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Daniel P. Toews - One of the best experts on this subject based on the ideXlab platform.

  • The dynamics of venous return and response to Hypervolemia in the toad, Bufo marinus (L.).
    BMC Physiology, 2001
    Co-Authors: Erin E Killorn, Daniel P. Toews
    Abstract:

    Background Venous return from the posterior region of amphibians travels by either two renal portal veins to the kidney or a central abdominal vein that drains into the hepatic portal system. The relative proportions of blood flow in these vessels has never been measured nor has a modification of flow been determined when venous return increases by changes in blood volume during Hypervolemia or during increased volume input from the posterior lymph hearts.

  • The dynamics of venous return and response to Hypervolemia in the toad, Bufo marinus (L.)
    BMC Physiology, 2001
    Co-Authors: Erin E Killorn, Daniel P. Toews
    Abstract:

    Background Venous return from the posterior region of amphibians travels by either two renal portal veins to the kidney or a central abdominal vein that drains into the hepatic portal system. The relative proportions of blood flow in these vessels has never been measured nor has a modification of flow been determined when venous return increases by changes in blood volume during Hypervolemia or during increased volume input from the posterior lymph hearts. Results Venous return from the posterior region of Bufo marinus was measured under resting conditions and in response to a systemic Hypervolemia. Doppler flow probes were positioned on the renal portal and ventral abdominal veins, and flow was recorded as injections of artificial plasma equaling 100% of the animal's plasma volume were administered through the sciatic artery. Resting flow was found to be 5.54 ± 2.03 ml min^-1 kg^-1 in the paired renal portal veins, and 7.31 ± 0.89 ml min^-1 kg^-1 in the ventral abdominal vein. While renal portal flow was found to increase by a factor of 2.4 times during the first 10 min of Hypervolemia, ventral abdominal flow only increased by a factor of 1.3. Conclusions Our results quantify the contribution to circulation from posterior venous return in the toad Bufo marinus. A preferential movement of excess fluid through the renal portal pathway was also demonstrated, supporting the possibility of water elimination via the renal portal circulation, especially during periods of high water influx into the animals.

D R Lamb - One of the best experts on this subject based on the ideXlab platform.

  • Spironolactone administration and training-induced Hypervolemia
    International Journal of Sports Medicine, 1994
    Co-Authors: M. J. Luetkemeier, Kenneth Michael FLOWERS, D R Lamb
    Abstract:

    The purpose of this study was to determine the contribution of aldosterone to plasma volume expansion accompanying short-term exercise training. Twelve healthy males (age = 26.5 +/- 5.8) cycled for 120 min on three consecutive days at a relative exercise intensity of 65% VO2max. Half of the subjects were treated with 25 mg of spironolactone taken four times daily to suppress the effects of aldosterone. Resting plasma volume increased significantly (501 +/- 83 ml, p < 0.05) from pretraining in control subjects, but not for drug-treated subjects (163 +/- 94 ml). Spironolactone attenuated gains in resting plasma volume, serum sodium content, and serum osmolal content by 67%, 79% and 66%, respectively. Spironolactone-treated and non-treated subjects experienced similar increases in total serum protein content sufficient to increase the plasma volume by approximately 290 ml. It was not determined why drug-treated subjects attained less of a plasma volume expansion than that expected by the increase in oncotic pressure. In conclusion, two-fifths of the plasma volume expansion induced by 3 d of endurance cycling could be attributed to aldosterone activity, and the remaining three-fifths could be explained by the expansion of intravascular protein mass. Other neurohormonal influences may have contributed to the overall plasma volume expansion but this experiment did not allow for their exclusion.

Aslam S. Hassan - One of the best experts on this subject based on the ideXlab platform.

  • Acute Hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses
    European Journal of Applied Physiology, 2005
    Co-Authors: Murli Manohar, Thomas E. Goetz, Aslam S. Hassan
    Abstract:

    Recently, it was reported that acute Hypervolemia improves arterial oxygen tension in human athletes known to experience exercise-induced arterial hypoxemia. Since exercise-induced arterial hypoxemia is routinely observed in racehorses and is known to limit performance, we examined whether pre-exercise induction of acute Hypervolemia would similarly benefit arterial oxygenation in maximally exercising thoroughbred horses. Two sets of experiments, namely, placebo [intravenous (IV) physiological saline] and acute Hypervolemia (IV 7.2% NaCl, causing an 18.2% expansion of plasma volume) studies were carried out in random order on 13 healthy, exercise-trained thoroughbred horses, 7 days apart. An incremental exercise protocol leading to 120 s of galloping at 14 m s^−1 on a 3.5% uphill incline was used. Galloping at this workload elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. In the placebo study, arterial oxygen tension decreased to 76.1 (2) mmHg ( P

  • acute Hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses
    European Journal of Applied Physiology, 2005
    Co-Authors: Murli Manohar, Thomas E. Goetz, Aslam S. Hassan
    Abstract:

    Recently, it was reported that acute Hypervolemia improves arterial oxygen tension in human athletes known to experience exercise-induced arterial hypoxemia. Since exercise-induced arterial hypoxemia is routinely observed in racehorses and is known to limit performance, we examined whether pre-exercise induction of acute Hypervolemia would similarly benefit arterial oxygenation in maximally exercising thoroughbred horses. Two sets of experiments, namely, placebo [intravenous (IV) physiological saline] and acute Hypervolemia (IV 7.2% NaCl, causing an 18.2% expansion of plasma volume) studies were carried out in random order on 13 healthy, exercise-trained thoroughbred horses, 7 days apart. An incremental exercise protocol leading to 120 s of galloping at 14 m s−1 on a 3.5% uphill incline was used. Galloping at this workload elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. In the placebo study, arterial oxygen tension decreased to 76.1 (2) mmHg (P<0.0001) at 30 s of maximal exertion, but further significant changes did not occur as exercise duration increased to 120 s [arterial oxygen tension 72.4 (2) mmHg]. A significant arterial hypoxemia also developed in galloping horses in the acute Hypervolemia study [arterial oxygen tension at 30 and 120 s was 76.7 (1.7) and 71.9 (1.6) mmHg, respectively], but significant differences between treatments could not be demonstrated. In both treatments, a similar desaturation of arterial hemoglobin was also observed at 30 s of maximal exercise, which intensified with increasing exercise duration as hyperthermia, acidosis and hypercapnia intensified. Thus, acute expansion of plasma volume did not benefit arterial oxygenation in maximally exercising thoroughbred horses.

Erin E Killorn - One of the best experts on this subject based on the ideXlab platform.

  • The dynamics of venous return and response to Hypervolemia in the toad, Bufo marinus (L.).
    BMC Physiology, 2001
    Co-Authors: Erin E Killorn, Daniel P. Toews
    Abstract:

    Background Venous return from the posterior region of amphibians travels by either two renal portal veins to the kidney or a central abdominal vein that drains into the hepatic portal system. The relative proportions of blood flow in these vessels has never been measured nor has a modification of flow been determined when venous return increases by changes in blood volume during Hypervolemia or during increased volume input from the posterior lymph hearts.

  • The dynamics of venous return and response to Hypervolemia in the toad, Bufo marinus (L.)
    BMC Physiology, 2001
    Co-Authors: Erin E Killorn, Daniel P. Toews
    Abstract:

    Background Venous return from the posterior region of amphibians travels by either two renal portal veins to the kidney or a central abdominal vein that drains into the hepatic portal system. The relative proportions of blood flow in these vessels has never been measured nor has a modification of flow been determined when venous return increases by changes in blood volume during Hypervolemia or during increased volume input from the posterior lymph hearts. Results Venous return from the posterior region of Bufo marinus was measured under resting conditions and in response to a systemic Hypervolemia. Doppler flow probes were positioned on the renal portal and ventral abdominal veins, and flow was recorded as injections of artificial plasma equaling 100% of the animal's plasma volume were administered through the sciatic artery. Resting flow was found to be 5.54 ± 2.03 ml min^-1 kg^-1 in the paired renal portal veins, and 7.31 ± 0.89 ml min^-1 kg^-1 in the ventral abdominal vein. While renal portal flow was found to increase by a factor of 2.4 times during the first 10 min of Hypervolemia, ventral abdominal flow only increased by a factor of 1.3. Conclusions Our results quantify the contribution to circulation from posterior venous return in the toad Bufo marinus. A preferential movement of excess fluid through the renal portal pathway was also demonstrated, supporting the possibility of water elimination via the renal portal circulation, especially during periods of high water influx into the animals.

Andreas Raabe - One of the best experts on this subject based on the ideXlab platform.

  • Hypervolemia in cerebral vasospasm
    Journal of Neurosurgery, 2006
    Co-Authors: Andreas Raabe, Bertil Romner
    Abstract:

    Object. Arterial vasospasm is the most common cause of delayed ischemic neurological deficits (DINDs) and one of the major causes of disability following subarachnoid hemorrhage (SAH). Current management of vasospasm involves intravascular volume expansion and hemodynamic augmentation with the goal of increasing cerebral blood flow (CBF). The purpose of this study was to examine the effects of volume expansion on regional (r)CBF in patients with DIND following SAH. Methods. The authors measured quantitative rCBF on positron emission tomography (PET) scans in six patients with aneurysmal SAH who had developed clinical signs of vasospasm. All patients were kept in a euvolemic state prior to the onset of vasospasm. At the onset of vasospasm, global and rCBF were measured before and after the administration of a normal saline bolus of 15 ml/kg administered over 1 hour. Two patients then received saline infusions of 5 ml/kg x hr over the following 2 to 3 hours and underwent hourly serial CBF measurements. Global and rCBF data were calculated in each patient. The mean rCBF in areas with low flow at baseline (<= 25 ml/[100 g x min]) increased from 19.1 +/- 3.0 to 29.9 +/- 9.7 ml/(100 g x min) (p = 0.02) with volume expansion. This change was sustained over the following 2 to 3 hours. Pulmonary capillary wedge pressure, mean arterial blood pressure, cardiac output, and central venous pressure did not change significantly during this intervention. Conclusions. In euvolemic patients with vasospasm, intravascular volume expansion with a normal saline bolus raised CBF in regions of the brain most vulnerable to ischemia. (Less)

  • relative importance of hypertension compared with Hypervolemia for increasing cerebral oxygenation in patients with cerebral vasospasm after subarachnoid hemorrhage
    Journal of Neurosurgery, 2005
    Co-Authors: Andreas Raabe, Jurgen Beck, Mike Keller, H Vatter, Michael Zimmermann, Volker Seifert
    Abstract:

    Object. Hypervolemia and hypertension therapy is routinely used for prophylaxis and treatment of symptomatic cerebral vasospasm at many institutions. Nevertheless, there is an ongoing debate about the preferred modality (Hypervolemia, hypertension, or both), the degree of therapy (moderate or aggressive), and the risk or benefit of Hypervolemia, moderate hypertension, and aggressive hypertension in patients following subarachnoid hemorrhage. Methods. Monitoring data and patient charts for 45 patients were retrospectively searched to identify periods of Hypervolemia, moderate hypertension, or aggressive hypertension. Measurements of central venous pressure, fluid input, urine output, arterial blood pressure, intracranial pressure, and oxygen partial pressure (PO2) in the brain tissue were extracted from periods ranging from 1 hour to 24 hours. For these periods, the change in brain tissue PO2 and the incidence of complications were analyzed. During the 55 periods of moderate hypertension, an increase in br...