Gastrointestinal hemodynamics during compensation for hemorrhage and measurement of Pmcf

1994 ◽  
Vol 266 (3) ◽  
pp. H1242-H1250
Author(s):  
C. F. Rothe ◽  
R. Maass-Moreno
Keyword(s):  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Peripheral Resistance ◽  
Portal Flow ◽  
Total Blood ◽  
Flow Measurements ◽  
Control Value ◽  
Vascular Compliance ◽  
Autonomic Blockade

To quantify the degree of autonomic reflex control of the gastrointestinal vasculature, we studied the responses to a 10-ml/kg hemorrhage or transfusion and autonomic blockade in fentanyl- and pentobarbital-anesthetized dogs. The active total blood volume was estimated by indocyanine green dilution. Transfusion and hemorrhage did not significantly change gastrointestinal vascular compliance [1.82 +/- 0.68 (SD) ml/mmHg], but autonomic blockade with hexamethonium and atropine increased it by 0.57 +/- 0.37 ml/mmHg. Neither hemorrhage nor autonomic blockade significantly changed gastrointestinal vascular resistance from its control value of 10.8 +/- 4 mmHg.ml-1.min.kg body wt, but transfusion reduced it by 3.0 +/- 1.2 mmHg.ml-1.min.kg body wt. The ratio of gastrointestinal vascular resistance to total peripheral resistance was not significantly changed, however. We conclude that vascular compliance and resistance of the gastrointestinal bed are minimally influenced by the autonomic nervous system under the conditions studied. Portal pressure and flow measurements (transit-time ultrasound) during the above maneuvers were also combined with estimations of mean circulatory filling pressure (Pmcf) to test the hypothesis that, when the heart is stopped to measure Pmcf, portal pressure equals central venous pressure (Pcv) and hence that portal flow is zero. Seven seconds after the heart was stopped, portal venous pressure (Ppv) remained 0.83 +/- 0.78 mmHg higher than Pcv and portal flow decreased to only 25% of its control value. However, gastrointestinal compliance times (Ppv-Pcv), an estimate of the extra distending volume, was only 0.07 +/- 0.07 ml/kg body wt. Thus we conclude that the error in estimating Pmcf, given this (Ppv-Pcv) difference, is physiologically insignificant.

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

1996 ◽  
Vol 271 (2) ◽  
pp. H602-H613 ◽  
Author(s):  
M. P. Kunert ◽  
J. F. Liard ◽  
D. J. Abraham
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Experimental Models ◽  
Metabolic Demand ◽  
Flow Probe ◽  
Inositol Hexaphosphate ◽  
Control Value ◽  
Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

In vivo characterization of vasocontractile activities in erythrocytes

1983 ◽  
Vol 58 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Michael P. McIlhany ◽  
Lydia M. Johns ◽  
Thomas Leipzig ◽  
Nicholas J. Patronas ◽  
Frederick D. Brown ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Content Type ◽  
Control Value ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Chronic Cerebral Vasospasm ◽  
In Vivo Characterization

✓ Partially purified protein from washed and artificially hemolyzed erythrocytes, known to cause significant contractions of isolated canine cerebral vessels in vitro, was injected into the cisterna magna of intact anesthetized dogs. Cerebral blood flow, measured by the xenon-133 washout technique, decreased from a control value of 49.5 ± 1.17 ml/100 gm/min to an experimental value of 34.1 ± 1.65 ml/100 gm/min at 2 hours. Cerebral vascular resistance rose from a control value of 2.05 ± 0.17 PRU (peripheral resistance units) to an experimental value of 2.91 ± 0.25 PRU at 2 hours. Mean arterial blood pressure, heart rate, intracranial pressure, and cerebral perfusion pressure remained stable. Cardiac output also fell significantly (in 2-hour control animals it was 2.89 ± 0.37 liter/min, and in 2-hour experimental animals 1.43 ± 0.13 liter/min) and peripheral vascular resistance rose. These changes were evident by 10 minutes after the cisternal injection of the hemolysate protein, and remained for the duration of the 2-hour monitoring period. Serial vertebrobasilar angiograms demonstrated marked narrowing of the intracranial basilar artery when compared to control values. The narrowing persisted for several days in most animals, and tended to increase with time. Relaxation occurred by the 10th through the 14th day. The authors conclude that this experimental preparation may be a useful model for both in vitro and in vivo investigation of chronic cerebral vasospasm.

Influence of nisoldipine on vascular resistance and vasoconstrictor responses in cats

1987 ◽  
Vol 252 (4) ◽  
pp. H816-H825
Author(s):  
W. M. Armstead ◽  
H. L. Lippton ◽  
A. L. Hyman ◽  
P. J. Kadowitz
Keyword(s):  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Blocking Agent ◽  
Calcium Entry ◽  
Inhibitory Effects ◽  
Specific Receptor ◽  
Control Value ◽  
Vascular Bed ◽  
Adrenoceptor Agonists ◽  
Stimulation Of

The influence of nisoldipine, a calcium entry antagonist, on vascular resistance and vasoconstrictor responses was investigated in the anesthetized cat. Nisoldipine, a dihydropyridine calcium entry blocking agent, decreased total peripheral resistance and dilated the intestinal vascular bed. This calcium antagonist blocked intestinal vasoconstrictor responses to BAY K 8644, a nifedipine analogue, which promotes calcium entry. The calcium entry antagonist decreased intestinal vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine, and tyramine. Nisoldipine also reduced intestinal vasoconstrictor responses to potassium chloride and agonists that elicit vasoconstriction by specific receptor-mediated actions including stimulation of alpha 1- and alpha 2-adrenoceptors. The vasodilator and inhibitory effects of nisoldipine on vasoconstrictor responses were reversible, and responses returned to control value over a 60-min period. The present data suggest that an extracellular source of calcium is required for maintenance of tone and for vasoconstriction induced by neuronally released or exogenous norepinephrine as well as a diverse group of agents that act through specific receptor mechanisms or depolarize vascular smooth muscle. The present results suggest that similar sources of calcium are required for vasoconstriction elicited by alpha 1- and alpha 2-adrenoceptor agonists in the feline intestinal vascular bed.

Diminished baroreflex control of forearm vascular resistance in physically fit humans

1987 ◽  
Vol 63 (1) ◽  
pp. 105-110 ◽  
Author(s):  
G. W. Mack ◽  
X. G. Shi ◽  
H. Nose ◽  
A. Tripathi ◽  
E. R. Nadel
Keyword(s):  
Linear Relationship ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Vo2 Max ◽  
Total Blood ◽  
Baroreflex Control ◽  
Stimulus Response ◽  
Forearm Vascular Resistance

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) were studied in five unfit [UF, maximal O2 consumption (VO2 max) = 38.5 ml X min-1 X kg-1] and six fit (F, VO2 max = 57.0 ml X min-1 X kg-1) subjects. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure (CVP) and response, i.e., FVR, during selective unloading of the cardiopulmonary mechanoreceptors with lower body negative pressure (0 to -20 mmHg). The linear relationship between FVR and CVP, the gain of this baroreflex, was significantly diminished in the F subjects, -2.42 +/- 0.57 U/mmHg, compared with the UF, -5.15 +/- 0.58 U/mmHg. Both groups, F and UF, had similar resting values for CVP and FVR; thus the diminished gain in F subjects was not simply an artifact resulting from a shift of the set point along the baroreflex stimulus-response curve. We also found a linear relationship between baroreflex gain and total blood volume (r = 0.59, P less than 0.05). We conclude that the gain of this vascular reflex is attenuated in trained individuals and is related to cardiovascular adaptations, such as an increased blood volume, associated with exercise training.

Fetal placental vascular responses to prostacyclin after angiotensin II-induced vasoconstriction

1989 ◽  
Vol 257 (1) ◽  
pp. E102-E107
Author(s):  
V. M. Parisi ◽  
S. W. Walsh
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Control Period ◽  
Vena Cava ◽  
Ang Ii ◽  
Flow Measurements ◽  
Control Value ◽  
Blood Flow Measurements ◽  
Infusion Period

The vasodilator prostacyclin is produced by many fetal tissues and may serve to protect umbilical placental blood flow. We hypothesized that prostacyclin could reverse fetoplacental vasoconstriction produced by angiotensin II (ANG II). Studies were done in eight unanesthetized near-term ovine fetuses. After a control period, ANG II was infused into the fetal inferior vena cava at a rate of 0.5 microgram/min for 40 min. Twenty minutes after starting the ANG II infusion, an infusion of prostacyclin at a rate of 5 micrograms/min was added to the ANG II infusion. Blood flows were measured by the radioactive microsphere technique. Blood flow measurements were made during the control period, 20 min after starting the ANG II infusion, and 20 min after adding prostacyclin to the ANG II infusion. ANG II produced significant fetal hypertension and renal, intestinal, and placental vasoconstriction. Placental vascular resistance rose from 0.14 +/- 0.01 to 0.18 +/- 0.01 mmHg.min.kg fetal wt.ml-1 during the ANG II infusion period (P less than 0.05). The addition of prostacyclin to the ANG II infusion resulted in a return to control values for fetal blood pressure and renal and intestinal resistance. However, placental vasoconstriction was not reversed by addition of prostacyclin as placental vascular resistance remained significantly elevated over the control value (0.17 +/- 0.01 mmHg.min.kg fetal wt.ml-1). Although unchanged by ANG II infusion, fetal pH decreased significantly during the ANG II plus prostacyclin infusion period. We conclude that ANG II causes fetal hypertension and renal and intestinal vasoconstriction, which are reversed by prostacyclin.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of orthotopic transplantation of liver on systemic and splanchnic hemodynamics in conscious rat

1995 ◽  
Vol 269 (1) ◽  
pp. G153-G159 ◽  
Author(s):  
L. V. Kuznetsova ◽  
D. Zhao ◽  
A. M. Wheatley
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Portal Pressure ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
Suture Technique ◽  
Arterial Blood Flow ◽  
Conscious Rat ◽  
Arterial Blood

The long-term cardiovascular effects of orthotopic liver transplantation (OLT) were studied in conscious Lewis rats with a radioactive microsphere technique. Three months after OLT with an all-suture technique for graft revascularization (s-OLT), all hemodynamic parameters were similar to control. OLT with "cuffs" fitted to the portal vein and infrahepatic inferior vena cava (c-OLT) led to prominent hemodynamic disturbances including 1) hyperkinetic circulation with increased cardiac index (CI; 22%; P < 0.05) and decreased mean arterial pressure (15%; P < 0.05) and total peripheral resistance (TPR; 28%; P < 0.05); 2) a slight increase in portal pressure (11.8 +/- 0.9 vs. 9.3 +/- 1.7 mmHg in control) and marked portal-systemic shunting (51 +/- 11 vs. 0.05 +/- 0.04% in control; P < 0.05); 3) increased hepatic arterial blood flow (0.49 +/- 0.06 vs. 0.27 +/- 0.04 ml.min-1.g liver wt-1; P < 0.05); 4) splanchnic vasodilation with vascular resistance significantly (P < 0.05) lower in the liver, stomach, and large intestine; and 5) increased blood flow and decreased vascular resistance in the kidneys and heart. Ganglionic blockade with chlorisondamine (5 mg/kg body wt iv) indicated that the increase in CI seen in the c-OLT rats was probably sympathetically mediated, whereas the increase in renal blood flow was a reflection of the increase in CI. After ganglionic blocker administration, TPR and regional vascular resistances decreased to approximately the same extent in the control and c-OLT groups, indicating that vascular sympathetic tone was unchanged in the c-OLT rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Splanchnic and systemic haemodynamic response to volume changes in patients with cirrhosis and portal hypertension

1999 ◽  
Vol 96 (5) ◽  
pp. 475-481 ◽  
Author(s):  
Panagiotis VLAVIANOS ◽  
Padraik MAC MATHUNA ◽  
Roger WILLIAMS ◽  
David WESTABY
Keyword(s):  
Cardiac Output ◽  
Portal Hypertension ◽  
Systemic Vascular Resistance ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Haemodynamic Response ◽  
Volume Depletion ◽  
Compensated Cirrhosis

We investigated the haemodynamic response to volume depletion and subsequent repletion in patients with cirrhosis and portal hypertension. Twelve patients with compensated cirrhosis and portal hypertension were included in the study. The haemodynamic changes occurring after removal of approx. 15% of the blood volume, and subsequently after isovolume repletion with colloid, were assessed. Baseline haemodynamic measurements showed increased cardiac output and a systemic vascular resistance at the lower limit of normal. The hepatic venous pressure gradient (HVPG) was increased, at 18 mmHg. After depletion, arterial pressure, cardiac output and all right-heart-sided pressures decreased, and systemic vascular resistance increased. HVPG decreased to 16.0 mmHg. All the above changes were statistically significant. After blood volume restitution, the haemodynamic values returned to baseline. In particular, an increase in HVPG was shown in four out of the twelve patients (two with ascites and two without), which was small in three of them. However, HVPG remained the same as or lower than the baseline in the other eight patients. Patients with cirrhosis and portal hypertension exhibit an abnormal haemodynamic response to blood volume depletion. After volume repletion, no increase in the portal pressure was noted in this group of patients as a whole, although four out of the twelve patients did show an increase, possibly due to extensive collateral circulation.

Cirrhosis regression: extrahepatic angiogenesis and liver hyperarterialization persist

2018 ◽  
Vol 132 (12) ◽  
pp. 1341-1343
Author(s):  
Audrey Payancé ◽  
Pierre-Emmanuel Rautou
Keyword(s):  
Vascular Resistance ◽  
Antiviral Treatment ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Systemic Hemodynamics ◽  
Marginal Effect ◽  
Hemodynamic Changes ◽  
Systemic Hemodynamic ◽  
Duct Ligation ◽  
Intrahepatic Vascular Resistance

Data on the consequences of cirrhosis regression on portal hypertension and on splanchnic and systemic hemodynamic are scarce. Previous studies have reported a decrease in hepatic venous pressure gradient following antiviral treatment in patients with hepatitis B or C related cirrhosis. However, these studies did not investigate splanchnic and systemic hemodynamic changes associated with virus control. To fill this gap in knowledge, in a recent issue of Clinical Science, Hsu et al. (vol. 132, issue 6, 669-683) used rat models of cirrhosis induced by thioacetamide and by bile duct ligation and provided a comprehensive analysis of the effects of cirrhosis regression on splanchnic and systemic hemodynamics. They observed a significant reduction in portal pressure accompanied by a normalization of systemic hemodynamic (normal cardiac index and systemic vascular resistance) and a decrease in intrahepatic vascular resistance. No change in extrahepatic vascular structures were observed despite normalization of collateral shunting, meaning that portosystemic collaterals persist but are not perfused. One intriguing part of their results is the only marginal effect of cirrhosis regression on liver hyperarterialisation. This result suggests that changes in splanchnic hemodynamic features induced by cirrhosis remain when hepatic vascular resistance decreases, raising the hypothesis of an autonomous mechanism persisting despite regression of intrahepatic vascular resistance. Microbiota changes and bacterial translocation might account for this effect. In conclusion cirrhosis regression normalizes systemic hemodynamics, but some splanchnic hemodynamic changes persist including extrahepatic angiogenesis and liver hyperarterialization.

Mechanism of action of isoproterenol on venous return

1977 ◽  
Vol 232 (2) ◽  
pp. H152-H156 ◽  
Author(s):  
J. F. Green
Keyword(s):  
Venous Return ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vascular Effects ◽  
Right Heart ◽  
Control Value ◽  
Anesthetized Dogs ◽  
Venous Resistance ◽  
Right Heart Bypass ◽  
Transient And Steady State

The systemic vascular effects of isoproterenol infused in a dose of 1 mug-kg-1-min-1 was studied in 10 anesthetized dogs. A right heart bypass preparation allowed the separation of venous return into splanchnic and extrasplanchnic flows. Each channel was drained by gravity into an external reservoir. Venous return was then pumped into the pulmonary artery. During the infusion of isoproterenol, the pump was set at sufficient speed to maintain a constant level of blood in the external reservoir. Venous resistances and compliances of both channels were calculated from transient and steady-state volume shifts that occurred after rapid drops in splanchnic and then extrasplanchnic venous pressures. Isoproterenol affected both arterial and venous systems. Venous return increased from 1.62+/-0.11 to 2.40+/-0.19 liter/min (P less than 0.001) while arterial pressure fell from 97.5+/-3.8 to 70.2+/-5.9 mmHg (P less than 0.01). The compliances of the splanchnic and extrasplanchnic channels did not change significantly from their control values of 0.025+/-0.004 and 0.024+/-0.002 liter/mmHg. The venous resistance of the extrasplanchnic channel also did not change from its control value of 5.0 mmHg-liter-1-min-1; however, the splanchnic venous resistance decreased from 16.3+/-3.2 to 9.4+/-2.8 mmHg-liter-1-min-1 (P less than 0.001). The effective splanchnic back pressure, estimated by measuring the level to which hepatic venous pressure had to be raised to cause a change in portal pressure, decreased from 3.9 to 3.0 mmHg (P less than 0.01).

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