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

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.

1959 ◽  
Vol 197 (2) ◽  
pp. 399-402 ◽  
Author(s):  
Julius J. Friedman

The effect of Nembutal on the circulating and tissue blood volumes and hematocrits was calculated by means of independent determinations of plasma and red cell volumes. Nembutal produced an increase in circulating blood volume accompanied by a reduction in the venous hematocrit. The blood volumes of liver, kidney, spleen and intestine rose following the administration of Nembutal, while the hematocrits of liver, lung, intestine and muscle declined, and that of kidney rose. The administration of Nembutal to splenectomized mice produces similar changes. The relationship of these alterations to changes in periphero-vascular tone are discussed.


1994 ◽  
Vol 266 (5) ◽  
pp. H2122-H2129 ◽  
Author(s):  
A. Deschamps ◽  
S. Magder

In dogs and humans, heat stress is associated with an increase in cardiac output that sustains blood flow to heat-dissipating organs. Because cardiac output and venous return are equal in the steady state, the circulation must also adjust in heat stress to allow the venous return to increase. To analyze these adjustments, we measured blood volumes, unstressed volumes, blood flow distribution, venous compliance, venous resistance, and the time constant of venous drainage of the splanchnic and extrasplanchnic vascular beds in dogs anesthetized with alpha-chloralose at normal and at high core temperatures. We repeated the measurements at high core temperatures with ganglionic blockade, alpha-adrenergic receptor blockade, or beta-adrenergic receptor blockade to determine the efferent neurohumoral pathway. When core temperature was increased from 37.8 +/- 0.2 to 41.9 +/- 0.1 degrees C, total splanchnic blood volume decreased 23% (4.6 +/- 1.4 ml/kg) and splanchnic unstressed volume decreased 38.5%. None of the other determinants of venous return changed. Ganglionic blockade shifted the total and unstressed splanchnic blood volume during heat stress back to normothermic values. However, beta- and alpha-blockade did not affect splanchnic volumes. We conclude that a decrease in splanchnic unstressed volume is an important factor for the increased venous return during heat stress. Although mediated through sympathetic ganglions, this decrease is not abolished by alpha- or beta-receptor blockade.


2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S94
Author(s):  
T Mimura ◽  
S Tanaka ◽  
T Kawarabayashi ◽  
K Ishihara ◽  
T Hara ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Kevin J Wu ◽  
T. Stan Gregory ◽  
Charles Reeder ◽  
Bobby Leitmann ◽  
Augustus Huffines ◽  
...  

Background: Blood volume assessment is a valuable clinical metric, which can diagnostically be used to assess tissue health, monitor patient rehabilitation, and track the progression of wound healing. Currently there exists several methods to assess flow (MRI, US), but are either limited in cost or portability, and may require injection of contrast agents. Magnetohydrodynamic voltages (VMHD) are induced through blood flow interactions with an external magnetic field, and have been successfully measured using a modified ECG recorder and software package [1]. We hypothesize that a portable device capable of measuring induced VMHD could be used to rapidly quantify changes in blood flow. Objectives: Develop a portable device capable of monitoring of variations in blood volumes using induced VMHD. Methods: A portable smartphone-based ECG monitor was developed to use methods proposed in [1] to extract a metric proportional to blood flow from acquired ECGs (Fig. 1a). ECGs were acquired in two healthy volunteers, the second being a trained athlete. VMHD was induced in the carotid artery while in the presence of 0.4T static magnetic field generated by a neodymium magnet embedded in the monitor (Fig. 1b). VMHD signal extraction was performed to isolate the voltage induced by the magnet. Integrating over the VMHD yielded a metric proportional to blood volume [1,2]. Trials were performed at rest and at an elevated heart rate (HR) from exercise stress. Results: Induced VMHD was shown to increase from the baseline during exercise by 59% and 106% for the healthy subject and the athlete, respectively; resulting in a 47% difference in VMHD variations between the trained athlete and the healthy subject (Fig. 1c). Conclusions: A stand-alone device capable of quickly assessing blood volumes in the field using custom hardware and smartphone technology was developed. The ability of the device to quantify VMHD-derived blood flow was demonstrated. Ref: [1] Tse, MRM, 2013. [2] Gregory, JCMR, 2015.


1986 ◽  
Vol 64 (5) ◽  
pp. 621-624 ◽  
Author(s):  
C. V. Greenway ◽  
F. Burczynski ◽  
I. R. Innes

Arterial pressures, portal pressures, and hepatic blood volumes were recorded after hepatic denervation in cats anesthetized with pentobarbital. Bromocryptine (50 μg/kg) lowered arterial pressure but did not significantly change portal pressure or hepatic blood volume. However, both portal pressure and hepatic blood volume responses to hepatic nerve stimulation were significantly depressed after bromocryptine especially at low frequencies of stimulation. Responses to intraportal infusions of norepinephrine were significantly impaired only at the highest dose. The inhibitory effect of bromocryptine on the neural responses may, therefore, involve a presynaptic inhibition of norepinephrine release, but the mechanism requires further study. These data provide further suport for the hypothesis that drugs which impair hepatic venous responses to sympathetic stimuli cause significant impairment of postural reflexes and orthostatic hypotension during clinical use.


1992 ◽  
Vol 262 (2) ◽  
pp. H432-H436 ◽  
Author(s):  
Y. Chien ◽  
B. L. Pegram ◽  
M. B. Kardon ◽  
E. D. Frohlich

To test the hypothesis that atrial natriuretic factor (ANF) increases total body venous compliance through venodilation and thereby reduces cardiac preload, we compared the systemic hemodynamic effects of ANF (99-126) with the venodilator nitroglycerin in conscious rats with myocardial infarction (mean infarct size 25%) induced by coronary artery ligation 3 wk previously. A 30-min ANF infusion (0.5 microgram.kg-1.min-1) decreased mean arterial pressure, central venous pressure, and blood volume by 11 mmHg, 0.8 mmHg, and 3 ml/kg, respectively (P less than 0.02). Nitroglycerin (10 micrograms.kg-1.min-1) similarly reduced arterial and venous pressures (7 and 0.6 mmHg; P less than 0.02) but increased blood volume by 2 ml/kg (P less than 0.05). Both ANF and nitroglycerin reduced mean circulatory filling pressure (MCFP) by 1 mmHg (P less than 0.05). Compared with vehicle infusion, nitroglycerin increased total body vascular compliance as derived from serial MCFP measurements taken during 10% blood volume changes (2.09 +/- 0.12 vs. 2.76 +/- 0.32 ml.kg-1.mmHg-1; P less than 0.05) and reduced extrapolated unstressed volume (34.96 +/- 1.10 vs. 23.79 +/- 3.80 ml/kg; P less than 0.02). In contrast, ANF had no effect on either measurement. These data suggest that ANF and nitroglycerin reduced cardiac filling pressure through different mechanisms; the lack of effects of ANF on total body venous compliance and unstressed volume does not support its venodilating effect in these rats postmyocardial infarction.


1985 ◽  
Vol 248 (4) ◽  
pp. H468-H476 ◽  
Author(s):  
C. V. Greenway ◽  
K. L. Seaman ◽  
I. R. Innes

Hemodynamic relationships between flows, pressures, and blood volume have been examined in the denervated liver of cats anesthetized with pentobarbital. Portal and hepatic lobar venous pressures, portal and total hepatic flows, and hepatic blood volume were recorded when portal flow was varied from 0 to 240 ml X min-1 X 100 g liver-1 and when hepatic outflow pressure was varied from 0 to 9.5 mmHg, before, during, and after intravenous infusion of norepinephrine (2 micrograms X min-1 X kg body wt-1). Portal pressure was 1-2 mmHg higher than lobar venous pressure and 8-9 mmHg higher than inferior vena caval pressure, showing that the major site of resistance in the portal circuit was in the large hepatic veins. Intrahepatic pressure was linearly related to total hepatic flow, and norepinephrine increased the intercept but not the slope of this relationship. Hepatic blood volume was linearly related to intrahepatic pressure with a calculated compliance of 2.5-3.0 ml X mmHg-1 X 100 g liver-1 and a calculated unstressed volume at zero pressure of 10-15 ml/100 g liver. Norepinephrine did not significantly change vascular compliance but caused a marked reduction of 15-20 ml/100 g liver in calculated unstressed volume. Thus norepinephrine reduced hepatic blood volume by 15-20 ml/100 g liver at any given intrahepatic pressure. It is concluded that venoconstriction in the hepatic bed occurs by a decrease in unstressed volume with little change in compliance. Unstressed volume represents a true blood volume reserve, independent of passive influences, which can be mobilized by the central nervous system.


VASA ◽  
2012 ◽  
Vol 41 (4) ◽  
pp. 275-281 ◽  
Author(s):  
da Rocha Chehuen ◽  
G. Cucato ◽  
P. dos Anjos Souza Barbosa ◽  
A. R. Costa ◽  
M. Ritti-Dias ◽  
...  

Background: This study assessed the relationship between lower limb hemodynamics and metabolic parameters with walking tolerance in patients with intermittent claudication (IC). Patients and methods: Resting ankle-brachial index (ABI), baseline blood flow (BF), BF response to reactive hyperemia (BFRH), oxygen uptake (VO2), initial claudication distance (ICD) and total walking distance (TWD) were measured in 28 IC patients. Pearson and Spearman correlations were calculated. Results: ABI, baseline BF and BF response to RH did not correlate with ICD or TWD. VO2 at first ventilatory threshold and VO2peak were significantly and positively correlated with ICD (r = 0.41 and 0.54, respectively) and TWD (r = 0.65 and 0.71, respectively). Conclusions: VO2peak and VO2 at first ventilatory threshold, but not ABI, baseline BF and BFHR were associated with walking tolerance in IC patients. These results suggest that VO2 at first ventilatory threshold may be useful to evaluate walking tolerance and improvements in IC patients.


1961 ◽  
Vol 201 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Noel M. Bass ◽  
Vincent V. Glaviano

Heart rate, mean blood pressure, adrenal blood flow, and adrenal plasma adrenaline and noradrenaline were compared before and after ligation of the anterior descending coronary artery in dogs anesthetized with chloralose. One group of 12 dogs responded to acute coronary occlusion with a sudden and marked decrease in mean blood pressure (mean, 31%) and heart rate (mean, 18%) followed by an early onset (mean, 227 sec) of ventricular fibrillation. Another group of nine dogs responded with slight decreases in mean blood pressure (mean, 13%) and heart rate (mean, 5%), during which time ventricular fibrillation occurred late (mean, 30 min) or not at all. While the two groups were statistically different in mean blood pressure and heart rate, the minute output of adrenal catecholamines in either group was not found to be related to the early or late occurrence of ventricular fibrillation.


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