Abstract P193: Effect Of Nitroglycerin And Sympathetic Withdrawal On Splanchnic Capacitance And Cardiac Blood Volumes

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Luis E Okamoto ◽  
William D Dupont ◽  
Sachin Y Paranjape ◽  
Jorge E Celedonio ◽  
Emily C Smith ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Blood Volume ◽  
Venous Return ◽  
Intrathoracic Pressure ◽  
Cardiac Volume ◽  
Parallel Shift ◽  
Cardiac Blood ◽  
Before And After ◽  
Autonomic Blockade ◽  
Blood Volumes

The splanchnic vasculature is the largest blood volume reservoir in the human body. Reduced capacitance of this vascular bed, in part due to sympathetic venoconstriction, is proposed to play a role in hypertension and heart failure. Thus, interventions that increase splanchnic capacitance or decrease sympathetic activity may be beneficial in these conditions. In a proof-of-concept study in healthy and hypertensive subjects, we evaluated whether venodilation with nitroglycerin (NTG; Study 1) or sympathetic withdrawal with trimethaphan (Study 2) increase splanchnic capacitance and reduce cardiac and stroke volumes. In Study 1 (n=10, 36±4 yrs, BMI 26.1±1.7, 4 men), abdominal and chest scintigrams, to measure regional blood volumes, were obtained before and after 0.6 mg sublingual NTG. Splanchnic capacitance (volume-pressure relationships, VPR) and compliance (VPR slope) were estimated by recording abdominal scintigrams during progressive escalation of intrathoracic pressure using continuous positive airway pressure (CPAP) at 0, 4, 8, 12, and 16 cm H 2 O, each for ≤2 min. We found that NTG increased splanchnic blood volume at rest (4%, IQR 1.81-9.95; P<0.01) resulting in a rightward parallel shift in splanchnic VPR (P slope =0.46 and P intercept =0.01), indicating an increase in splanchnic capacitance. This was associated with a decrease in cardiac blood volume (-9%, IQR 2.2-10.3; P<0.01). In Study 2, we measured blood pressure (BP) and stroke volume, used as a surrogate of venous return, during the same CPAP protocol before and during autonomic blockade with trimethaphan in 12 hypertensive subjects (49±2 yrs, BMI 29.9±1.7, 5 men). Sympathetic withdrawal decreased systolic BP (-27±14 mmHg) and produced a leftward parallel shift in VPR (i.e. reduced stroke volume; P slope =0.12 and P intercept <0.01), indicating a reduction in venous return likely due to an increase in splanchnic capacitance. In conclusion, venodilation with NTG increased splanchnic capacitance and decreased cardiac volume. Sympathetic withdrawal had similar hemodynamic effects. These findings highlight the importance of splanchnic capacitance in cardiovascular regulation.

Changes in stroke volume and maximal aerobic capacity with increased blood volume in men women

1996 ◽  
Vol 80 (4) ◽  
pp. 1180-1186 ◽  
Author(s):  
C. M. Mier ◽  
M. A. Domenick ◽  
N. S. Turner ◽  
J. H. Wilmore
Keyword(s):  
Stroke Volume ◽  
Blood Volume ◽  
Hemoglobin Concentration ◽  
Cycle Ergometer ◽  
Maximal Aerobic Capacity ◽  
Plasma Volume Expansion ◽  
Men And Women ◽  
Women Subjects ◽  
Before And After ◽  
Blood Pressures

This study determined whether the effects of acute plasma volume expansion (PVX) or 10 days of training on stroke volume during submaximal cycling and on treadmill maximal oxygen uptake (VO2max) were similar between men and women. Subjects performed a submaximal cycle test and a treadmill test to exhaustion under three conditions: control, PVX, and after training. Cycle peak VO2 (VO2peak) and blood volume were measured before and after training. Training consisted of daily 1-h bouts [30 min at 80% peak heart rate (HRpeak) and ten 2-min intervals at 95% HRpeak alternating with 1-min low-intensity pedaling] on a cycle ergometer for 10 consecutive days. Training increased cycle VO2peak in men [P < 0.05; 3.14 +/- 0.13 vs. 3.42 +/- 0.13 (SE) l/min] and women (2.11 +/- 0.10 vs. 2.37 +/- 0.12 l/min) and increased blood volume in men (67.6 +/- 3.0 vs. 72.3 +/- 3.1 ml/kg) and women (62.7 +/- 2.2 vs. 65.6 +/- 2.4 ml/kg). As a result of the greater blood volume with PVX and with training, stroke volume (ml) during submaximal cycling increased in men (control 110 +/- 4; PVX 123 +/- 4; trained 121 +/- 4) and women (control 87 +/- 5; PVX 95 +/- 6, trained 96 +/- 7). Treadmill VO2max (ml.kg-1.min-1) did not change with PVX despite a 6-7% reduction in hemoglobin concentration, whereas training resulted in an increase in VO2max in men (control 47.9 +/- 2.8; PVX 46.7 +/- 2.8; trained 49.9 +/- 2.6) and women (control 38.0 +/- 1.2; PVX 36.9 +/- 1.2; trained 39.2 +/- 1.2). The effects of PVX or training on stroke volume or VO2max did not differ between men and women. An additional finding was an increase in diastolic and mean blood pressures at 65% of cycle VO2peak with PVX and with training in women. Thus men and women hold similar cardiac reserve capacities for increasing stroke volume and, as a result, VO2max is maintained despite a reduction in hemoglobin concentration. However, gender differences in blood pressure regulation with increased blood volume might exist.

Determinants of cardiac augmentation by elevations in intrathoracic pressure

1985 ◽  
Vol 58 (4) ◽  
pp. 1189-1198 ◽  
Author(s):  
M. R. Pinsky ◽  
G. M. Matuschak ◽  
M. Klain
Keyword(s):  
Stroke Volume ◽  
Cardiac Function ◽  
Blood Volume ◽  
Intrathoracic Pressure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Respiratory Frequency ◽  
Stroke Work ◽  
Inspiratory Time ◽  
Ventricular Failure

We studied the cardiovascular effects of phasic increases in intrathoracic pressure (ITP) by high-frequency jet ventilation in an acute pentobarbital-anesthetized intact canine model both before and after the induction of acute ventricular failure by large doses of propranolol. Chest and abdominal pneumatic binders were used to further increase ITP. Respiratory frequency, percent inspiratory time, mean ITP, and swings in ITP throughout the respiratory cycle were independently varied at a constant-circulating blood volume. We found that pertubations in mean ITP induced by ventilator adjustments accounted for all observable steady-state hemodynamic changes independent of respiratory frequency, inspiratory time, or phasic respiratory swings in ITP. Changes in ITP were associated with reciprocal changes in both intrathoracic vascular pressures (P less than 0.01) and blood volume (P less than 0.01). When cardiac function was normal, left ventricular (LV) stroke volume decreased, whereas in acute ventricular failure, LV stroke volume increased in response to increasing ITP when apneic LV filling pressure was high (greater than or equal to 17 Torr) and did not change if apneic LV filling pressure was low (less than or equal to 12 Torr). However, in all animals in acute ventricular failure, LV stroke work increased with increasing ITP. Our study demonstrates that the improved cardiac function seen with increasing ITP in acute ventricular failure is dependent upon adequate LV filling and decreased LV afterload in a manner analogous to that seen with arterial vasodilator therapy in heart failure.

scholarly journals Expanded blood volumes contribute to the increased cardiovascular performance of endurance-trained older men

1998 ◽  
Vol 85 (2) ◽  
pp. 484-489 ◽  
Author(s):  
James M. Hagberg ◽  
Andrew P. Goldberg ◽  
Loretta Lakatta ◽  
Frances C. O’Connor ◽  
Lewis C. Becker ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Blood Volume ◽  
Left Ventricular ◽  
Fat Free Mass ◽  
Peak Exercise ◽  
Red Cell ◽  
Total Blood ◽  
End Diastolic Volume ◽  
Ergometer Exercise ◽  
Blood Volumes

To determine whether expanded intravascular volumes contribute to the older athlete’s higher exercise stroke volume and maximal oxygen consumption (V˙o 2 max), we measured peak upright cycle ergometry cardiac volumes (99mTc ventriculography) and plasma (125I-labeled albumin) and red cell (NaCr51) volumes in 7 endurance-trained and 12 age-matched lean sedentary men. The athletes had ∼40% higherV˙o 2 max values than did the sedentary men and larger relative plasma (46 vs. 38 ml/kg), red cell (30 vs. 26 ml/kg), and total blood volumes (76 vs. 64 ml/kg) (all P < 0.05). Athletes had larger peak cycle ergometer exercise stroke volume indexes (75 vs. 57 ml/m2, P < 0.05) and 17% larger end-diastolic volume indexes. In the total group,V˙o 2 maxcorrelated with plasma, red cell, and total blood volumes ( r = 0.61–0.70, P < 0.01). Peak exercise stroke volume was correlated directly with the blood volume variables ( r = 0.59–0.67, P < 0.01). Multiple regression analyses showed that fat-free mass and plasma or total blood volume, but not red cell volume, were independent determinants ofV˙o 2 max and peak exercise stroke volume. Plasma and total blood volumes correlated with the stroke volume and end-diastolic volume changes from rest to peak exercise. This suggests that expanded intravascular volumes, particularly plasma and total blood volumes, contribute to the higher peak exercise left ventricular end-diastolic volume, stroke volume, and cardiac output and hence the higherV˙o 2 max in master athletes by eliciting both chronic volume overload and increased utilization of the Frank-Starling effect during exercise.

Platelet Distribution and Survival in Plasma Clots and Thrombi

1961 ◽  
Vol 06 (03) ◽  
pp. 470-484 ◽  
Author(s):  
Peter Wolf
Keyword(s):  
Blood Vessels ◽  
Calcium Ions ◽  
Paraffin Sections ◽  
Cardiac Infarction ◽  
Cardiac Blood ◽  
Before And After

SummaryViscous metamorphosis of platelets in native and sequestrene plasma, before and after thrombin and plasmin action, has been studied. A method for the examination of platelet distribution in plasma clots and tissue paraffin sections is described.It was found that not all platelets undergo viscous metamorphosis in plasma clots or in intravascular thrombi. Platelets before and after viscous metamorphosis are not digested by plasmin. After plasmin action intact platelets can still undergo viscous metamorphosis and the fibrils which are then produced are not made of fibrin.Thrombin in the absence of calcium ions will not cause platelets to undergo viscous metamorphosis.Total blockage of cardiac blood vessels by platelet masses in cases of cardiac infarction is demonstrated. The significance of these findings in relation to blood sludging, and future lines of treatment are discussed.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

Modulation of carotid baroreflex responsiveness in man: effects of posture and propranolol

1976 ◽  
Vol 41 (3) ◽  
pp. 383-387 ◽  
Author(s):  
D. L. Eckberg ◽  
F. M. Abboud ◽  
A. L. Mark
Keyword(s):  
Angina Pectoris ◽  
Supine Position ◽  
Baroreflex Sensitivity ◽  
Pulse Interval ◽  
Upright Posture ◽  
Adrenergic Stimulation ◽  
Interval Prolongation ◽  
Carotid Baroreflex ◽  
Before And After ◽  
Autonomic Blockade

Carotid baroreceptors were stimulated with graded neck suction in supine and standing volunteers, before and after autonomic blockade, to determine the influence of posture on baroreflex responsiveness. Propranolol significantly augmented baroreflex pulse interval prolongation in the supine position. Upright posture did not modify baroreflex pulse interval responses prior to propranolol, but significantly augmented responses after propranolol. The results suggest that standing enhances baroreflex sensitivity, but that under normal circumstances, this effect is masked by beta-adrenergic stimulation. Augmentation of baroreflex pulse interval prolongation in the supine and standing positions by propranolol may contribute to the effectiveness of this drug in angina pectoris and labile hypertension.

Effects of hemorrhage and hepatic nerve stimulation on venous compliance and unstressed volume in cat liver

1987 ◽  
Vol 65 (11) ◽  
pp. 2168-2174 ◽  
Author(s):  
C. V. Greenway
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Nerve Stimulation ◽  
Marked Decrease ◽  
Venous Compliance ◽  
Remarkable Feature ◽  
Unstressed Volume ◽  
Passive Response ◽  
The Relationship ◽  
Blood Volumes

Intrahepatic blood volume–pressure relationships were studied using plethysmography to measure hepatic blood volume and a hepatic venous long-circuit to control intrahepatic pressure. In cats anesthetized with pentobarbital or with ketamine–chloralose, hemorrhage (to reduce hepatic blood flow to 60% of control) caused marked reductions in hepatic blood volume and intrahepatic pressure but did not significantly change hepatic blood volume–pressure relationships. We were unable to demonstrate an active reflex venous response to hemorrhage in these preparations, although a large passive response occurred. The volume–pressure relationships in innervated livers were different from those in denervated livers: apparent venous compliance was much greater and apparent unstressed volume was zero or negative. Hepatic nerve stimulation in denervated livers caused a marked decrease in hepatic blood volume at low intrahepatic pressures but failed to alter hepatic blood volumes at high intrahepatic pressures (15 mmHg) (1 mmHg = 133.3 Pa). This resulted in large apparent compliances and apparently negative unstressed volumes, as seen in the innervated livers. Thus blood volume–pressure relationships in innervated livers may not give valid measurements of compliance and unstressed volume. A remarkable feature in all these experiments was the linearity of the relationship between hepatic blood volume and intrahepatic pressure. Exudation of fluid begins at higher intrahepatic pressures in innervated compared with denervated livers.

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