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Jarogniew J Luszczki - One of the best experts on this subject based on the ideXlab platform.

  • Effects of arachidonyl-2’-chloroethylamide (ACEA) on the protective action of various antiepileptic drugs in the 6-Hz corneal stimulation model in mice
    2017
    Co-Authors: Jarogniew J Luszczki, Miroslaw Zagaja, Pawel Patrzylas, Marta Andres-mach, Katarzyna Zaluska, Maria W. Kondrat-wrobel, Monika Szpringer, Jaroslaw Chmielewski, Magdalena Florek-luszczki
    Abstract:

    Accumulating evidence indicates that cannabinoid CB1 receptor ligands play a pivotal role in seizures, not only in preclinical studies on animals, but also in clinical settings. This study was aimed at characterizing the influence of arachidonyl-2′-chloroethylamide (ACEA–a selective cannabinoid CB1 receptor agonist) co-administered with phenylmethylsulfonyl fluoride (PMSF) on the anticonvulsant potency of various antiepileptic drugs (clobazam, lacosamide, levetiracetam, phenobarbital, tiagabine and valproate) in the 6-Hz corneal stimulation model. Psychomotor seizures in male albino Swiss mice were evoked by a current (32 mA, 6 Hz, 3 s stimulus duration) delivered via corneal electrodes. Potential adverse effects produced by the antiepileptic drugs in combination with ACEA+PMSF were assessed using the chimney test (motor performance), passive avoidance task (remembering and acquisition of learning), and grip-strength test (muscular strength). Brain concentrations of antiepileptic drugs were measured by HPLC to exclude any pharmacokinetic contribution to the observed effect. ACEA (5 mg/kg, i.p.) + PMSF (30 mg/kg, i.p.) significantly potentiated the anticonvulsant potency of levetiracetam (P

  • Effects of arachidonyl-2’-chloroethylamide (ACEA) on the protective action of various antiepileptic drugs in the 6-Hz corneal stimulation model in mice - Fig 1
    2017
    Co-Authors: Jarogniew J Luszczki, Miroslaw Zagaja, Pawel Patrzylas, Marta Andres-mach, Katarzyna Zaluska, Maria W. Kondrat-wrobel, Monika Szpringer, Jaroslaw Chmielewski, Magdalena Florek-luszczki
    Abstract:

    A-L. Influence of ACEA, PMSF and their combination on the anticonvulsant activity of clobazam (CLB), lacosamide (LCM), levetiracetam (LEV), phenobarbital (PB), tiagabine (TGB) and valproate (VPA) in the 6-Hz corneal stimulation model in mice. Dose–response functions (sigmoidal curves) for the anticonvulsant activity of various antiepileptic drugs [CLB (A), LCM (C), LEV (E), PB (G), TGB (I) and VPA (K)] alone and in combination with ACEA and PMSF in the 6-Hz corneal stimulation model. Structural formulas of antiepileptic drugs are placed above sigmoidal curves. Each data point corresponds to percent of mice protected (n = 8 mice/data point) from the 6-Hz corneal stimulation model at a given dose (in mg/kg). Points of intersections with the dashed line at 50% reflect approximate ED50 values of antiepileptic drugs administered alone and in combination with ACEA and PMSF. Columns represent median effective doses (ED50 in mg/kg ± S.E.M.) of antiepileptic drugs [CLB (B), LCM (D), LEV (F), PB (H), TGB (J) and VPA (L)] that protected 50% of the mice from the 6-Hz corneal stimulation model. The log-probit method was used for calculating the ED50 values. Data were statistically analyzed with one-way ANOVA and post-hoc Tukey-Kramer test. *P

  • Effects of ACEA and PMSF in combinations with clobazam (CLB), lacosamide (LCM), levetiracetam (LEV) and tiagabine (TGB) on long-term memory in the passive avoidance task, muscular strength in the grip-strength test and motor performance in the chimne
    2017
    Co-Authors: Jarogniew J Luszczki, Miroslaw Zagaja, Pawel Patrzylas, Marta Andres-mach, Katarzyna Zaluska, Maria W. Kondrat-wrobel, Monika Szpringer, Jaroslaw Chmielewski, Magdalena Florek-luszczki
    Abstract:

    Effects of ACEA and PMSF in combinations with clobazam (CLB), lacosamide (LCM), levetiracetam (LEV) and tiagabine (TGB) on long-term memory in the passive avoidance task, muscular strength in the grip-strength test and motor performance in the chimney test in mice.

  • acea a highly selective cannabinoid cb1 receptor agonist stimulates hippocampal neurogenesis in mice treated with antiepileptic drugs
    Brain Research, 2015
    Co-Authors: Marta Andresmach, Agnieszka Haratymmaj, Radoslaw Rola, Magdalena Chrościnskakrawczyk, Miroslaw Zagaja, Jarogniew J Luszczki
    Abstract:

    Abstract Hippocampal neurogenesis plays a very important role in learning and memory functions. In a search for best neurological drugs that protect neuronal cells and stimulate neurogenesis with no side effects, cannabinoids proved to be a strong group of substances having many beneficial properties. The aim of this study was to evaluate the impact of ACEA (arachidonyl-2′-chloroethylamide—a highly selective cannabinoid CB1 receptor agonist) combined with a classical antiepileptic drug sodium valproate (VPA) on neural precursor cells׳ proliferation and differentiation in the mouse brain. All experiments were performed on adolescent CB57/BL male mice injected i.p. with VPA (10 mg/kg), ACEA (10 mg/kg) and PMSF (30 mg/kg) (phenylmethylsulfonyl fluoride—a substance protecting ACEA against degradation by the fatty-acid amidohydrolase) for 10 days. Next an acute response of proliferating neural precursor cells to ACEA and VPA administration was evaluated with Ki-67 staining (Time point 1). Next, in order to determine whether acute changes translated into long-term alterations in neurogenesis, proliferating cells were labeled with 5-bromo-2deoxyuridine (BrdU) followed by confocal microscopy used to determine the percentage of BrdU-labeled cells that showed mature cell phenotypes (Time point 2). Results indicate that ACEA with PMSF significantly increase the total number of Ki-67-positive cells when compared to the control group. Moreover, ACEA in combination with VPA increased the number of Ki-67-positive cells, whereas VPA administered alone had no impact on proliferating cells׳ population. Accordingly, neurogenesis study results indicate that the combination of ACEA+PMSF administered alone and in combination with VPA considerably increases the total number of BrdU-positive cells in comparison to the control group while ACEA+PMSF alone and in combination with VPA increased total numbers of BrdU-positive cells, newly born neurons and astrocytes as compared to VPA group but not to the control group. VPA administered alone decreased the number of newly born neurons with no significant impact on neurogenesis. These data provide substantial evidence that VPA administered chronically slightly decreases the proliferation and differentiation of newly born cells while combination of VPA+ACEA significantly increases the level of newborn neurons in the dentate subgranular zone.

  • effect of acea a selective cannabinoid cb1 receptor agonist on the protective action of different antiepileptic drugs in the mouse pentylenetetrazole induced seizure model
    Progress in Neuro-psychopharmacology & Biological Psychiatry, 2012
    Co-Authors: Marta Andresmach, Dorota Zolkowska, Agnieszka Haratymmaj, Magdalena Florekluszczki, Beata Barcickaklosowska, Jarogniew J Luszczki
    Abstract:

    Endogenous cannabinoid ligands and cannabinoid CB1 receptor agonists have been shown to exert anticonvulsant effects in various experimental models of epilepsy. The purpose of this study was to determine the effects of arachidonyl-2′-chloroethylamide (ACEA—a highly selective cannabinoid CB1 receptor agonist) on the protective action of clonazepam, ethosuximide, phenobarbital, and valproate against pentylenetetrazole (PTZ)-induced clonic seizures in mice. To ascertain any pharmacokinetic contribution of ACEA to the observed interactions between tested drugs, free (non-protein bound) plasma and total brain concentrations of the antiepileptic drugs were estimated. Additionally, acute adverse-effect profiles of the combination of ACEA and different classical antiepileptic drugs (clonazepam, ethosuximide, phenobarbital and valproate) with respect to motor performance, long-term memory and skeletal muscular strength were measured. Results indicated that ACEA (10 mg/kg, i.p.) co-administered with phenylmethylsulfonyl fluoride (PMSF—a substance protecting ACEA against degradation by the fatty-acid hydrolase; 30 mg/kg, i.p.) significantly potentiated the anticonvulsant activity of ethosuximide, phenobarbital and valproate in the mouse PTZ-induced clonic seizure model by reducing their median effective doses (ED50 values) from 122.8 mg/kg to 71.7 mg/kg (P < 0.01; for ethosuximide), from 13.77 mg/kg to 5.26 mg/kg (P < 0.05; for phenobarbital), and from 142.7 mg/kg to 87.3 mg/kg (P < 0.05; for valproate), respectively. In contrast, ACEA (10 mg/kg, i.p.) in combination with PMSF (30 mg/kg, i.p.) had no impact on the protective action of clonazepam against PTZ-induced seizures in mice. However, ACEA (10 mg/kg) + PMSF (30 mg/kg) considerably increased free plasma and total brain concentrations of ethosuximide and valproate in mice suggesting a pharmacokinetic nature of interaction between drugs. In contrast, free plasma and total brain concentrations of clonazepam and phenobarbital remained unchanged after ACEA + PMSF administration and thus, indicating pharmacodynamic interactions. Moreover, none of the examined combinations of ACEA (10 mg/kg, i.p.) + PMSF (30 mg/kg, i.p.) with clonazepam, ethosuximide, phenobarbital, and valproate (at their ED50 values from the PTZ-induced seizure test) affected motor coordination in the chimney test, long-term memory in the passive avoidance task, and muscular strength in the grip-strength test in mice, indicating no possible acute adverse effects in animals. In conclusion, pharmacodynamic enhancement of the anticonvulsant potency of phenobarbital by ACEA + PMSF is worthy of recommendation for further clinical settings. Pharmacokinetic interactions of ACEA + PMSF with ethosuximide and valproate seem to be responsible for a significant suppression of PTZ-induced seizures in mice. The combination of ACEA + PMSF with clonazepam seems to be neutral from a preclinical viewpoint.

Marta Andresmach - One of the best experts on this subject based on the ideXlab platform.

  • levetiracetam combined with acea highly selective cannabinoid cb1 receptor agonist changes neurogenesis in mouse brain
    Neuroscience Letters, 2019
    Co-Authors: Miroslaw Zagaja, Agnieszka Haratymmaj, Radoslaw Rola, Aleksandra Szewczyk, Jarogniew J. Łuszczki, Marta Andresmach
    Abstract:

    Abstract The aim of the study was to evaluate the impact of second generation antiepileptic drug levetiracetam (LEV) with arachidonyl-2′-chloroethylamide (ACEA) on proliferating neural precursor cells in mouse brain. Additionally, we established the relationship between treatment with ACEA in combination with LEV and hippocampal neurogenesis in mouse brain. All experiments were performed on male CB57/BL mice injected i.p. with LEV (10 mg/kg), ACEA (10 mg/kg) and PMSF (30 mg/kg) for 10 days. Experiments were provided in two stages: stage 1- an acute response of proliferating neural precursor cells to ACEA and LEV administration (Ki-67 staining), stage 2 – a long term response to ACEA and LEV administration (BrDU, NeuN, GFAP staining). Results indicate that ACEA + PMSF and ACEA + PMSF + LEV significantly increased the total number of Ki-67 positive cells comparing to the control group. PMSF and LEV administered alone and in combination had no significant impact on cell proliferation compared to the control group. Results from neurogenesis study indicated that ACEA + PMSF administered alone and in combination with LEV increased the total number of BrDU cells compared to the control group, although LEV on its own decreased the number of BrDU cells. Moreover, the combination of ACEA + PMSF + LEV significantly increased the total number of newborn neurons compared to the control group. In turn, LEV significantly decreased the process of neurogenesis. Astrocytes were considerably reduced in all treated groups as compare to the control mice. These data provide substantial evidence that LEV administered chronically decreases the proliferation and differentiation of newly born cells while combination of LEV + ACEA significantly increases the level of newborn neurons in the dentate subgranular zone.

  • acea a highly selective cannabinoid cb1 receptor agonist stimulates hippocampal neurogenesis in mice treated with antiepileptic drugs
    Brain Research, 2015
    Co-Authors: Marta Andresmach, Agnieszka Haratymmaj, Radoslaw Rola, Magdalena Chrościnskakrawczyk, Miroslaw Zagaja, Jarogniew J Luszczki
    Abstract:

    Abstract Hippocampal neurogenesis plays a very important role in learning and memory functions. In a search for best neurological drugs that protect neuronal cells and stimulate neurogenesis with no side effects, cannabinoids proved to be a strong group of substances having many beneficial properties. The aim of this study was to evaluate the impact of ACEA (arachidonyl-2′-chloroethylamide—a highly selective cannabinoid CB1 receptor agonist) combined with a classical antiepileptic drug sodium valproate (VPA) on neural precursor cells׳ proliferation and differentiation in the mouse brain. All experiments were performed on adolescent CB57/BL male mice injected i.p. with VPA (10 mg/kg), ACEA (10 mg/kg) and PMSF (30 mg/kg) (phenylmethylsulfonyl fluoride—a substance protecting ACEA against degradation by the fatty-acid amidohydrolase) for 10 days. Next an acute response of proliferating neural precursor cells to ACEA and VPA administration was evaluated with Ki-67 staining (Time point 1). Next, in order to determine whether acute changes translated into long-term alterations in neurogenesis, proliferating cells were labeled with 5-bromo-2deoxyuridine (BrdU) followed by confocal microscopy used to determine the percentage of BrdU-labeled cells that showed mature cell phenotypes (Time point 2). Results indicate that ACEA with PMSF significantly increase the total number of Ki-67-positive cells when compared to the control group. Moreover, ACEA in combination with VPA increased the number of Ki-67-positive cells, whereas VPA administered alone had no impact on proliferating cells׳ population. Accordingly, neurogenesis study results indicate that the combination of ACEA+PMSF administered alone and in combination with VPA considerably increases the total number of BrdU-positive cells in comparison to the control group while ACEA+PMSF alone and in combination with VPA increased total numbers of BrdU-positive cells, newly born neurons and astrocytes as compared to VPA group but not to the control group. VPA administered alone decreased the number of newly born neurons with no significant impact on neurogenesis. These data provide substantial evidence that VPA administered chronically slightly decreases the proliferation and differentiation of newly born cells while combination of VPA+ACEA significantly increases the level of newborn neurons in the dentate subgranular zone.

  • effect of acea a selective cannabinoid cb1 receptor agonist on the protective action of different antiepileptic drugs in the mouse pentylenetetrazole induced seizure model
    Progress in Neuro-psychopharmacology & Biological Psychiatry, 2012
    Co-Authors: Marta Andresmach, Dorota Zolkowska, Agnieszka Haratymmaj, Magdalena Florekluszczki, Beata Barcickaklosowska, Jarogniew J Luszczki
    Abstract:

    Endogenous cannabinoid ligands and cannabinoid CB1 receptor agonists have been shown to exert anticonvulsant effects in various experimental models of epilepsy. The purpose of this study was to determine the effects of arachidonyl-2′-chloroethylamide (ACEA—a highly selective cannabinoid CB1 receptor agonist) on the protective action of clonazepam, ethosuximide, phenobarbital, and valproate against pentylenetetrazole (PTZ)-induced clonic seizures in mice. To ascertain any pharmacokinetic contribution of ACEA to the observed interactions between tested drugs, free (non-protein bound) plasma and total brain concentrations of the antiepileptic drugs were estimated. Additionally, acute adverse-effect profiles of the combination of ACEA and different classical antiepileptic drugs (clonazepam, ethosuximide, phenobarbital and valproate) with respect to motor performance, long-term memory and skeletal muscular strength were measured. Results indicated that ACEA (10 mg/kg, i.p.) co-administered with phenylmethylsulfonyl fluoride (PMSF—a substance protecting ACEA against degradation by the fatty-acid hydrolase; 30 mg/kg, i.p.) significantly potentiated the anticonvulsant activity of ethosuximide, phenobarbital and valproate in the mouse PTZ-induced clonic seizure model by reducing their median effective doses (ED50 values) from 122.8 mg/kg to 71.7 mg/kg (P < 0.01; for ethosuximide), from 13.77 mg/kg to 5.26 mg/kg (P < 0.05; for phenobarbital), and from 142.7 mg/kg to 87.3 mg/kg (P < 0.05; for valproate), respectively. In contrast, ACEA (10 mg/kg, i.p.) in combination with PMSF (30 mg/kg, i.p.) had no impact on the protective action of clonazepam against PTZ-induced seizures in mice. However, ACEA (10 mg/kg) + PMSF (30 mg/kg) considerably increased free plasma and total brain concentrations of ethosuximide and valproate in mice suggesting a pharmacokinetic nature of interaction between drugs. In contrast, free plasma and total brain concentrations of clonazepam and phenobarbital remained unchanged after ACEA + PMSF administration and thus, indicating pharmacodynamic interactions. Moreover, none of the examined combinations of ACEA (10 mg/kg, i.p.) + PMSF (30 mg/kg, i.p.) with clonazepam, ethosuximide, phenobarbital, and valproate (at their ED50 values from the PTZ-induced seizure test) affected motor coordination in the chimney test, long-term memory in the passive avoidance task, and muscular strength in the grip-strength test in mice, indicating no possible acute adverse effects in animals. In conclusion, pharmacodynamic enhancement of the anticonvulsant potency of phenobarbital by ACEA + PMSF is worthy of recommendation for further clinical settings. Pharmacokinetic interactions of ACEA + PMSF with ethosuximide and valproate seem to be responsible for a significant suppression of PTZ-induced seizures in mice. The combination of ACEA + PMSF with clonazepam seems to be neutral from a preclinical viewpoint.

  • effect of arachidonyl 2 chloroethylamide a selective cannabinoid cb1 receptor agonist on the protective action of the various antiepileptic drugs in the mouse maximal electroshock induced seizure model
    Progress in Neuro-psychopharmacology & Biological Psychiatry, 2010
    Co-Authors: Jarogniew J Luszczki, Monika Dudrajastrzebska, Piotr Czuczwar, Anna Cioczekczuczwar, Marta Andresmach
    Abstract:

    Abstract The aim of this study was to determine the influence of arachidonyl-2′-chloroethylamide (ACEA — a highly selective cannabinoid type 1 [CB1] receptor agonist) on the protective action and acute adverse effects of carbamazepine, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, and topiramate in the maximal electroshock seizure model and chimney test in mice. Tonic hind limb extension (seizure activity) was evoked in adult male albino Swiss mice by a current (sine-wave, 25 mA, 500 V, 50 Hz, 0.2 s stimulus duration) delivered via auricular electrodes. Acute adverse-effect profiles of the studied antiepileptic drugs with respect to motor coordination was assessed in the chimney test. Additionally, long-term memory and skeletal muscular strength were measured along with free plasma (non-protein bound) and total brain antiepileptic drug concentrations. To inhibit the rapid metabolic degradation of ACEA by the fatty-acid amide hydrolase, phenylmethylsulfonyl fluoride (PMSF) was used at a constant ineffective dose of 30 mg/kg. Results indicate that ACEA (2.5 mg/kg, i.p.) co-administered with PMSF (30 mg/kg, i.p.), significantly enhanced the anticonvulsant activity of phenobarbital, but not that of carbamazepine, lamotrigine, oxcarbazepine, phenytoin, or topiramate in the maximal electroshock seizure test in mice. Moreover, ACEA (2.5 mg/kg) with PMSF (30 mg/kg) had no significant impact on the acute adverse effects of all examined antiepileptic drugs in the chimney test in mice. The protective index values (as quotients of the respective TD 50 and ED 50 values denoted from the chimney and maximal electroshock seizure tests, respectively) for the combinations of ACEA (2.5 mg/kg) and PMSF (30 mg/kg) with carbamazepine, oxcarbazepine, phenobarbital, and topiramate were greater than those denoted for the antiepileptic drugs administered alone. Only, the protective index values for the combination of ACEA (2.5 mg/kg) and PMSF (30 mg/kg) with lamotrigine and phenytoin were lower than those determined for the antiepileptic drugs administered alone. Pharmacokinetic experiments revealed that ACEA (2.5 mg/kg) and PMSF (30 mg/kg) affected neither free plasma (non-protein bound) nor total brain concentrations of phenobarbital in mice. Moreover, ACEA and PMSF in combination with carbamazepine, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, and topiramate did not alter long-term memory or skeletal muscular strength in experimental animals. In conclusion, the enhanced anticonvulsant action of phenobarbital by ACEA and PMSF, lack of pharmacokinetic interaction and no acute adverse effects between the examined compounds, make the combination of ACEA and PMSF with phenobarbital of pivotal importance for further experimental and clinical studies. The combinations of ACEA and PMSF with carbamazepine, lamotrigine, oxcarbazepine, phenytoin, and topiramate are neutral from a preclinical viewpoint.

Jos R C Jansen - One of the best experts on this subject based on the ideXlab platform.

  • bedside assessment of total systemic vascular compliance stressed volume and cardiac function curves in intensive care unit patients
    Anesthesia & Analgesia, 2012
    Co-Authors: Jacinta J Maas, Leon Aarts, Michael R Pinsky, Jos R C Jansen
    Abstract:

    Background: Mean systemic filling pressure (PMSF) can be measured at the bedside with minimally invasive monitoring in ventilator-dependent patients using inspiratory hold maneuvers (PMSFhold) as the zero flow intercept of cardiac output (CO) to central venous pressure (CVP) relation. We compared PMSFhold with arm vascular equilibrium pressure during vascular occlusion (PMSFarm) and their ability to assess systemic vascular compliance (Csys) and stressed volume by intravascular fluid administration. Methods: In mechanically ventilated postoperative cardiac surgery patients, inspiratory holds at varying airway pressures and arm stop-flow maneuvers were performed during normovolemia and after each of 10 sequential 50-mL bolus colloid infusions. We measured CVP, PMSFarm, stroke volume, and CO during fluid administration steps to construct CVP to CO (cardiac function) curves and Δvolume/ΔPMSF (compliance) curves. PMSFhold was measured before and after fluid administration. Stressed volume was determined by extrapolating the PMSF-volume curve to zero pressure intercept. Results: Fifteen patients were included. PMSFhold and PMSF arm were closely correlated. Csys was linear (64.3 ± 32.7 mL • mm Hg, 0.97 ± 0.49 mL • mm Hg • kg predicted body weight). Stressed volume was estimated to be 1265 ± 541 mL (28.5% ± 15% predicted total blood volume). Cardiac function curves of patients with an increase of >12% to 500 mL volume extension (volume responsive) were steep, whereas the cardiac function curves of the remaining patients were flat. Conclusions: Csys, stressed volume, and cardiac function curves can be determined at the bedside and can be used to characterize patients' hemodynamic status. Copyright © 2012 International Anesthesia Research Society.

  • determination of vascular waterfall phenomenon by bedside measurement of mean systemic filling pressure and critical closing pressure in the intensive care unit
    Anesthesia & Analgesia, 2012
    Co-Authors: Jacinta J Maas, Rob B P De Wilde, Leon Aarts, Michael R Pinsky, Jos R C Jansen
    Abstract:

    BACKGROUND: Mean systemic filling pressure (PMSF) can be determined at the bedside by measuring central venous pressure (Pcv) and cardiac output (CO) during inspiratory hold maneuvers. Critical closing pressure (Pcc) can be determined using the same method measuring arterial pressure (Pa) and CO. If Pcc > PMSF, there is then a vascular waterfall. In this study, we assessed the existence of a waterfall and its implications for the calculation of vascular resistances by determining PMSF and Pcc at the bedside. METHODS: In 10 mechanically ventilated postcardiac surgery patients, inspiratory hold maneuvers were performed, transiently increasing Pcv and decreasing Pa and CO to 4 different steady-state levels. For each patient, values of Pcv and CO were plotted in a venous return curve to determine PMSF. Similarly, Pcc was determined with a ventricular output curve plotted for Pa and CO. Measurements were performed in each patient before and after volume expansion with 0.5 L colloid, and vascular resistances were calculated. RESULTS: For every patient, the relationship between the 4 measurements of Pcv and CO and of Pa and CO was linear. Baseline PMSF was 18.7 ± 4.0 mm Hg (mean ± SD) and differed significantly from Pcc 45.5 ± 11.1 mm Hg (P < 0.0001). The difference of Pcc and PMSF was 26.8 ± 10.7 mm Hg, indicating the presence of a systemic vascular waterfall. Volume expansion increased PMSF (26.3 ± 3.2 mm Hg), Pcc (51.5 ± 9.0 mm Hg), and CO (5.5 ± 1.8 to 6.8 ± 1.8 L · min). Arterial (upstream of Pcc) and venous (downstream of PMSF) vascular resistance were 8.27 ± 4.45 and 2.75 ± 1.23 mm Hg · min · L; the sum of both (11.01 mm Hg · min · L) was significantly different from total systemic vascular resistance (16.56 ± 8.57 mm Hg · min · L; P = 0.005). Arterial resistance was related to total resistance. CONCLUSIONS: Vascular pressure gradients in cardiac surgery patients suggest the presence of a vascular waterfall phenomenon, which is not affected by CO. Thus, measures of total systemic vascular resistance may become irrelevant in assessing systemic vasomotor tone. Copyright © 2012 International Anesthesia Research Society.

  • evaluation of mean systemic filling pressure from pulse contour cardiac output and central venous pressure
    Journal of Clinical Monitoring and Computing, 2011
    Co-Authors: Jacinta J Maas, Bart F Geerts, Jos R C Jansen
    Abstract:

    Objective The volemic status of a patient can be determined by measuring mean systemic filling pressure (PMSF). PMSF is obtained from the venous return curve, i.e. the relationship between central venous pressure (Pcv) and blood flow. We evaluated the feasibility and precision of PMSF measurement.

  • assessment of venous return curve and mean systemic filling pressure in postoperative cardiac surgery patients
    Critical Care Medicine, 2009
    Co-Authors: Jacinta J Maas, Michael R Pinsky, Bart F Geerts, Paul C M Van Den Berg, Jos R C Jansen
    Abstract:

    OBJECTIVE:: To measure the relationship between blood flow and central venous pressure (Pcv) and to estimate mean systemic filling pressure (PMSF), circulatory compliance, and stressed volume in patients in the intensive care unit. DESIGN:: Intervention study. SETTING:: Intensive care unit of a university hospital. PATIENTS:: Twelve mechanically ventilated postoperative cardiac surgery patients. INTERVENTIONS:: Inspiratory holds were performed during normovolemia in supine position (baseline), relative hypovolemia by placing the patients in 30 degree head-up position (hypo), and relative hypervolemia by volume loading with 0.5 L colloid (hyper). MEASUREMENTS AND MAIN RESULTS:: We measured the relationship between blood flow and Pcv using 12-second inspiratory-hold maneuvers transiently increasing Pcv to three different steady-state levels and monitored the resultant blood flow via the pulse contour method during the last 3 seconds. The Pcv to blood flow relation was linear for all measurements with a slope unaltered by relative volume status. PMSF decreased with hypo and increased with hyper (18.8 ± 4.5 mm Hg, to 14.5 ± 3.0 mm Hg, to 29.1 ± 5.2 mm Hg [baseline, hypo, hyper, respectively, p < 0.05]). Baseline total circulatory compliance was 0.98 mL•mm Hg•kg and stressed volume was 1677 mL. CONCLUSIONS:: PMSF can be determined in intensive care patients with an intact circulation with use of inspiratory pause procedures, making serial measures of circulatory compliance and circulatory stressed volume feasible. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

Jacinta J Maas - One of the best experts on this subject based on the ideXlab platform.

  • bedside assessment of total systemic vascular compliance stressed volume and cardiac function curves in intensive care unit patients
    Anesthesia & Analgesia, 2012
    Co-Authors: Jacinta J Maas, Leon Aarts, Michael R Pinsky, Jos R C Jansen
    Abstract:

    Background: Mean systemic filling pressure (PMSF) can be measured at the bedside with minimally invasive monitoring in ventilator-dependent patients using inspiratory hold maneuvers (PMSFhold) as the zero flow intercept of cardiac output (CO) to central venous pressure (CVP) relation. We compared PMSFhold with arm vascular equilibrium pressure during vascular occlusion (PMSFarm) and their ability to assess systemic vascular compliance (Csys) and stressed volume by intravascular fluid administration. Methods: In mechanically ventilated postoperative cardiac surgery patients, inspiratory holds at varying airway pressures and arm stop-flow maneuvers were performed during normovolemia and after each of 10 sequential 50-mL bolus colloid infusions. We measured CVP, PMSFarm, stroke volume, and CO during fluid administration steps to construct CVP to CO (cardiac function) curves and Δvolume/ΔPMSF (compliance) curves. PMSFhold was measured before and after fluid administration. Stressed volume was determined by extrapolating the PMSF-volume curve to zero pressure intercept. Results: Fifteen patients were included. PMSFhold and PMSF arm were closely correlated. Csys was linear (64.3 ± 32.7 mL • mm Hg, 0.97 ± 0.49 mL • mm Hg • kg predicted body weight). Stressed volume was estimated to be 1265 ± 541 mL (28.5% ± 15% predicted total blood volume). Cardiac function curves of patients with an increase of >12% to 500 mL volume extension (volume responsive) were steep, whereas the cardiac function curves of the remaining patients were flat. Conclusions: Csys, stressed volume, and cardiac function curves can be determined at the bedside and can be used to characterize patients' hemodynamic status. Copyright © 2012 International Anesthesia Research Society.

  • determination of vascular waterfall phenomenon by bedside measurement of mean systemic filling pressure and critical closing pressure in the intensive care unit
    Anesthesia & Analgesia, 2012
    Co-Authors: Jacinta J Maas, Rob B P De Wilde, Leon Aarts, Michael R Pinsky, Jos R C Jansen
    Abstract:

    BACKGROUND: Mean systemic filling pressure (PMSF) can be determined at the bedside by measuring central venous pressure (Pcv) and cardiac output (CO) during inspiratory hold maneuvers. Critical closing pressure (Pcc) can be determined using the same method measuring arterial pressure (Pa) and CO. If Pcc > PMSF, there is then a vascular waterfall. In this study, we assessed the existence of a waterfall and its implications for the calculation of vascular resistances by determining PMSF and Pcc at the bedside. METHODS: In 10 mechanically ventilated postcardiac surgery patients, inspiratory hold maneuvers were performed, transiently increasing Pcv and decreasing Pa and CO to 4 different steady-state levels. For each patient, values of Pcv and CO were plotted in a venous return curve to determine PMSF. Similarly, Pcc was determined with a ventricular output curve plotted for Pa and CO. Measurements were performed in each patient before and after volume expansion with 0.5 L colloid, and vascular resistances were calculated. RESULTS: For every patient, the relationship between the 4 measurements of Pcv and CO and of Pa and CO was linear. Baseline PMSF was 18.7 ± 4.0 mm Hg (mean ± SD) and differed significantly from Pcc 45.5 ± 11.1 mm Hg (P < 0.0001). The difference of Pcc and PMSF was 26.8 ± 10.7 mm Hg, indicating the presence of a systemic vascular waterfall. Volume expansion increased PMSF (26.3 ± 3.2 mm Hg), Pcc (51.5 ± 9.0 mm Hg), and CO (5.5 ± 1.8 to 6.8 ± 1.8 L · min). Arterial (upstream of Pcc) and venous (downstream of PMSF) vascular resistance were 8.27 ± 4.45 and 2.75 ± 1.23 mm Hg · min · L; the sum of both (11.01 mm Hg · min · L) was significantly different from total systemic vascular resistance (16.56 ± 8.57 mm Hg · min · L; P = 0.005). Arterial resistance was related to total resistance. CONCLUSIONS: Vascular pressure gradients in cardiac surgery patients suggest the presence of a vascular waterfall phenomenon, which is not affected by CO. Thus, measures of total systemic vascular resistance may become irrelevant in assessing systemic vasomotor tone. Copyright © 2012 International Anesthesia Research Society.

  • evaluation of mean systemic filling pressure from pulse contour cardiac output and central venous pressure
    Journal of Clinical Monitoring and Computing, 2011
    Co-Authors: Jacinta J Maas, Bart F Geerts, Jos R C Jansen
    Abstract:

    Objective The volemic status of a patient can be determined by measuring mean systemic filling pressure (PMSF). PMSF is obtained from the venous return curve, i.e. the relationship between central venous pressure (Pcv) and blood flow. We evaluated the feasibility and precision of PMSF measurement.

  • assessment of venous return curve and mean systemic filling pressure in postoperative cardiac surgery patients
    Critical Care Medicine, 2009
    Co-Authors: Jacinta J Maas, Michael R Pinsky, Bart F Geerts, Paul C M Van Den Berg, Jos R C Jansen
    Abstract:

    OBJECTIVE:: To measure the relationship between blood flow and central venous pressure (Pcv) and to estimate mean systemic filling pressure (PMSF), circulatory compliance, and stressed volume in patients in the intensive care unit. DESIGN:: Intervention study. SETTING:: Intensive care unit of a university hospital. PATIENTS:: Twelve mechanically ventilated postoperative cardiac surgery patients. INTERVENTIONS:: Inspiratory holds were performed during normovolemia in supine position (baseline), relative hypovolemia by placing the patients in 30 degree head-up position (hypo), and relative hypervolemia by volume loading with 0.5 L colloid (hyper). MEASUREMENTS AND MAIN RESULTS:: We measured the relationship between blood flow and Pcv using 12-second inspiratory-hold maneuvers transiently increasing Pcv to three different steady-state levels and monitored the resultant blood flow via the pulse contour method during the last 3 seconds. The Pcv to blood flow relation was linear for all measurements with a slope unaltered by relative volume status. PMSF decreased with hypo and increased with hyper (18.8 ± 4.5 mm Hg, to 14.5 ± 3.0 mm Hg, to 29.1 ± 5.2 mm Hg [baseline, hypo, hyper, respectively, p < 0.05]). Baseline total circulatory compliance was 0.98 mL•mm Hg•kg and stressed volume was 1677 mL. CONCLUSIONS:: PMSF can be determined in intensive care patients with an intact circulation with use of inspiratory pause procedures, making serial measures of circulatory compliance and circulatory stressed volume feasible. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

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  • effect of phenylmethyl sulfonylfluoride PMSF on total differential expression proteins in the spinal cord tissue of tocp treated hens
    Chinese Journal of Public Health, 2011
    Co-Authors: Piao Fengyuan
    Abstract:

    Objective To screen differential expression proteins in the lumbar spinal cord tissue of triorthocresyl phosphate(TOCP)-treated hens and to provide evidence for mass spectroscopy.Methods Twenty-four adult Roman hens were randomly divided into three groups and 8 hens in each group.The hens in TOCP group were treated with a single oral dosage of 1 000 mg/kg TOCP.The hens in the PMSF intervention group first were given 40 mg/kg PMSF and then treated with 1 000 mg/kg TOCP 24 hours later.The control group received the same volume of sodium chloride.On the 5th day after the exposure,the hens were sacrificed and their lumbar spinal cord tissue were dissected and homogenized in ice bath.Total proteins of the lumbar spinal cord tissue were separated by isoelectric focusing as the first dimension and sodium dodecyl sulfate-ployacrylanide gel electrophoresis(SDS-PAGE) as the second dimension.The two-dimensional electrophoresis maps were visualized after silver staining and analyzed by Image Master 2D software.Results According to the PMSF features,there were 23 up and 113 down protein match spots in TOCP group,which were significantly different compared with those of the control group,and there was no significant difference compared with that of PMSF intervention group.The up and down protein spots with the changes of more than 4 folds were 7 and 10.Conclusion The 7 up and 10 down differential expression proteins in the lumbar spinal cord of TOCP-treated hens may be closely involved in the pathogenesis of organophosphorus ester-induced delayed neurotoxicity(OPIDN).

  • effect of PMSF on gene expression profiles in the brain tissue of tocp treated hens
    Journal of Dalian Medical University, 2010
    Co-Authors: Wang Xianghu, Piao Fengyuan
    Abstract:

    [Objective] To screen the organophosphorus-induced delayed neurotoxicity(OPIDN)-related genes from the brain tissue of tri-ortho-cresyl phosphate(TOCP)-treated hens by means of pretreatment of phenylmethylsulfonyl fluoride(PMSF) and to provide the information of target gene profiles for exploring mechanisms of OPIDN.[Methods] Twelve hens were randomly divided into three groups including TOCP group,PMSF interfering group and control group.Hens in the TOCP group were treated with 1000 mg/kg TOCP.Hens in the PMSF interfering group were given with TOCP after 40 mg / kg PMSF administration.The hensin control group were received the saline.On the 5th day,the hens were sacrificed.The brains were dissected and homogenized.Total RNA in the brain tissue was extracted,purifled,and transcribed to cRNA probe.Then cRNA probe was biotin labeled and hybridized with Chicken Genome 430 2.0 Araay.Hybridization signals were scaned and genechip data was analyzed.[Results] It was found that 311 genes were significant difference compared with control group,but no significant difference compared with PMSF interfering group.There were 36 genes over 3 fold expressions among these genes found.[Conclusion] The 311 genes may be related to OPIDN in the brain tissue of TOCP-treated hens.Among these genes,the 36 genes may be closely associated with OPIDN.