Effective Vascular Compliance of Dogs in Acute Heart Failure

1975 ◽  
Vol 53 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Pierre Larochelle ◽  
Richard I. Ogilvie

Effective vascular compliance was measured repeatedly in dogs without circulatory arrest utilizing a closed-circuit venous bypass system and constant cardiac output. Compliance, determined by the ΔV/ΔP relationship at the end of a 1-min infusion of 5% of the circulating volume into the inferior vena cava, was independent of the initial venous pressure, total circulating volume and systemic arterial pressure. It remained constant over a 3 h experimental period at 1.55 ± 0.05 ml (mm Hg)−1 kg−1 body weight. Elevation of mean left atrial pressure and mean pulmonary arterial pressure by gradual aortic constriction was associated with a large and significant reduction in vascular compliance to a value of 1.14 ± 0.06 ml (mm Hg)−1 kg−1 after 2 h. This reduction was independent of the initial venous pressure and total circulating volume but was associated with the changes in left atrial and pulmonary artery pressures and an increase in plasma catecholamine concentrations. The mechanism responsible for the reduction in effective compliance is not clear from the present experiments. Increased circulating catecholamines and sympathetic nerve traffic resulting from baro- and volume receptor stimulation in the vascular tree may be the causative mechanism.

1984 ◽  
Vol 56 (5) ◽  
pp. 1403-1410 ◽  
Author(s):  
J. Malo ◽  
H. Goldberg ◽  
R. Graham ◽  
H. Unruh ◽  
C. Skoog

Effects of hypoxic hypoxia (HH) on cardiac output (CO), CO distribution, arterial and venous pressure-flow curves, vascular compliance, vascular time constant (tau), and resistance to venous return (RVR) were evaluated on six dogs. The vascular bed was isolated into four compartments depending on venous drainage: superior vena cava (SVC), splanchnic, renal and adrenal, and the remainder of the inferior vena cava (IVC). Low arterial O2 content and PO2 produced a threefold increase in CO at the same mean arterial pressure and a significant redistribution of CO to the SVC. Arterial pressure-flow curves decreased their slope (i.e., flow resistance) by a factor of two in the IVC and renal beds and by a factor of three in the splanchnic and SVC beds. Venous pressure-flow curves for the animal also decreased their slope significantly. HH causes a twofold increase in venous compliance and in mean venous pressure; tau did not change, but RVR halved. Seventy percent of the CO increase is explained by the increase in mean venous pressure and 30% by the reduction in RVR.


1994 ◽  
Vol 267 (1) ◽  
pp. R97-R106 ◽  
Author(s):  
H. S. Huang ◽  
J. C. Longhurst

The cardiovascular effects of regional abdominal ischemia and reperfusion were studied in cats anesthetized with alpha-chloralose. In group 1 (n = 9), central venous pressure was kept constant by a servo-controller while the celiac and superior mesenteric arteries were occluded by loop snares for 10 min. In group 2 (n = 9), a constant-perfusion circuit to the celiac and superior mesenteric arteries that could divert flow to the femoral vein was used to induce abdominal ischemia. In group 3 (n = 7), venous return from the inferior vena cava was controlled, and a constant-perfusion circuit was used to induce abdominal ischemia. Abdominal ischemia significantly (P < 0.05) increased portal venous blood lactate from 4.3 +/- 0.6 to 6.0 +/- 0.6 mM in group 3. The early increases in blood pressure caused by passive volume shifts in groups 1 and 2 were abolished in group 3. The late, i.e., 10 min, response to abdominal ischemia consisted of significant (P < 0.05) increases in mean arterial pressure (29 +/- 7, 24 +/- 7, and 33 +/- 8 mmHg in groups 1, 2, and 3, respectively). Abdominal ischemia also significantly (P < 0.05) increased the first derivative of left ventricular pressure at 40 mmHg developed pressure from 4,355 +/- 377 to 4,839 +/- 407 mmHg/s in group 3. Celiac and superior mesenteric ganglionectomy abolished the late but not the early hemodynamic changes. Ganglionectomy also significantly (P < 0.05) enhanced the decrease in mean arterial pressure during reperfusion in all groups. We conclude that the pressor and contractile responses during 10 min of abdominal ischemia and the relative maintenance of blood pressure during reperfusion after ischemia are reflex in nature.


1975 ◽  
Vol 53 (5) ◽  
pp. 850-858 ◽  
Author(s):  
Pierre Larochelle ◽  
Richard I. Ogilvie

Effective vascular compliance determined by the ΔV/ΔP relationship was measured repeatedly in anesthetized open-chest dogs without circulatory arrest utilizing a closed circuit venous bypass system with a constant cardiac output. Production of acute heart failure by gradual aortic constriction was associated with a significant decrease in total effective vascular compliance. The effect of loading and 20-min maintenance doses of different drugs on vascular compliance of animals in acute heart failure was studied. Phenoxybenzamine (total dose 2 mg/kg) produced a rapid and sustained increase in effective vascular compliance and theophylline (12 mg/kg) produced an increase which was more gradual in development than with phenoxybenzamine. Morphine (1 mg/kg) produced a rapid but transient increase in compliance. In contrast, ethacrynic acid (100 mg) or nitroglycerin (0.6 or 1.2 mg) did not alter vascular compliance significantly. These agents differ markedly in the magnitude and time-course of effect on effective vascular compliance.


1995 ◽  
Vol 82 (4) ◽  
pp. 877-883. ◽  
Author(s):  
Rom A. Stevens ◽  
David Beardsley ◽  
J. Lee White ◽  
Tzu-Cheg Kao ◽  
Rod Gantt ◽  
...  

Background Spinal and epidural injection of local anesthetics are used to produce sympathetic block to diagnose and treat certain chronic pain syndromes. It is not clear whether either form of regional anesthesia produces a complete sympathetic block. Spinal anesthesia using tetracaine has been reported to produce a decrease in plasma catecholamine concentrations. This has not been demonstrated for epidural anesthesia in humans with level of anesthesia below C8. One possible explanation is that spinal anesthesia results in a more complete sympathetic block than epidural anesthesia. To examine this question, a cross-over study was performed in young, healthy volunteers. Methods Ten subjects underwent both spinal and epidural anesthesia with lidocaine (plain) on the same day with complete recovery between blocks. By random assignment, spinal anesthesia and epidural anesthesia were induced via lumbar injection. Before and 30 min after local anesthetic injection, a cold pressor test (CPT) was performed. Blood was obtained to determine epinephrine and norepinephrine plasma concentrations at four stages: (1) 20 min after placing peripheral catheters, (2) at the end of a 2-min CPT (before conduction block), (3) 30 min after injection of epidural or spinal lidocaine, and (4) at the end of a second CPT (during anesthesia). Mean arterial pressure, heart rate, noninvasive cardiac index, and analgesia to pin-prick were monitored. Results Neither spinal nor epidural anesthesia changed baseline resting values of catecholamines or any hemodynamic variable, except heart rate, which was slightly decreased during spinal anesthesia. Median level of analgesia was T4 during spinal and T3 during epidural anesthesia. CPT before conduction block reliably increased heart rate, mean arterial pressure, cardiac index, epinephrine, and norepinephrine. Conduction block attenuated the increase in response to CPT only in mean arterial pressure (spinal and epidural) and cardiac index (spinal only). Neither technique blocked the increase in heart rate, norepinephrine, or epinephrine to CPT. Conclusions Spinal anesthesia did not result in a more complete attenuation of the sympathetic response to a CPT than did epidural anesthesia. In response to the CPT, spinal anesthesia blocked the increase in cardiac index, and epidural anesthesia resulted in a decrease in total peripheral resistance compared to the pre-anesthesia state. The differences between the techniques are not significant and are of uncertain clinical implications.


1996 ◽  
Vol 84 (3) ◽  
pp. 672-685 ◽  
Author(s):  
Toshiaki Nishikawa ◽  
Hiroshi Naito

Background Hypoxia or hypercapnia elicits cardiovascular responses associated with increased plasma catecholamine concentrations, whereas clonidine, an alpha(2)- adrenergic agonist, decreases plasma catecholamine concentrations. The authors examined whether systemic clonidine administration would alter the hemodynamic and catecholamine responses to hypoxia or hypercapnia in anesthetized dogs. Methods Pentobarbital-anesthetized dogs whose lungs were mechanically ventilated were instrumented for measurement of mean arterial pressure, heart rate, mean pulmonary artery pressure, right atrial pressure, cardiac output, left ventricular end-diastolic pressure, and the peak of first derivative of left ventricular pressure. The dogs were randomly assigned to receive an intravenous bolus injection of 10 microg/kg clonidine followed by continous infusion at a rate of 1 microg. kg (-1). min (-1)(clonidine-10 group, n = 7), an intravenous bolus injection of microg/kg clonidine followed by continuous infusion at a rate of 0.5 micro.kg(-).min(-1)(clonidine-5 group, n = 7), or an equivalent volume of 0.9% saline (control group = 7). Each dog underwent random challenges of hypoxia (PaO2 30, 40, and 50 mmHg) and hypercapnia (PaCO2 60, 80, and 120 mmHg). Measurements of hemodynamic and plasma norepinephrine and epinephrine concentrations were made after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia. Results Although significant increases from prehypoxic values in mean arterial pressure (39 +/- 10 mmHg) and plasma norepinephrine (291 +/- 66 pg/ml) and epinephrine (45 +/- 22 pg/ml) concentrations were noted during hypoxia of PaO2 30, mmHg in the control group (P&lt;0.05), such changes were absent in both clonidine groups. During hypercapnia of PaCo2 120 mmHg, changes from prehypercapnic values in mean arterial pressure, mean pulmonary artery pressure, the peak of first derivative of left ventricular pressure, and plasma norepinephrine and epinephrine concentrations in the clonidine-10 and clonidine-5 groups were significantly less than those in the control group. Plasma clonidine concentrations in the clonidine-10 and clonidine-5 groups were 16.8 +/- 1.7 and 8.9 =/- 1.0, 42.5 =/- 2.9 and 21.5 +/- 1.5, and 51.1 +/- 3.2 and 26.7 +/- 1.0 ng/ml after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia, respectively. Conclusions Systemic clonidine administration alter the hemodynamic changes associated with hypoxia or hypercapnia and suppresses plasma catecholamine responses in anesthetized dogs when a larger dose of clonidine is administered. catecholamines: epinephrine; norepinephrine.)


1999 ◽  
Vol 87 (3) ◽  
pp. 928-932 ◽  
Author(s):  
Bettina Pump ◽  
Regitze Videbæk ◽  
Anders Gabrielsen ◽  
Peter Norsk

Results from our laboratory have indicated that, compared with those of the 1-G supine (Sup) position, left atrial diameter (LAD) and transmural central venous pressure increase in humans during weightlessness (0 G) induced by parabolic flights (R. Videbæk and P. Norsk. J. Appl. Physiol. 83: 1862–1866, 1997). Therefore, because cardiopulmonary low-pressure receptors are stimulated during 0 G, the hypothesis was tested that mean arterial pressure (MAP) in humans decreases during 0 G to values below those of the 1-G Sup condition. When the subjects were Sup, 0 G induced a decrease in MAP from 93 ± 4 to 88 ± 4 mmHg ( P< 0.001), and LAD increased from 30 ± 1 to 33 ± 1 mm ( P < 0.001). In the seated position, MAP also decreased from 93 ± 6 to 87 ± 5 mmHg ( P < 0.01) and LAD increased from 28 ± 1 to 32 ± 1 mm ( P < 0.001). During 1-G conditions with subjects in the horizontal left lateral position, LAD increased compared with that of Sup ( P < 0.001) with no further effects of 0 G. In conclusion, MAP decreases during short-term weightlessness to below that of 1-G Sup simultaneously with an increase in LAD. Therefore, distension of the heart and associated central vessels during 0 G might induce the hypotensive effects through peripheral vasodilatation. Furthermore, the left lateral position in humans could constitute a simulation model of weightlessness.


1976 ◽  
Vol 54 (2) ◽  
pp. 154-159 ◽  
Author(s):  
Pierre Larochelle ◽  
Richard I. Ogilvie

Total effective vascular compliance was measured repeatedly in open-chest dogs without circulatory arrest, utilizing a closed-circuit venous bypass system with a constant cardiac output. Mutual inductance coils were used to measure the diameter of the inferior vena cava above the diaphragm at the position where the pressure change was recorded during a volume load (ΔV). In all experiments, there was a relationship which tended to be curvilinear between the diameter of the inferior vena cava and the venous pressure before ΔV. No relationship was demonstrated between the initial diameter or pressure and the calculated effective vascular compliance. During aortic constriction or infusion of noradrenaline, the effective compliance was reduced in value at any given initial venous diameter and pressure. An unaltered venous diameter and plasma volume excluded the possibility of a large change in initial venous volume as a cause of the observed changes in compliance during aortic constriction or during infusion of noradrenaline. A relationship was observed between compliance and calculated venous wall tension so that as the wall tension, developed during a fixed volume load, increased, there was an associated reduction in compliance. These results demonstrate that the measurement of effective compliance provides an assessment of combined active and passive venous wall tension and venous tone.


1983 ◽  
Vol 11 (2) ◽  
pp. 103-106 ◽  
Author(s):  
M. F. Cummings ◽  
W. J. Russell ◽  
D. B. Frewin ◽  
J. R. Jonsson

Changes in mean arterial pressure (MAP) and plasma catecholamine concentrations in response to endotracheal intubation were examined in 8 patients who had received d-tubocurarine and 10 who had received suxamethonium. MAP fell after induction of anaesthesia and administration of the relaxant by a mean of 11 mmHg in those who had received suxamethonium and 19 mmHg in those who had received d-tubocurarine (p <0.05 for each). MAP rose sharply when the trachea was intubated, by a mean of 29 mmHg for the suxamethonium group, and 35 mmHg for the curare group (p <0.001 for each). A significant rise in plasma noradrenaline was also noted after intubation in each group, 51% (p <0.01) for the suxamethonium group and 28% (p <0.05) for the d-tubocurarine. The results suggest that the fall in MAP after administration of d-tubocurarine does not attenuate the pressor response associated with intubation.


2015 ◽  
Vol 61 (2) ◽  
pp. 132-135
Author(s):  
IA Nechifor-Boila ◽  
H Suciu ◽  
Loghin Andrada ◽  
Borda Angela ◽  
A Maier ◽  
...  

Abstract Surgery for renal cell carcinomas with tumor thrombus extending in the Inferior Vena Cava (IVC) can be particularly challenging, especially in the retrohepatic and intraatrial situations (T3b and T3c). Classically, these tumors require the intraoperative use of cardio-pulmonary by-pass (CPB) and deep hypothermic circulatory arrest (DHCA), that can result in specific complications (stroke, platelet dysfunction), with increased postoperative morbidity rates. In urological practice, a particular IVC preparation method is currently in use, allowing full control both upon the IVC and its tributaries. It is derived from the “piggy-back” liver transplantation technique and implies the resection of all hepatic ligaments, leaving the hepatic vascular connections intact. This procedure is joined by a form of veno-venous bypass (between the right atrium and the infrarenal IVC) that allows a constant central venous pressure (by assuring blood return), with less bleeding and without the need for CPB and DHCA (avoiding, in this way, their inherent complications). All in all, these recently-introduced procedures can offer better thrombus control, improved oncologic outcomes and smaller complication rates. We aim to present a case of borderline T3b/T3c renal tumor that was successfully treated in our university center using these techniques.


1981 ◽  
Vol 241 (3) ◽  
pp. H449-H454
Author(s):  
G. Simon

Arterial pressure-flow and venous pressure-volume relationships were measured at maximal vasodilatation in the denervated pump-perfused hindquarters of four groups of rats: 1) neonatally sympathectomized (guanethidine-injected and adrenal-demedullated), one-kidney, one-clip hypertensive (n = 9); 2) sympathectomized, sham-operated, unilaterally nephrectomized control (n = 10); 3) sham-sympathectomized, one-kidney, one-clip hypertensive (n = 8); and 4) sham-sympathectomized, sham-operated, unilaterally nephrectomized control (n = 9). Dry defatted weight of anatomically defined segments of the aorta and vena cava in the four groups of rats also was measured. Significant rises in arterial pressure developed in sympathectomized rats after clipping of the renal artery and contralateral nephrectomy. Arterial pressure-flow curves were shifted toward the pressure axis (P less than 0.01) in clipped rats whether sympathectomized or not. In sympathectomized clipped rats, there was also a shift of the venous pressure-volume curves toward the pressure axis (P less than 0.05). The same degree of hypertrophy of the aorta was found in sympathectomized and sham-sympathectomized clipped rats. The findings indicate that in renal hypertensive rats structural changes of both large arteries and veins may develop in the absence of an intact sympathoadrenergic system.


Sign in / Sign up

Export Citation Format

Share Document