The Experts below are selected from a list of 5313 Experts worldwide ranked by ideXlab platform

Kenneth D Mitchell - One of the best experts on this subject based on the ideXlab platform.

  • enhancement of renin and prorenin receptor in collecting duct of cyp1a1 ren2 rats may contribute to development and progression of Malignant Hypertension
    American Journal of Physiology-renal Physiology, 2011
    Co-Authors: Minolfa C Prieto, Dustyn E Williams, John J Mullins, Liu Liu, Kimberly L Kavanagh, Kenneth D Mitchell
    Abstract:

    To determine whether in the transgenic rat model [TGR(Cyp1a1Ren2)] with inducible ANG II-dependent Malignant Hypertension changes in the activation of intrarenal renin-angiotensin system may contribute to the pathogenesis of Hypertension, we examined the gene expression of angiotensinogen (AGT) in renal cortical tissues and renin and prorenin receptor [(P)RR] in the collecting duct (CD) of the kidneys from Cyp1a1Ren2 rats (n = 6) fed a normal diet containing 0.3% indole-3-carbinol (I3C) for 10 days and noninduced rats maintained on a normal diet (0.6% NaCl diet; n = 6). Rats induced with I3C developed Malignant Hypertension and exhibited alterations in the expression of renin and (P)RR expressed by the CD cells. In the renal medullary tissues of the Cyp1a1Ren2 transgenic rats with Malignant Hypertension, renin protein levels in CD cells were associated with maintained renin content and lack of suppression of the endogenous Ren1c gene expression. Furthermore, these tissues exhibited increased levels of (P)RR transcript, as well as of the protein levels of the soluble form of this receptor, the s(P)RR. Intriguingly, although previous findings demonstrated that urinary AGT excretion is augmented in Cyp1a1Ren2 transgenic rats with Malignant Hypertension, in the present study we did not find changes in the gene expression of AGT in renal cortical tissues of these rats. The data suggest that upregulation of renin and the s(P)RR in the CD, especially in the renal medullary tissues of Cyp1a1Ren2 transgenic rats with Malignant Hypertension, along with the previously demonstrated increased availability of AGT in the urine of these rats, may constitute a leading mechanism to explain elevated formation of kidney ANG II levels in this model of ANG II-dependent Hypertension.

  • transient induction of ang ii dependent Malignant Hypertension causes sustained elevation of blood pressure and augmentation of the pressor response to ang ii in cyp1a1 ren2 transgenic rats
    The American Journal of the Medical Sciences, 2010
    Co-Authors: Catherine G Howard, John J Mullins, Kenneth D Mitchell
    Abstract:

    Abstract Introduction Transgenic rats with inducible expression of the mouse Ren2 renin gene [strain name: TGR(Cyp1a1Ren2)] allow induction of various degrees of ANG II-dependent Hypertension. Dietary administration of the aryl hydrocarbon indole-3-carbinol (I3C) at a dose of 0.15% induces a slowly developing form of ANG II-dependent Hypertension, whereas dietary administration of a higher dose (0.3%) of I3C results in the development of ANG II-dependent Malignant Hypertension. Cessation of administration of 0.15% I3C results in the normalization of blood pressure, indicating the reversibility of Hypertension induced by this dose of I3C. The present study was performed to determine if ANG II-dependent Malignant Hypertension is similarly reversible following cessation of dietary administration of 0.3% I3C. Methods Cyp1a1-Ren2 rats (n = 6) were fed a normal diet containing 0.3% I3C for 11 days to induce Malignant Hypertension. Results Cyp1a1-Ren2 rats induced with I3C exhibited pronounced increases in systolic blood pressure (SBP) (132 ± 3–229 ± 11 mm Hg, P P P P P P Conclusions The present findings demonstrate that transient induction of ANG II-dependent Malignant Hypertension results in prolonged elevations of arterial blood pressure and marked augmentation of the magnitude of the pressor response to ANG II in Cyp1a1-Ren2 transgenic rats.

  • at1 receptor blockade prevents the increase in blood pressure and the augmentation of intrarenal ang ii levels in hypertensive cyp1a1 ren2 transgenic rats fed with a high salt diet
    The American Journal of the Medical Sciences, 2010
    Co-Authors: Dustyn E Williams, Gabriel L Navar, Minolfa C Prieto, Kenneth D Mitchell, John J Mullins
    Abstract:

    Abstract Introduction This study was performed to determine the effects of high-salt diet on the magnitude of the increases in systolic blood pressure (SBP) and kidney tissue angiotensin (ANG) II levels that occur after induction of ANG II-dependent Malignant Hypertension in Cyp1a1-Ren2 transgenic rats with inducible expression of the mouse Ren2 renin gene [strain name: TGR(Cyp1a1Ren2)]. Methods Cyp1a1- Ren2 rats (n=6) were fed a normal diet containing 0.3% indole-3- carbinol (I3C) for 10days to induce ANG II-dependent Malignant Hypertension. Results Rats induced with I3C exhibited increases in SBP and elevations of ANG II levels in kidney cortex and medulla. In a second group of rats (n=6), high-salt intake alone did not alter basal SBP; however, subsequent dietary administration of 0.3% I3C during continued high-salt intake elicited a substantially greater increase in SBP than observed in rats fed a normal salt diet. ANG II levels in kidney cortex and medulla of rats induced with I3C and fed a high-salt diet were elevated similarly to those in rats induced with I3C alone. Chronic administration of the AT 1 receptor antagonist, losartan (100mg/L in drinking water, n=6), markedly attenuated the I3C-induced increase in SBP and prevented the augmentation of ANG II levels in kidney cortex and medulla in rats induced with I3C and maintained on a high-salt diet. Conclusions Activation of AT 1 receptors contributes to the augmented blood pressure and elevated kidney tissue ANG II levels that occur in Cyp1a1-Ren2 transgenic rats with Malignant Hypertension maintained on a high-salt diet.

Johannes J Van Lieshout - One of the best experts on this subject based on the ideXlab platform.

  • Cerebral Hemodynamics During Treatment With Sodium Nitroprusside Versus Labetalol in Malignant Hypertension
    2016
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    Abstract—In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler–determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n8) or labetalol (n7). The reduction in mean arterial blood pressure with sodium nitroprusside (283%; meanSEM) and labetalol (284%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (1310% and 175%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (534 % and74%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.450.05 % versus 0.780.04 % cm s1 %mm Hg1; P0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flo

  • cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in Malignant Hypertension
    Hypertension, 2008
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler-determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n=8) or labetalol (n=7). The reduction in mean arterial blood pressure with sodium nitroprusside (-28+/-3%; mean+/-SEM) and labetalol (-28+/-4%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (-13+/-10% and -17+/-5%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (-53+/-4% and -7+/-4%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.45+/-0.05% versus 0.78+/-0.04% cm.s(-1).%mm Hg(-1); P<0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flow to the low resistance systemic vascular bed rather than the cerebral vascular bed.

  • impaired cerebral autoregulation in patients with Malignant Hypertension
    Circulation, 2004
    Co-Authors: Rogier V Immink, John M Karemaker, Bertjan H Van Den Born, Gert A Van Montfrans, Richard P. Koopmans, Johannes J Van Lieshout
    Abstract:

    Background— In patients with a Malignant Hypertension, immediate parenteral treatment with blood pressure–lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients. Methods and Results— In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA Vmean to MAP phase lead and static CA as the MCA Vmean to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA Vmean to MAP phase lead was lower (30±8° versus 58±5°, mean±SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA Vmean decrease was 22±4%, along with...

Gert A Van Montfrans - One of the best experts on this subject based on the ideXlab platform.

  • Cerebral Hemodynamics During Treatment With Sodium Nitroprusside Versus Labetalol in Malignant Hypertension
    2016
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    Abstract—In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler–determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n8) or labetalol (n7). The reduction in mean arterial blood pressure with sodium nitroprusside (283%; meanSEM) and labetalol (284%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (1310% and 175%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (534 % and74%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.450.05 % versus 0.780.04 % cm s1 %mm Hg1; P0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flo

  • Microangiopathic Hemolysis and Renal Failure in Malignant Hypertension
    2016
    Co-Authors: Bert Jan, H. Born, Uwkje P. F. Honnebier, Richard P. Koopmans, Gert A Van Montfrans
    Abstract:

    Abstract—Renal dysfunction is an important cause of morbidity and mortality in patients with Malignant Hypertension. Microangiopathic hemolysis (MAHA) related to Malignant Hypertension may cause renal insufficiency by obstruction of interlobular arteries. We hypothesized that the presence of MAHA is an important indicator of renal dysfunction and recovery in Malignant Hypertension. We retrospectively analyzed 97 patients admitted between April 1994 and April 2004 with Malignant Hypertension. MAHA was defined as a low platelet count (150109/L) with either an elevated lactic dehydrogenase (220 U/L) or presence of schistocytes. MAHA was present in 26 of 97 patients (27%). Serum creatinine levels at admission were significantly higher in those with than in those without MAHA: median serum creatinine 690 mol/L (interquartile range [IQR] 394 to 1105) and 120 mol/L (IQR 82 to 211), respectively (P0.01). Macroalbuminuria was present in 88 % with versus 41 % without MAHA (P0.01). Patients with MAHA were more often black (73%; P0.01) and had higher systolic blood pressure (mean 242 mm Hg versus 225 mm Hg; P0.01). Dialysis was needed in 15 patients with MAHA (58%) versus 2 patients (3%) without MAHA. In 6 patients with MAHA, dialysis could be stopped. Cox regression analysis showed that MAHA and systolic blood pressure were the most important indicators of renal improvement during follow-up, with a hazard ratio of 0.24 (95 % confidence interva

  • cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in Malignant Hypertension
    Hypertension, 2008
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler-determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n=8) or labetalol (n=7). The reduction in mean arterial blood pressure with sodium nitroprusside (-28+/-3%; mean+/-SEM) and labetalol (-28+/-4%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (-13+/-10% and -17+/-5%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (-53+/-4% and -7+/-4%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.45+/-0.05% versus 0.78+/-0.04% cm.s(-1).%mm Hg(-1); P<0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flow to the low resistance systemic vascular bed rather than the cerebral vascular bed.

  • microangiopathic hemolysis and renal failure in Malignant Hypertension
    Hypertension, 2005
    Co-Authors: Bertjan H Van Den Born, Uwkje P. F. Honnebier, Richard P. Koopmans, Gert A Van Montfrans
    Abstract:

    Renal dysfunction is an important cause of morbidity and mortality in patients with Malignant Hypertension. Microangiopathic hemolysis (MAHA) related to Malignant Hypertension may cause renal insufficiency by obstruction of interlobular arteries. We hypothesized that the presence of MAHA is an important indicator of renal dysfunction and recovery in Malignant Hypertension. We retrospectively analyzed 97 patients admitted between April 1994 and April 2004 with Malignant Hypertension. MAHA was defined as a low platelet count ( 9 /L) with either an elevated lactic dehydrogenase (>220 U/L) or presence of schistocytes. MAHA was present in 26 of 97 patients (27%). Serum creatinine levels at admission were significantly higher in those with than in those without MAHA: median serum creatinine 690 μmol/L (interquartile range [IQR] 394 to 1105) and 120 μmol/L (IQR 82 to 211), respectively ( P P P P P =0.01) and 1.02 per mm Hg increase in systolic blood pressure (95% CI, 1.01 to 1.05; P =0.01). In conclusion, MAHA is an important indicator of renal insufficiency and recovery in patients with Malignant Hypertension.

  • impaired cerebral autoregulation in patients with Malignant Hypertension
    Circulation, 2004
    Co-Authors: Rogier V Immink, John M Karemaker, Bertjan H Van Den Born, Gert A Van Montfrans, Richard P. Koopmans, Johannes J Van Lieshout
    Abstract:

    Background— In patients with a Malignant Hypertension, immediate parenteral treatment with blood pressure–lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients. Methods and Results— In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA Vmean to MAP phase lead and static CA as the MCA Vmean to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA Vmean to MAP phase lead was lower (30±8° versus 58±5°, mean±SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA Vmean decrease was 22±4%, along with...

Bertjan H Van Den Born - One of the best experts on this subject based on the ideXlab platform.

  • Cerebral Hemodynamics During Treatment With Sodium Nitroprusside Versus Labetalol in Malignant Hypertension
    2016
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    Abstract—In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler–determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n8) or labetalol (n7). The reduction in mean arterial blood pressure with sodium nitroprusside (283%; meanSEM) and labetalol (284%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (1310% and 175%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (534 % and74%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.450.05 % versus 0.780.04 % cm s1 %mm Hg1; P0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flo

  • cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in Malignant Hypertension
    Hypertension, 2008
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler-determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n=8) or labetalol (n=7). The reduction in mean arterial blood pressure with sodium nitroprusside (-28+/-3%; mean+/-SEM) and labetalol (-28+/-4%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (-13+/-10% and -17+/-5%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (-53+/-4% and -7+/-4%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.45+/-0.05% versus 0.78+/-0.04% cm.s(-1).%mm Hg(-1); P<0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flow to the low resistance systemic vascular bed rather than the cerebral vascular bed.

  • microangiopathic hemolysis and renal failure in Malignant Hypertension
    Hypertension, 2005
    Co-Authors: Bertjan H Van Den Born, Uwkje P. F. Honnebier, Richard P. Koopmans, Gert A Van Montfrans
    Abstract:

    Renal dysfunction is an important cause of morbidity and mortality in patients with Malignant Hypertension. Microangiopathic hemolysis (MAHA) related to Malignant Hypertension may cause renal insufficiency by obstruction of interlobular arteries. We hypothesized that the presence of MAHA is an important indicator of renal dysfunction and recovery in Malignant Hypertension. We retrospectively analyzed 97 patients admitted between April 1994 and April 2004 with Malignant Hypertension. MAHA was defined as a low platelet count ( 9 /L) with either an elevated lactic dehydrogenase (>220 U/L) or presence of schistocytes. MAHA was present in 26 of 97 patients (27%). Serum creatinine levels at admission were significantly higher in those with than in those without MAHA: median serum creatinine 690 μmol/L (interquartile range [IQR] 394 to 1105) and 120 μmol/L (IQR 82 to 211), respectively ( P P P P P =0.01) and 1.02 per mm Hg increase in systolic blood pressure (95% CI, 1.01 to 1.05; P =0.01). In conclusion, MAHA is an important indicator of renal insufficiency and recovery in patients with Malignant Hypertension.

  • impaired cerebral autoregulation in patients with Malignant Hypertension
    Circulation, 2004
    Co-Authors: Rogier V Immink, John M Karemaker, Bertjan H Van Den Born, Gert A Van Montfrans, Richard P. Koopmans, Johannes J Van Lieshout
    Abstract:

    Background— In patients with a Malignant Hypertension, immediate parenteral treatment with blood pressure–lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients. Methods and Results— In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA Vmean to MAP phase lead and static CA as the MCA Vmean to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA Vmean to MAP phase lead was lower (30±8° versus 58±5°, mean±SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA Vmean decrease was 22±4%, along with...

Rogier V Immink - One of the best experts on this subject based on the ideXlab platform.

  • Cerebral Hemodynamics During Treatment With Sodium Nitroprusside Versus Labetalol in Malignant Hypertension
    2016
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    Abstract—In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler–determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n8) or labetalol (n7). The reduction in mean arterial blood pressure with sodium nitroprusside (283%; meanSEM) and labetalol (284%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (1310% and 175%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (534 % and74%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.450.05 % versus 0.780.04 % cm s1 %mm Hg1; P0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flo

  • cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in Malignant Hypertension
    Hypertension, 2008
    Co-Authors: Rogier V Immink, Bertjan H Van Den Born, Gert A Van Montfrans, Yusok Kim, Markus W Hollmann, Johannes J Van Lieshout
    Abstract:

    In patients with Malignant Hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler-determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for Malignant Hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n=8) or labetalol (n=7). The reduction in mean arterial blood pressure with sodium nitroprusside (-28+/-3%; mean+/-SEM) and labetalol (-28+/-4%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (-13+/-10% and -17+/-5%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (-53+/-4% and -7+/-4%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.45+/-0.05% versus 0.78+/-0.04% cm.s(-1).%mm Hg(-1); P<0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flow to the low resistance systemic vascular bed rather than the cerebral vascular bed.

  • impaired cerebral autoregulation in patients with Malignant Hypertension
    Circulation, 2004
    Co-Authors: Rogier V Immink, John M Karemaker, Bertjan H Van Den Born, Gert A Van Montfrans, Richard P. Koopmans, Johannes J Van Lieshout
    Abstract:

    Background— In patients with a Malignant Hypertension, immediate parenteral treatment with blood pressure–lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients. Methods and Results— In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA Vmean to MAP phase lead and static CA as the MCA Vmean to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA Vmean to MAP phase lead was lower (30±8° versus 58±5°, mean±SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA Vmean decrease was 22±4%, along with...