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PubMed1979

Effects of neurolept anaesthesia (NLA) on haemodynamics and oxygen consumption in the dog with special reference to the liver and preportal tissues.

The effects of neurolept anaesthesia (NLA) on central circulation, total oxygen uptake and splanchnic circulation and oxygen uptake were studied in 12 artificially ventilated dogs, basally anaesthetized with thiopental and nitrous oxide. Hepatic arterial, superior mesenteric arterial and portal venous blood flows were measured with electromagnetic flowmetry. Cardiac output was measured by thermodilution. Determinations of oxygen contents were made in arterial, pulmonary arterial, portal venous and hepatic venous blood. NLA was induced with droperidol 0.5 mg . kg-1 b.w. and fentanyl 0.01 mg . kg-1 b.w. Arterial blood pressure decreased to 63% of control value due to reductions of cardiac output to 78% and of total peripheral vascular resistance to 81% of control values. Hepatic arterial, superior mesenteric arterial and portal venous blood flows all diminished to 75% of control values. Hepatic arterial, superior mesenteric arterial and preportal tissue vascular resistances all decreased. Total oxygen uptake declined to the same extent as cardiac output, leaving the arterio-venous oxygen difference unchanged. Oxygen uptake of the preportal tissues was unaffected and hepatic oxygen uptake was not significantly reduced, although there were decreases of hepatic oxygen uptake in some of the individual dogs. It is suggested that the cardiovascular depression following NLA was due to adaptation to a lowered total oxygen uptake. It is further concluded that splanchnic circulation was well preserved due to decreases in splanchnic vascular resistances, and that splanchnic oxygen consumption was maintained by means of increased oxygen extraction.

Anesthetics↗

PubMed2001

Splanchnic and systemic hemodynamic effects of sustained euglycemic hyperinsulinemia in rats.

Insulin, in addition to its metabolic function, was found to induce skeletal muscle vasodilatation after acute administration. The vasoactive effects of sustained euglycemic hyperinsulinemia, especially in the splanchnic circulation, are less well known. The aim of this study was to evaluate the systemic and splanchnic hemodynamic effects of sustained euglycemic hyperinsulinemia. Hyperinsulinemia was induced by a sustained-release insulin implant in the scurf area of male rats (release rate -1 U/day). Beginning on the 3rd day, the study group was fed a glucose-rich diet. Hemodynamic studies were performed on the 5th day using the radioactive microsphere technique. Serum insulin was measured by radioimmunoassay. At the time of the hemodynamic measurements, plasma insulin level was higher in the insulin-treated (n=8) compared to control rats (n=8) (23.6 +/- 4.7 vs. 13.2+/-3.9 microu/mL, respectively; p<0.001). Plasma glucose level of the two groups was similar (5.43 +/- 1.07 vs. 5.83 +/- 1.44 mmol/L, respectively). Abdominal skeletal muscle blood flow was higher in the insulin-treated group (0.11 +/- 0.05 vs. 0.05 +/- 0.04 mL x min(-1) x g(-1), respectively; p<0.02). No significant changes were observed in cardiac output and renal blood flow. In the splanchnic circulation: stomach, pancreatic, intestinal, splenic, hepatic arterial and total hepatic blood flow were also not significantly different. In summary, short-term, sustained euglycemic hyperinsulinemia in rats increased blood flow to skeletal muscle but had no hemodynamic effects on cardiac output or splanchnic circulation.

Animals↗

PubMed1995

Cavernous transformation of the portal vein: patterns of intrahepatic and splanchnic collateral circulation detected with Doppler sonography.

OBJECTIVE: Cavernous transformation of the portal vein is defined as the formation of venous channels within or around a previously thrombosed portal vein. The purpose of this work was to study the hemodynamic consequences of cavernous transformation of the portal vein in a group of afflicted patients by use of Doppler sonography. We wished to study the evolution from portal vein thrombosis to the formation of cavernous transformation, the extent of resulting extrahepatic collateral channels, and the patterns of splanchnic collateral circulation. MATERIALS AND METHODS: Seventy-five patients (48 adults and 27 children) with cavernous transformation of the portal vein were studied with color and/or pulsed Doppler sonography. Blood flow in the extrahepatic portal vein, in its segmental branches, in the hepatic veins and artery, and in the splanchnic veins was examined. Collateral pathways were sought. For nine patients with acute thrombosis of the portal vein, serial examinations were performed during the formation of cavernous transformation. RESULTS: In nine patients, a fresh thrombus filled and distended the portal vein and became recanalized within a few days. Tortuous vessels appeared at the porta hepatis. These were characterized as veins or arteries with Doppler sonography. Soon the portal vein could no longer be identified within the mass of tortuous vessels. The cavernous transformation developed within 6-20 days of the acute thrombosis. A spongelike mass of collateral vessels around the main portal vein was seen in all but two patients. Intrahepatic extension of the cavernous transformation was seen in 57 patients (76%) and involved one or more intrahepatic portal veins. Two types of collateral circulation were observed: portosystemic, mainly through the left gastric and the perisplenic veins (the caput medusae, i.e., the paraumbilical-to-abdominal venous route, was never seen); and portoportal, from the periportal or pericholecystic venous channels to the intrahepatic portal veins. In nine patients, flow within unaffected intrahepatic branches of the portal vein was reversed as directed toward the cavernous transformation surrounding other, thrombosed intrahepatic segments of the portal vein. CONCLUSION: After thrombosis of the portal vein, portoportal venous channels may form not only at the porta hepatis but also within the liver. Intrahepatic blood may be shunted from one segmental portal vein to another. In addition, portosystemic collateral channels are formed, suggesting that, despite extensive hemodynamic adaptations, portal hypertension ensues.

Acute Disease↗

PubMed2001

Vascular smooth muscle cell signaling in cirrhosis and portal hypertension.

Abnormal vascular responsiveness to ligands has been frequently observed in cirrhosis and portal hypertension, but its existence is not proven. The signaling pathways in vascular smooth muscle cells (VSMCs) have been studied only in animal models of cirrhosis and portal hypertension. Emerging evidence suggests that active relaxation, expressed as augmented content or activity of effectors within the cyclic AMP signaling pathway and suppressed content or activity of effectors in the inositol 1,4,5-trisphosphate/1,2-diacylglycerol signaling pathway, may be occurring in VSMCs of the splanchnic circulation in portal hypertension. The evidence supporting the existence of this phenomenon in the VSMCs of extrasplanchnic circulations in portal hypertension, as well as in the splanchnic circulation when chronic cellular damage is present, is very limited. The status of the other signaling pathways associated with contractile functions of the VSMCs, viz., cyclic GMP and tyrosine kinase-linked pathways, is unknown. The status of all the signaling pathways in non-contractile functions of VSMCs, such as growth and remodeling, has not been studied. As our overall understanding on the signaling pathways in VSMCs is only emerging, it is premature to implicate altered activity of the signaling pathways as the underlying basis of vascular hyporesponsiveness in cirrhosis and portal hypertension, and to extrapolate these limited observations to the human condition.

Animals↗

PubMed1998

Superior mesenteric artery impedance in chronic liver diseases: relationship with disease severity and portal circulation.

OBJECTIVE: The increase of splanchnic blood flow volume in liver cirrhosis is attributed to decreased arterial resistance. The aim of this study was to noninvasively investigate superior mesenteric artery impedance in patients with chronic liver diseases and to assess its relationship with portal hemodynamics and with clinical parameters. METHODS: Superior mesenteric artery (SMA) pulsatility (SMA-PI) and resistance (SMA-RI) indices and portal vein flow parameters (velocity, volume, and congestion index) were measured by duplex-Doppler ultrasound in 14 patients with chronic hepatitis, in 73 cirrhotics, in 30 liver transplant recipients, and in 31 control subjects. RESULTS: SMA-PI significantly differed among the five groups (p < 0.0001), being lower in cirrhotics (2.55+/-0.70) and transplanted patients (2.77+/-0.69) than in chronic hepatitis (3.28+/-0.57) and control subjects (3.42+/-0.92). SMA-PI was lower in ascitic cirrhosis (2.40+/-0.71) than in compensated cirrhosis (2.71+/-0.70) (p < 0.01) and in cirrhotics with large varices (2.30+/-0.67) than in those without varices (2.75+/-0.65) (p < 0.05). Moreover SMA-PI correlated with numeric Child-Pugh score (r=-0.28) and portal vein congestion index (r=-0.36). CONCLUSION: Hyperdynamic splanchnic circulation, noninvasively assessed by a decrease of mesenteric artery impedance, occurs in cirrhosis since the early stage of the disease and tends to worsen in relation to liver failure and the severity of portal hypertension. Furthermore, the persistent SMA-PI decrease in transplant recipients suggests a consistent contribution to this circulatory alteration from a patent portosystemic collateral circulation.

Adult↗

PubMed1994

Role of EDRF in the regulation of regional blood flow and vascular resistance at rest and during exercise in conscious dogs.

The contribution of endothelium-derived relaxing factor (EDRF) to the regulation of regional vascular resistance and tissue blood flow at rest and during acute moderate exercise was studied in chronically instrumented conscious dogs. Radioactive microspheres were injected before and during exercise to measure regional blood flow. An infusion of nitro-L-arginine (L-NA), an analogue of L-arginine, was used to inhibit the synthesis of EDRF and resulted in a significant increase in mean arterial pressure, associated with significantly elevated vascular resistance in heart, skeletal muscle, renal and splanchnic circulations and with decreases in tissue blood flow in those regions at rest. Acute exercise caused a typical redistribution of blood flow, in which there was vasodilation in heart and working skeletal muscles, accompanied by vasoconstriction in kidney and splanchnic circulations. L-NA resulted in significantly elevated vascular resistance during vasodilation in heart and working skeletal muscles and also significantly increased vasoconstriction in renal cortex, stomach, pancreas, liver, and colon during exercise. Blood flows during exercise were largely unaffected by L-NA treatment. Our results suggest that whereas EDRF functions to regulate basal vascular tone and vascular resistance during exercise, EDRF has a minor role in determining the pattern of the redistribution of tissue blood flow during exercise.

Acetylcholine↗

PubMed2003

Mechanisms of water and sodium retention in cirrhosis and the pathogenesis of ascites.

Patients with advanced cirrhosis and portal hypertension often show an abnormal regulation of extracellular fluid volume, resulting in the accumulation of fluid as ascites, pleural effusion or oedema. The mechanisms responsible for ascites formation include alterations in the splanchnic circulation as well as renal functional abnormalities that favour sodium and water retention. Renal abnormalities occur in the setting of a hyperdynamic state characterized by an increase cardiac output, a reduction in total vascular resistance and an activation of neurohormonal vasoactive systems. This circulatory dysfunction, due mainly to intense arterial vasodilation in the splanchnic circulation, is considered to be a primary feature in the pathogenesis of ascites. A major factor involved in the development of splanchnic arterial vasodilation is nitric oxide (NO), a potent vasodilator that is elevated in the splanchnic circulation of patients with cirrhosis. This event decreases effective arterial blood volume and leads to fluid accumulation and renal function abnormalities which are a consequence of the homeostatic activation of vasoconstrictor and antinatriuretic factors triggered to compensate for a relative arterial underfilling. The net effect is avid retention of sodium and water as well as renal vasoconstriction. The mechanisms of sodium and water retention and ascites formation in patients with cirrhosis are discussed in this review.

Ascites↗

PubMed1994

The effect of adenosine-induced hypotension on systemic and splanchnic hemodynamics during halothane or sevoflurane anesthesia in the rat.

BACKGROUND: It has been suggested that the liver may be at risk for ischemic damage during adenosine-induced hypotension. This notion, however, is somewhat inconsistent with the understanding that adenosine is a powerful vasodilator of the splanchnic circulation. To help clarify the effect of adenosine-induced hypotension on splanchnic hemodynamics, we studied the systemic and splanchnic hemodynamic responses to adenosine, both alone and in the presence of halothane or sevoflurane. METHODS: Systemic and splanchnic hemodynamics were determined during the infusion of adenosine in 36 rats allocated randomly to one of three study groups: (1) awake, (2) halothane anesthesia (1.0 MAC), or (3) sevoflurane anesthesia (1.0 MAC). Adenosine was infused at a rate sufficient to decrease the mean arterial pressure by 35-38% from awake control values. Cardiac output and organ blood flows were measured using the radiolabeled microsphere technique. RESULTS: Adenosine infusion produced stable hypotension of rapid onset due to a reduction in systemic vascular resistance. Stroke volume increased, but cardiac output remained unchanged in the awake and sevoflurane groups because of a decrease in heart rate. Infusion of adenosine during halothane anesthesia increased cardiac output enough to compensate for the decrease in cardiac output due to halothane alone. In the splanchnic circulation, there was an increase in portal tributary (42%, P < 0.01) and hepatic arterial (38%, P < 0.05) blood flows during adenosine infusion in awake rats. This resulted in an overall increase in total liver blood flow (42%, P < 0.01). Halothane anesthesia was associated with a decrease in portal tributary blood flow (28%, P < 0.05). In contrast, sevoflurane anesthesia was associated with an increase in hepatic arterial flow (35%, P < 0.05) but with no change in portal tributary blood flow. During halothane anesthesia, adenosine infusion increased portal tributary (90%, P < 0.01) and hepatic arterial (37%, P < 0.05) blood flows, thereby increasing total liver blood flow to values similar to those in awake adenosine-infused rats. During sevoflurane anesthesia, adenosine infusion increased portal tributary blood flow (48%, P < 0.01), but hepatic arterial blood flow did not increase beyond the values observed during sevoflurane anesthesia alone. CONCLUSIONS: These findings demonstrate that adenosine is a potent vasodilator of portal tributary and hepatic arterial vasculature in the rat and that the splanchnic hemodynamic effects of adenosine predominate over those of halothane and sevoflurane.

Adenosine↗

PubMed1979

Effects of enflurane on haemodynamics and oxygen consumption in the dog with special reference to the liver and preportal tissues.

The effects of enflurane anaesthesia on central circulation, total oxygen uptake, splanchnic circulation and splanchnic oxygen uptake were studied in 10 artifically ventilated dogs, basally anaesthetized with thiopental and nitrous oxide. Hepatic arterial, superior mesenteric arterial and portal venous blood flows were measured with electromagnetic flowmetry. Cardiac output was measured by thermodilution. Determinations of oxygen contents were made in arterial, pulmonary arterial, portal venous and hepatic venous blood. The end-tidal enflurane concentration was kept at about 1 MAC (= 2.2%). Arterial blood pressure diminished 54% of control value due to decreases of cardiac output to 65% and of total peripheral vascular resistance to 81% of control values. Hepatic arterial, superior mesenteric arterial and portal venous blood flows decreased to 65-70% of control levels and the corresponding vascular resistances all declined to about 80-85% of control values. Total oxygen uptake decreased, but less than cardiac output, leading to an increased arterio-venous oxygen content difference. Oxygen uptake of the preportal tissues was unchanged and hepatic oxygen uptake was not significantly altered, although there were decreases in hepatic oxygen uptake in some of the individual experiments. It is suggested that the cardiovascular depression following enflurane anaesthesia in the dog was due, to a great extent, to a primary myocardial depression. It is further concluded that the splanchnic blood flows were relatively well preserved, due to decreases in splanchnic vascular resistances, and that hepatic and preportal tissue oxygen consumptions were maintained by increased oxygen extraction.

Anesthesia, General↗

PubMed1999

[The status of splanchnic blood circulation in patients with varicose veins of the esophagus and stomach in liver cirrhosis].

Complex hemodynamical investigations were done in 166 patients with liver cirrhosis and the portal hypertension syndrome. Patients with varicose veins of the esophagus and stomach versus patients with isolated varicose veins of the esophagus have significantly higher resistance of vessels of the a. hepatica and v. porta systems, more pronounced losses of portal perfusion at the expense of varicose veins of stomach, gastro- and splenorenal shunts and lower volumetric blood flow in v. lienalis. While varicose veins of the esophagus and stomach occur an absolute values of the arterial and portal blood flow in liver are lowering, common hepatic blood flow reduces. The varicose veins of the stomach existence testifies high degree of the portosystemic shunting development with subsequent lowering of volumetric blood flow in v. lienalis in comparison with such in isolated varicose veins of the esophagus.

Adult↗

PubMed2004

Review article: pharmacological treatment of hepatorenal syndrome.

Hepatorenal syndrome (HRS) is a common complication of advanced cirrhosis characterized not only by renal failure but also by marked alterations in systemic haemodynamics and activity of endogenous vasoactive systems. Renal failure is due to a severe vasoconstriction of the renal circulation. The pathogenesis of HRS is not completely understood but it is probably the result of extreme underfilling of the arterial circulation secondary to arterial vasodilation located in the splanchnic circulation. As well as the renal circulation, all other extrasplanchnic vascular beds appear to be vasoconstricted. The diagnosis of HRS is currently based on the exclusion of nonfunctional causes of renal failure; prognosis of patients with HRS is very poor. Liver transplantation is the best option in selected patients, but it is not always applicable as survival expectancy is short. Vasoconstrictor drugs with preferential effect on the splanchnic circulation (vasopressin analogues with a predominant V1 receptor effect, such as terlipressin--Glypressin) are very effective in improving renal function, with reversal of HRS being achieved in approximately two-thirds of patients. There is no agreement as to the terlipressin treatment regimen that is associated with a greater efficacy and lower incidence of side-effects. It appears that the administration of albumin together with terlipressin improves the therapeutic response rate. The impact of treatment on the natural course of HRS remains to be assessed in prospective investigations, but it seems that the reversal of HRS is associated with improved survival. Finally, treatment of patients with HRS with terlipressin before transplantation seems to improve post-transplantation outcome.

Adrenergic alpha-Agonists↗

PubMed1993

Persistence of systemic and splanchnic hyperkinetic circulation in liver transplant patients.

Portal pressure and portal-systemic collateral circulation after orthotopic liver transplantation have not been investigated. We studied systemic and splanchnic hemodynamics in 17 patients with cirrhosis before and 205 +/- 146 days after orthotopic liver transplantation. Among the 17 orthotopic liver transplantation patients, 12 had undergone hemodynamic study in the 6 mo before orthotopic liver transplantation. Controls were 50 patients with normal liver architecture. Cardiac index remained elevated in orthotopic liver transplantation patients compared with controls (3.6 +/- 0.9 vs 3.1 +/- 0.4 L/min.m2; p < 0.05). Azygos blood flow, which was elevated before orthotopic liver transplantation (585 +/- 402 ml/min), remained elevated after orthotopic liver transplantation (553 +/- 343 ml/min). In transplant patients, hepatic blood flow was higher than it was in controls (2.26 +/- 0.86 vs. 1.38 +/- 0.57 L/min; p < 0.05). Elevated hepatic blood flow correlated with cardiac index (r = 0.647, p < 0.025). In patients with normal graft function, hepatic venous pressure gradient was normal (2 +/- 1 mm Hg). In a patient with acute rejection, a sharp elevation in the hepatic venous pressure gradient was observed; it returned to normal 45 days after treatment. We conclude that despite normal portal pressure, portal-systemic collateral blood flow remains elevated after orthotopic liver transplantation. Possibly because of persistent collateral circulation, which may keep portal tributary blood flow elevated, hepatic blood flow is increased after orthotopic liver transplantation. Elevated splanchnic blood flow, in turn, contributes to the high cardiac index in liver recipients. Finally, a sharp elevation in portal pressure, which may be observed during acute rejection and subsides after treatment, merits further study.

Adult↗

PubMed2000

Hepatorenal syndrome: new perspectives in pathophysiology and management.

Hepatorenal syndrome (HRS) is a unique form of acute renal failure occurring in patients with advanced liver disease. Despite the severe derangement of renal function and ominous prognosis, minimal pathologic abnormalities of the kidneys are found at autopsy. The kidneys, if transplanted, are capable of normal function, which supports the concept that renal failure is functional and potentially reversible. The pathogenesis of HRS is not completely known, but it is probably the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in splanchnic circulation. Besides the renal circulation, all other extrasplanchnic vascular beds also appear to be vasoconstricted. The diagnosis of HRS is currently based on several widely accepted diagnostic criteria aimed at excluding nonfunctional causes of renal failure. Recently initiated therapeutic approaches lend a note of optimism to the future management of HRS. These include liver transplantation as definitive treatment for patients with end-stage liver disease, and introduction of new vasoconstrictor drugs with the preferential effect on the splanchnic circulation. The development of HRS after spontaneous bacterial peritonitis may be effectively prevented by the administration of albumin together with antibiotic therapy.

Hepatorenal Syndrome↗

PubMed2000

Diagnosis and treatment of hepatorenal syndrome.

Hepatorenal syndrome (HRS) is a common complication of advanced cirrhosis characterized not only by renal failure due to a marked vasoconstriction of the renal circulation but also by marked alterations in systemic haemodynamics and activity of endogenous vasoactive systems. The pathogenesis of HRS is not completely known but it is probably the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. Besides the renal circulation all other extrasplanchnic vascular beds appears to be vasoconstricted. The diagnosis of HRS is currently based on the exclusion of non-functional causes of renal failure. Prognosis of patients with HRS is very poor. Liver transplantation is the best option in selected patients, but is seldom applicable due to the short survival expectancy of most patients with HRS, particularly those with the progressive type (type I HRS). Therapies introduced during the last few years, such as transjugular intrahepatic portosystemic shunts or, particularly, vasoconstrictor drugs with preferential effect on the splanchnic circulation (V1 receptor agonists) are very effective in improving renal function and reverting HRS. However, the impact of the improvement of renal function on the natural course of HRS is unknown. Finally, the development of HRS after spontaneous bacterial peritonitis can be effectively prevented by the administration of albumin together with antibiotic therapy.

Female↗

PubMedDate not supplied

Hepatorenal syndrome.

The hepatorenal syndrome is a severe and common complication of patients with advanced cirrhosis and ascites. It is characterised not only by renal failure but also by marked alterations in systemic haemodynamics. Renal failure is due to a marked hypoperfusion of the kidney secondary to renal vasoconstriction. Although the pathogenesis of hepatorenal syndrome is not completely understood, it is thought to be the extreme manifestation of the underfilling of the arterial circulation secondary to an arterial vasodilation, located mainly in the splanchnic circulation. Recently, a revised definition and diagnostic criteria of hepatorenal syndrome have been proposed. The prognosis of patients with hepatorenal syndrome is very poor. Liver transplantation is the only effective treatment but it is not applicable in most cases due to short survival. New therapies developed during the last years, such as the use of systemic vasoconstrictors or transjugular intra-hepatic portosystemic shunts appear to be promising, but prospective investigations are needed to delineate their real usefulness.

Ascites↗

PubMed1995

Hereditary haemorrhagic telangiectasia and secondary biliary cirrhosis.

We report the case of a 65-year-old woman with a 10-year history of biliary disease and a 3-year history of anaemia, lethargy, angina and recurrent ascending cholangitis; she had hereditary haemorrhagic telangiectasia (HHT) with aneurysms in the splanchnic circulation, and was assumed to have secondary biliary cirrhosis with portal hypertension and hypertrophic obstructive cardiomyopathy. Her portal hypertension was caused by secondary biliary cirrhosis induced by intrahepatic gallstones; this was associated with left ventricular hypertrophy and a high cardiac output, caused by increased splanchnic circulation, and with aneurysms in the superior mesenteric and pancreaticoduodenal arteries, which were visualized by angiography. We conclude that HHT can produce abnormal abdominal vascular anatomy, which affects haemodynamic performance and makes it difficult to manage a patient with portal hypertension caused by secondary biliary cirrhosis. HHT has been shown to be associated with intrahepatic biliary stones and might have a causal role. When assessing patients with this type of condition for liver transplantation, particular attention should be paid to haemodynamic and circulatory abnormalities.

Aged↗

PubMed1987

Splenic artery and superior mesenteric artery blood flow: nonsurgical Doppler US measurement in healthy subjects and patients with chronic liver disease.

The accuracy of the duplex Doppler ultrasound system in the measurement of blood flow in the splenic artery and the superior mesenteric artery was evaluated in seven anesthetized dogs by comparing blood flow recordings obtained simultaneously with the electromagnetic flowmeter, with those obtained with the combination of B-mode and M-mode scanning. Various flow rates were produced by the infusion of dopamine. Splenic artery blood flow and superior mesenteric artery blood flow measured with the duplex system exhibited significant correlations with corresponding values obtained with electromagnetic flow measurements (r = .93 and r = .93, respectively). Changes in splanchnic circulation with the progression of chronic liver disease in humans were then investigated with the use of the duplex system. Splenic artery blood flow and superior mesenteric artery blood flow were significantly increased in patients with cirrhosis compared with patients with chronic hepatitis and healthy subjects. These results indicate that a hyperdynamic circulatory state may develop in the splanchnic circulation of the intestine and spleen in cirrhotic patients.

Adult↗

PubMed2002

Haemodynamic and splanchnic organ blood-flow responses to hypotension induced by the calcitonin gene-related peptide and sodium nitroprusside in dogs.

BACKGROUND AND OBJECTIVE: To elucidate the effects of various degrees of hypotension induced by the calcitonin gene-related peptide (CGRP) on the splanchnic circulation, we investigated the renal and hepatic blood flow during hypotension induced by either the calcitonin gene-related peptide or sodium nitroprusside in the isoflurane-anaesthetized dog. METHODS: Anaesthesia was maintained with 1.3% isoflurane in oxygen. After the baseline period, mean arterial pressure was reduced to 60 mmHg in the CGRP60 and nitroprusside groups, and to 50 mmHg in the CGRP50 group. The splanchnic organ blood flow was measured by hydrogen clearance. RESULTS: The cardiac index in the CGRP60 group increased (P < 0.01), but in the CGRP50 group it decreased (P < 0.01), and in the nitroprusside group it remained unchanged during hypotension. Mean pulmonary artery and pulmonary capillary wedge pressures in the CGRP60 group remained unchanged, but in the CGRP50 and nitroprusside groups they decreased (P < 0.01) during hypotension. Cardiac contractility in the CGRP60 group remained unchanged, whereas in the CGRP50 and nitroprusside groups it was reduced (P < 0.01) during hypotension. Renal blood flow in the CGRP60 group was relatively well maintained but in the CGRP50 and nitroprusside groups it was reduced (P < 0.01) throughout the observation. Hepatic blood flow in all three groups was reduced (P < 0.01) during hypotension. The reductions in hepatic blood flow between the Calcitonin gene-related peptide groups were associated with a dose-dependent decrease in mean arterial pressure. CONCLUSIONS: The results suggest that calcitonin gene-related peptide acts as an arteriolar vasodilator at low doses but as a vasodilator of the arteriolar and venous systems at higher doses, and that profound hypotension induced by the calcitonin gene-related peptide may impair splanchnic circulation.

Analysis of Variance↗