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PubMed1996

Systemic and splanchnic hemodynamic changes in patients with hepatic schistosomiasis.

Although hepatic schistosomiasis is a common cause of portal hypertension, only a few hemodynamic studies, in humans, have been published on this subject. The aim of this study was to determine the systemic and splanchnic hemodynamic changes in hepatic schistosomiasis and to evaluate the influence of liver fibrosis on these changes. A retrospective analysis of a series of 13 patients with hepatic schistosomiasis who had undergone hemodynamic studies was performed. Portal or perisinusoidal fibrosis was present at liver biopsy in 8 patients. The control group included 22 patients with chronic hepatitis and normal hepatic venous pressure gradients. Patients with schistosomiasis exhibited high cardiac index (4.11 +/- 1.15 l.min-1.m-2 vs 2.99 +/- 0.85 l.min-1.m-2; p < 0.05) and low systemic vascular resistance (1039 +/- 316 dyn.s.cm-5 vs 1334 +/- 336 dyn.s.cm-5; p < 0.05). The hepatic venous pressure gradient and hepatic blood flow were normal. Azygos blood flow was markedly increased (0.90 +/- 0.66 l.min-1 vs 0.13 +/- 0.04 l.min-1; p < 0.05). Hemodynamic values were not significantly different between patients with liver fibrosis and those without fibrosis at liver biopsy. In conclusion, patients with hepatic schistosomiasis had a hyperkinetic systemic and splanchnic circulation. In patients with esophageal varices, a normal hepatic venous pressure gradient confirmed presinusoidal portal hypertension. The presence of portal or perisinuoidal fibrosis did not influence hyperdynamic splanchnic state.

Adult↗
PubMed2005

Bench-to-bedside review: Is there a place for epinephrine in septic shock?

The use of epinephrine in septic shock remains controversial. Nevertheless, epinephrine is widely used around the world and the reported morbidity and mortality rates with it are no different from those observed with other vasopressors. In volunteers, epinephrine increases heart rate, mean arterial pressure and cardiac output. Epinephrine also induces hyperglycemia and hyperlactatemia. In hyperkinetic septic shock, epinephrine consistently increases arterial pressure and cardiac output in a dose dependent manner. Epinephrine transiently increases lactate levels through an increase in aerobic glycolysis. Epinephrine has no effect on splanchnic circulation in dopamine-sensitive septic shock. On the other hand, in dopamine-resistant septic shock, epinephrine has no effect on tonometric parameters but decreases fractional splanchnic blood flow with an increase in the gradient of mixed venous oxygen saturation (SVO2) and hepatic venous oxygen saturation (SHO2). In conclusion, epinephrine has predictable effects on systemic hemodynamics and is as efficient as norepinephrine in correcting hemodynamic disturbances of septic shock. Moreover, epinephrine is cheaper than other commonly used catecholamine regimens in septic shock. The clinical impact of the transient hyperlactatemia and of the splanchnic effects are not established.

Animals↗
PubMed1999

Angiotensin II receptor antagonism increases gut oxygen delivery but fails to improve intestinal mucosal acidosis in porcine endotoxin shock.

The renin angiotensin system is highly activated in shock states and has been suggested to be involved in the pathophysiology of the markedly deteriorated splanchnic circulation seen in septic shock. The purpose of the present study was to elucidate the capability of losartan, a nonpeptide angiotensin II type 1 (AT1) receptor antagonist, to attenuate splanchnic blood flow disturbances and counteract intestinal mucosal acidosis in endotoxin shock. A total of 20 pigs were anesthetized and catheterized. Central and regional hemodynamics were monitored. A tonometer in the ileum was used for measurement of mucosal pH. Onset of endotoxin challenge was followed by losartan administration (n = 10) 2 h later. Ten animals receiving endotoxin only served as controls. The experiments were terminated 5 h after onset of endotoxin challenge. Endotoxin infusion induced an hypodynamic shock with a reduction in cardiac index and systemic oxygen delivery. Losartan reduced both systemic vascular resistance and pulmonary capillary wedge pressure while stroke volume was improved. Pulmonary hypertension induced by endotoxin was significantly reduced by losartan without further changes in gas exchange. The profound reduction in gut oxygen delivery in response to endotoxin was counteracted by losartan administration. However, losartan failed to improve the markedly deteriorated intestinal mucosal pH and mucosal-arterial PCO2gap (i.e., difference in intestinal mucosal PCO2 and arterial PCO2). Also the mucosal-portal venous PCO2gap, used as a monitor of the mucosa in relation to the gut as a whole (including the spleen and pancreas), was greatly increased by endotoxemia but unaffected by losartan administration. In summary, although the angiotensin II type 1 receptor antagonist losartan improved gut oxygen delivery and reduced pulmonary hypertension during established endotoxin shock, it had no effect on intestinal mucosal acidosis. These findings suggest contribution of the angiotensin II type 1 receptor to perfusion disturbances, but not to deterioration of intestinal mucosal homeostasis seen during endotoxemia.

Acidosis↗
PubMedDate not supplied

Pathophysiology, diagnosis and treatment of ascites in cirrhosis.

The mechanism by which ascites develops in cirrhosis is multifactorial Severe sinusoidal portal hypertension and hepatic insufficiency are the initial factors. They lead to a circulatory dysfunction characterized by arterial vasodilation, arterial hypotension, high cardiac output and hypervolemia and to renal sodium and water retention. There are evidences that arterial vasodilation in cirrhosis occurs in the splanchnic circulation and is related to an increased synthesis of local vasodilators. Vascular resistance is normal or increased in the remaining major vascular territories (kidney, muscle and skin and brain). Splanchnic arterial vasodilation not only impairs systemic hemodynamics and renal function but also alters hemodynamics in the splanchnic microcirculation. The rapid and high inflow of arterial blood into the splanchnic microcirculation is the main factor increasing hydrostatic pressure in the splanchnic capillaries leading to an excessive production of splanchnic lymph over lymphatic return. Lymph leakage from the liver and other splanchnic organs is the mechanism of fluid accumulation in the abdominal cavity. Continuous renal sodium and water retention perpetuates ascites formation. Large volume paracentesis associated with albumin infusion is the treatment of choice of tense ascites because it is very effective and rapid and is associated with fewer complications that the traditional treatment (sodium restriction and diuretics). However, diuretic should be given after paracentesis to prevent reaccumulation of ascites. In patients with moderate ascites diuretics should be preferred as initial therapy. Patients with refractory ascites could be treated by paracentesis or percutaneous transjugular portacaval shunt (TIPS). TIPS is more effective in the long term control of ascites but may impair hepatic function and induce chronic hepatic encephalopathy.

Ascites↗
PubMed1998

Effects of fenoldopam on systemic and splanchnic haemodynamics and oxygen delivery/consumption relationship during hyperdynamic ovine endotoxaemia.

OBJECTIVE: To evaluate the use of a selective dopamine-1 agonist (fenoldopam) to provide selective splanchnic vasodilatation during sustained hypotensive endotoxaemia in sheep. DESIGN: Randomised, controlled, experimental study. SETTING: Animal research laboratory. SUBJECTS: 12 adult instrumented, midazolam-sedated sheep. INTERVENTIONS: The animals were randomised to receive a 20-min continuous infusion of dopamine (10 microg x kg(-1) x min(-1), fenoldopam (10 microg x kg(-1) x min(-1) and noradrenaline (1 microg x kg(-1) x min(-1)) under control conditions and 12 h after endotoxaemia was induced by a continuous infusion of Escherichia coli endotoxin producing a stable hyperdynamic state simulating human septic shock. This drug dosage was selected to produce a 25-30% increase in cardiac output by all three drugs during control conditions. MEASUREMENTS AND RESULTS: Systemic and splanchnic haemodynamic data were continuously obtained and systemic and splanchnic oxygen delivery (DO2) and consumption (VO2) were calculated. Hyperdynamic hypotensive endotoxaemia did not modify the splanchnic and renal reduction in DO2 and the vasoconstrictive reactivity to noradrenaline observed during control conditions. In contrast, endotoxaemia abolished the fenoldopam and dopamine-induced increase in splanchnic DO2 (especially in the coeliac trunk) observed during control conditions. CONCLUSIONS: During sustained hyperdynamic endotoxaemia, the dopaminergic-induced selective increase in coeliac trunk blood flow is abolished, most probably because of an already maximally vasodilated splanchnic circulation which prevented dopamine or fenoldopam to vasodilate this area further. Contrary to common belief, selective dopamine-1 agonist administration under these conditions may therefore not be beneficial to the splanchnic organs, though it improves whole body DO2 and VO2.

Animals↗
PubMed1995

Why portal hypertensive varices bleed and bleed: a hypothesis.

Continued bleeding or early rebleeding is associated with a poor prognosis in patients with variceal haemorrhage. It is not clear why bleeding stops in some patients and continues or restarts in others. It is suggested that secondary haemodynamic changes in the splanchnic circulation after a bleed may contribute to the risk of further bleeding. These changes include the effects of hypotension on portocollateral resistance, the effects of blood in the gut on splanchnic blood flow, and the effects of blood volume expansion on portal venous pressure during resuscitation. These factors, working in concert, cause a secondary rise in portal venous pressure, which may precipitate further bleeding. Treatment aimed at preventing these secondary haemodynamic changes may be beneficial. It is probable that somatostatin and octreotide could act in this way, which may explain their therapeutic efficacy.

Animals↗
PubMed1993

Changes in liver blood flow associated with the growth of hepatic LV10 and MC28 sarcomas in rats.

Abnormalities in liver blood flow are known to occur in patients and animals with overt hepatic tumour. This study investigated the changes in liver blood flow associated with the development of overt hepatic tumour in two different models. Hepatic tumour was induced by intraportal inoculation of either 300 LV10 sarcoma cells or 10(5) MC28 sarcoma cells in rats. Liver blood flow and hepatic haemodynamics were measured 3 weeks later when overt liver tumour was present. The hepatic perfusion index (HPI), the ratio of hepatic arterial to total liver blood flow, was raised and portal venous inflow reduced in rats with LV10 tumours, but not in those with MC28 lesions. Hepatic arterial flow was unchanged in LV10 tumours when the HPI was raised and neither model demonstrated arteriosystemic or portosystemic shunting. The changes in portal venous inflow were associated with a significant increase in portal and splanchnic vascular resistance. These studies suggest that liver blood flow changes in the presence of overt hepatic tumour are not related to portal venous obstruction but may be caused by a circulating splanchnic vasoconstrictor.

Animals↗
PubMed1988

Carotid sinus baroreceptor control of splanchnic resistance and capacity.

The contribution of the splanchnic vascular bed in the carotid sinus baroreceptor reflex control of vascular resistance and capacity was studied in nine pentobarbital-anesthetized dogs. The splanchnic circulation was vascularly isolated in an unopened abdomen and perfused at constant flow and venous pressure. Decreasing carotid sinus pressure from 200 to 50 mmHg resulted in a 72% increase in splanchnic vascular resistance and a decrease in splanchnic blood volume of 4.7 ml/kg. Changes in splanchnic inflow from 0 to 70 ml.min-1.kg-1 resulted in linear changes in splanchnic arterial pressure. Increasing carotid sinus pressure significantly decreased the slope (P less than 0.005) and intercept (P less than 0.025) of the splanchnic pressure-flow relationship. It is concluded that in the dog, the splanchnic vascular bed contributes a major portion of blood volume mobilized by the carotid sinus reflex.

Animals↗
PubMed1991

Catecholamine concentrations in the hepatic portal system: effect of surgical stress upon portal levels.

The biological effects of a hormone are dependent on the concentration delivered to the target tissue. This is generally best reflected in the arterial concentration. However, the liver is unique in that it receives substantial additional blood flow from the portal venous system. This may be important in the case of the catecholamines, where extraction or spillover from the splanchnic circulation may occur. In this study we examined portal venous catecholamine concentrations in anesthetized, laparotomized rabbits. We compared the values with simultaneously sampled arterial levels to evaluate the effects of the splanchnic tissues upon a wide range of catecholamine concentrations delivered to the liver during a state of stress. Spillover of norepinephrine and extraction of epinephrine were observed in all rabbits. Mean (+/- SEM) arterial norepinephrine concentrations were elevated, 716 +/- 167 pg/ml (n = 11); mean portal concentrations were 178 +/- 37% higher (p less than 0.01), at 1,425 +/- 301 pg/ml, representing net spillover from splanchnic tissues. In addition, significant extraction of epinephrine was observed; arterial concentrations were 2,144 +/- 580 pg/ml (n = 11). Portal levels were 1,205 +/- 382 pg/ml, 38 +/- 7.45% lower than corresponding arterial concentrations (p less than 0.02). Furthermore, there was a concentration-dependent effect upon norepinephrine spillover; the highest arterial norepinephrine concentrations were associated with the lowest splanchnic spillover. This resulted in a negative correlation between the arterial norepinephrine levels and the percent increase from spillover into the portal vein (r = -0.81, p less than 0.003). We conclude that portal venous catecholamine concentrations are significantly different from arterial levels in anesthetized, laparotomized rabbits over a wide range of concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Effect of acetylcholine on vascular capacity in the dog.

Acetylcholine produces venoconstriction of isolated vein strip preparations. However, the effect of acetylcholine on overall vascular capacity is not known. To investigate this effect and to elucidate the mechanisms involved, 38 anesthetized dogs were placed on total cardiopulmonary bypass, splenectomized, and given intraarterial infusions of acetylcholine. Almost all of the effect on vascular volume was found to be in the splanchnic circulation, because in four eviscerated animals there was no significant change in capacity. In the animals in which the mesenteric arteries were cannulated to provide constant inflow, and the hepatic vein was cannulated to measure splanchnic venus outflow, acetylcholine infusion for 5 and 21 min increased splanchnic vascular capacity in all animals by 107 +/- 28 (SEM)ml (p less than 0.01) and 291 +/- 132 ml (p less than 0.05), respectively. This increase in splanchnic vascular volume was associated with a rapid and sustained increase in transhepatic resistance to portal blood flow for the duration of the infusions (p less than 0.01). In the animals in which the portal vein was vented proximal to the liver, no significant volume change occurred in the splanchnic vasculature with acetylcholine infusion. Increasing hepatic venous pressure to elevate portal venous pressure to the same level as that achieved with acetylcholine resulted in a similar increase in splanchnic vascular volume. Atropine, but not adrenergic blockade, blocked the acetylcholine-induced volume retention, indicating that the effect of acetylcholine was direct. Substantial volume retention was also achieved by stimulation of the distal ends of the sectioned cervical vagi. Thus, acetylcholine administration directly increases transhepatic resistance and is associated with a pooling of volume in the splanchnic vasculature that would, in the intact animal, result in a decrease in venous return to the heart.

Acetylcholine↗
PubMed2005

A novel technique to measure splanchnic transit time using microbubble ultrasound.

OBJECTIVE: The objective of this study was to measure splanchnic transit time by intravenous injection of a microbubble. MATERIALS AND METHODS: Ten volunteers were examined before and after eating. After Doppler indices of splanchnic circulation were obtained, the superior mesenteric artery (SMA) and vein (SMV) were simultaneously interrogated using power Doppler ultrasound after intravenous injection of a microbubble. Contrast arrival in the SMA and subsequently the SMV was recorded and splanchnic transit time calculated from differences in the time-intensity curves. RESULTS: Splanchnic transit time decreased significantly after eating (mean 11 vs. 6.9 seconds; P = 0.007), reflecting splanchnic hemodynamics. Between-subject variability attributable to repeated measurements was least for the SMA resistive index (17%) but 56% for the new index, suggesting poor reproducibility. CONCLUSION: Splanchnic transit time may be measured by microbubble injection but is subject to considerable measurement error. Newer microbubbles and imaging methods may allow more reproducible measurements.

Adult↗
PubMedDate not supplied

Endoscopic demonstration that vasopressin but not propranolol produces gastric mucosal ischemia in dogs with portal hypertension.

Endoscopic reflectance spectrophotometry was used to compare the effect of vasopressin and propranolol on gastric mucosal hemodynamics in dogs with surgically induced esophageal varices and prehepatic portal hypertension. Reflectance spectrophotometry provides indices of mucosal hemoglobin concentration (IHB) and oxygen saturation (ISO2). Hyperemia (increased IHB, normal ISO2), ischemia without congestion (decreased IHB, decreased ISO2), and ischemia with congestion (increased IHB, decreased ISO2) are accompanied by characteristic patterns of IHB and ISO2. Under anesthesia, measurements were obtained on separate days from the gastric corpus mucosa of eight dogs before and 2 to 10 min after either 1 to 5 units of intravenous vasopressin or 1 mg of propranolol. Results revealed that vasopressin (in doses that significantly reduced variceal and portal venous pressure in this animal model) produced a reduction in both IHB and ISO2, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. On the other hand, propranolol in a dose that significantly reduced pulse rate by 27 +/- 2% had no effect on IHB or ISO2, suggesting that this dose of propranolol has no direct vasoactive effect on the gastric (splanchnic) circulation.

Animals↗
PubMed1994

Favorable effects of total paracentesis on splanchnic hemodynamics in cirrhotic patients with tense ascites.

Total paracentesis is widely used in the treatment of patients with cirrhosis and tense ascites. However, very little information is available regarding its consequences on splanchnic circulation, and its effects on portocollateral blood flow have not been investigated. Ten cirrhotic patients admitted because of tense ascites had measurements of hepatic and systemic hemodynamics, renal function and endogenous vasoactive neurohumoral systems at baseline, just after total paracentesis and 1 hr later. Total paracentesis caused a significant increase in cardiac output (+11%; 95% confidence interval, +4% to +19%) and a rapid fall in portal pressure, as shown by significant decreases in both the wedged hepatic venous pressure (-27% +/- 8%; p < 0.005) and the hepatic venous pressure gradient (-10%; 95% confidence interval, -3% to -18%). This was accompanied by a marked decrease in azygos blood flow (-28%; 95% confidence interval, -13% to -43%). These favorable hemodynamic effects were associated with a fall of the elevated levels of plasma renin activity (-47% +/- 9%; p < 0.05), plasma aldosterone (-31% +/- 21%; p < 0.05) and plasma norepinephrine and by a decrease in levels of serum creatinine (-24% +/- 15%; p < 0.05) and blood urea nitrogen (-4% +/- 3%; p < 0.05). These changes were maintained 1 hr later. This study indicates that in patients with cirrhosis and tense ascites total paracentesis favorably influences the systemic hemodynamics, portocollateral blood flow and portal pressure.

Aged↗
PubMed1993

Comparison of plasma androgen glucuronide levels after percutaneous or peroral androgen treatment in men: evidence for important splanchnic contribution to plasma 17 beta-hydroxyandrogen glucuronides.

To investigate whether glucuronides of 17 beta-hydroxyandrogens are formed mainly in peripheral tissues or in splanchnic tissues, we compared androstanediol (AD) glucuronide (ADG) and dihydrotestosterone (DHT) glucuronide (DHTG) levels as well as the ratios of glucuronides over free steroids after transcutaneous DHT gel administration to levels and ratios found after oral administration of testosterone undecanoate. Whereas DHT and AD plasma levels were much higher after transcutaneous DHT gel administration, ADG and DHTG levels as well as glucuronide/free androgen ratios were an order of a magnitude higher after oral TU. This indicates that 17 beta-hydroxyandrogen glucuronides cannot be considered specific metabolites of androgen target tissues and are formed to a large extent in the splanchnic circulation.

Administration, Cutaneous↗
PubMed2003

Effects of xenon on mesenteric blood flow.

BACKGROUND AND OBJECTIVE: The effects of xenon on mesenteric vascular resistance have not been investigated. Because human beings anaesthetized with xenon show good cardiovascular stability, we believed that the agent would have little or no effect on vascular resistance in the splanchnic bed. We determined the effects of different inhaled xenon concentrations on mesenteric blood flow and mesenteric oxygen consumption in pigs sedated with intravenous propofol. METHODS: Twenty-three minipigs were instrumented with transit time flow probes around the pulmonary and superior mesenteric arteries as well as with pulmonary artery and portal venous catheters. A 14 h recovery was allowed followed by recordings of baseline values. Xenon was then randomly administered in 0.30, 0.50, and 0.70 end-tidal fractions. RESULTS: The administration of xenon resulted in an 8% (not dose dependent) decrease in mean arterial pressure (from 99 +/- 15 to 91 +/- 19 mmHg; P < 0.05), a 20% decrease in calculated systemic oxygen consumption (from 0.23 +/- 0.07 to 0.19 +/- 0.04L min(-1); P < 0.01), a 20% reduction in mesenteric oxygen delivery (from 41 +/- 12 to 33 +/- 11 mL min; P < 0.001), a 37% reduction in mesentericmetabolic rate of oxygen (from 11.3 +/- 3.6 to 7.1 +/- 3.2 mL min(-1); P < 0.01) and an 8% decrease in mesenteric artery blood flow (0.22 +/- 0.07 to 0.20 +/- 0.07 L min(-1); P < 0.05) in a dose-dependent fashion. Heart rate, cardiac output, systemic vascular resistance, mesenteric vascular resistance, mesenteric oxygen extraction fraction and portal lactate concentration were not significantly altered by xenon. CONCLUSIONS: Xenon inhalation in the propofol-sedated pig had no measurable effects on mesenteric vascular resistance. This finding may partly explain the well-known cardiovascular stability observed in patients anaesthetized with xenon. Although mesenteric artery blood flow and mesenteric oxygen delivery decreased during xenon administration, unchanged mesenteric oxygen extraction fraction and portal lactate suggest that metabolic regulation of the splanchnic circulation remained unaltered.

Anesthetics, Inhalation↗
PubMed1989

Tryglycylvasopressin-reduced portal and systemic concentrations of serum bile acids after exogenous chenodeoxycholic acid load in rats as a reflection of reduced splanchnic blood flow.

The effect of triglycylvasopressin (TGVP) on the absorption of chenodeoxycholic acid (CDCA) was investigated in three groups of six rats (controls, CDCA, CDCA + TGVP) through the evaluation of portal and caval serum bile acids (SBA) concentrations after an oral load with CDCA to investigate whether changes in this parameter reflect variations in splanchnic blood flow induced by a vasoconstrictor. The results indicate that CDCA was absorbed and led to a significant increase in SBA. This increase was reduced by TGVP administration: portal blood 380.0 +/- 61.2 vs 279.7 +/- 45.3; caval blood 151.8 +/- 45.7 vs 41.7 +/- 12.5 (mumol/l; mean +/- s.d.). This suggests that variations in SBA concentrations could reflect changes in splanchnic circulation.

Animals↗
PubMed1996

Postprandial splanchnic hemodynamic response in patients with cirrhosis of the liver: evaluation with "triple-vessel" duplex US.

PURPOSE: To investigate the effect of a meal on splanchnic circulation in patients with cirrhosis of the liver. MATERIALS AND METHODS: Ten adult patients with cirrhosis and 10 adult control subjects (mean age, 54 years) underwent duplex ultrasonography. Flow volumes of the portal vein, superior mesenteric artery, splenic artery, and collateral vessels (difference between the splanchnic inflow [the sum of the superior mesenteric arterial and the splenic arterial blood flows] and the portal venous blood flow) were measured before and after a meal every 15 minutes for 60 minutes. Integrated post-prandial changes (the sum of the changes at each time point) were also calculated. RESULTS: Portal venous blood flow increased after the meal in control subjects (P < .01) and patients (P < .01). The integrated postprandial change in the portal venous blood flow was lower in patients than in control subjects (P < .05). Superior mesenteric arterial blood flow increased after the meal in control subjects (P < .01) and patients (P < .01); the integrated postprandial change in the superior mesenteric arterial blood flow was similar. In the two groups, splenic arterial blood flow remained unchanged after the meal. Collateral blood flow increased after the meal in patients (P < .01). CONCLUSION: Postprandial portal hyperemia is mainly due to mesenteric arterial vasodilation; reduced postprandial portal hyperemia in patients with cirrhosis is attributable to portocollateral runoff.

Adult↗
PubMed1996

Regulation of atrial natriuretic factor receptors in portal hypertensive rabbits.

BACKGROUND/AIMS: Portal hypertension is characterized by a marked splanchnic hyperemia due to a reduction in mesenteric vascular resistance. Possible mediators of this decreased resistance include an increased amount of and/or responsiveness to vasodilatory substances. Previous studies have demonstrated an enhanced hypotensive effect of exogenous atrial natriuretic factor in portal hypertension. We hypothesized that changes in the atrial natriuretic factor hormone receptor system may contribute to this response and hence underlie the marked hyperemia of portal hypertension. METHODS: We used a portal-vein-ligated rabbit model of portal hypertension to study the integrity of the atrial natriuretic factor receptor system within the hyperemic vasculature. RESULTS: There was no significant difference in the serum concentrations of sodium, potassium, atrial natriuretic factor, ANG-II, cGMP, serum osmolality, or hematocrit between normal and portal hypertensive rabbits. Superior mesenteric artery, thoracic aorta and portal vein atrial natriuretic factor receptor number and affinity were determined using [125I]-rANF99-126 binding analysis and affinity cross-linking studies. Receptor classification using specific atrial natriuretic factor-C receptor ligands, along with affinity cross-linking studies revealed two receptor subtypes present on these vessels. There was a significant decrease in the number of atrial natriuretic factor receptors in the portal vein and a significant increase in the superior mesenteric artery in portal hypertension without any significant change in affinity. Thoracic aortic atrial natriuretic factor receptors were increased with a concurrent decrease in affinity in portal hypertension. There was a concomitant increase in tissue cGMP levels within the superior mesenteric artery and thoracic aorta of portal hypertensive animals but not the portal vein. CONCLUSION: These data suggest the increased number of functional atrial natriuretic factor receptors may in part contribute to the hyperdynamic splanchnic circulation peculiar to portal hypertension.

Animals↗