Measurement of Splanchnic Circulation in Dogs: Changes Induced by Prostaglandin E1

In seven anesthetized dogs the effects of intravenously administered prostaglandin E₁ on mesenteric arterial and portal venous blood flows and pancreatic capillary blood flow were measured with a transit-time ultrasonic volume flowmeter and a laser Doppler flowmeter. Basal blood flow of the superior mesenteric artery and of the portal vein were 5.7 ± 0.6 and 11.2 ± 1.0 ml/min/kg, respectively. Prostaglandin E₁ caused a dose-dependent increase in these blood flows. The maximal effect was observed at a dose of 10μg/kg, when the superior mesenteric arterial blood flow increased 117.9 ± 3.2% and the portal venous blood flow increased 99.4 ± 1.7%. Prostaglandin E₁ produced an initial rapid increase, followed by a decrease in pancreatic capillary blood flow. The results indicate that the flowmeters used in the present study are widely available for the study of splanchnic circulation and may have a possibility for clinical application.     

Portal Hemodynamic Responses after Oral Intake of Glucose in Patients with Cirrhosis

Changes of portal, superior mesenteric, and splenic venous flows, and portohepatic gradient (portal vein pressure minus free hepatic vein pressure) after a meal were studied in patients with cirrhosis using the duplex ultrasonic Doppler flowmeter, and portal and hepatic vein catheterizations after ingestion of 227 ml of 33% glucose solution (300 kcal). As a control, changes of portal venous flow and portohepatic gradient after drinking 227 ml of water, were studied. Portal and superior mesenteric venous flows increased significantly at 30 min after glucose intake, and they returned gradually to the basal values, whereas no significant postprandial change occurred in splenic venous flow. The sum of superior mesenteric and splenic venous flows was greater than the estimated portal venous flow before glucose intake, and the difference widened during post-prandial mesenteric hyperemia, indicating an increase of blood flow into the portal-systemic shunts. After glucose intake, portohepatic gradient elevated immediately, in parallel with an increase of portal venous flow, and these changes persisted for the 30 min studied; however, no significant change occurred in these parameters after drinking water. In conclusion: 1) In patients with cirrhosis, hyperemia occurs in the intestine but not in the spleen after glucose intake, and 2) postprandial mesenteric hyperemia causes an increase of portal venous inflow, portal-systemic collateral flow, portal venous flow, and an elevation of portohepatic gradient.     

Portal Hemodynamics after Meal in Normal Subjects and in Patients with Chronic Liver Disease Studied by Echo-Doppler Flowmeter

Changes of portal, superior mesenteric, and splenic venous flows after a meal were studied with the duplex ultrasonic Doppler flowmeter in normal subjects, in patients with chronic active hepatitis, and in those with cirrhosis for 2 h after ingestion of a liquid meal (14% protein, 56% lipid, 30% carbohydrate, 300 kcal). Portal and superior mesenteric venous flows increased significantly throughout the experiment, whereas no significant change occurred in splenic venous flow after the meal in all three groups. The extent of the increase in portal venous flow was significantly lower in patients with cirrhosis, compared with normal subjects and patients with chronic active hepatitis, whereas superior mesenteric venous flow increased to the same extent in all three groups. The sum of superior mesenteric and splenic venous flows was less than the estimated portal venous flow in both normal subjects and patients with chronic active hepatitis; however, this value was greater than the portal venous flow in patients with cirrhosis. The difference widened during postprandial mesenteric hyperemia, indicating an increase of blood flow into the portal-systemic shunts. In conclusion 1) postprandial hyperemia occurs in the intestine, but not in the spleen, to the same extent in patients with chronic active hepatitis or with cirrhosis, as in normal subjects, and 2) a considerable amount of postprandial mesenteric hyperemia bypasses the liver into the systemic circulation of patients with cirrhosis but not in patients with chronic active hepatitis and normal subjects.     

Changes of Splanchnic Circulation with Progression of Chronic Liver Disease Studied by Echo-Doppler Flowmetry

Changes that occurred in splanchnic circulation with the progression of chronic liver disease were investigated using an ultrasonic Doppler flowmeter in healthy adults and in patients with chronic active hepatitis and liver cirrhosis in the supine position after an overnight fast. Superior mesenteric venous flow, splenic venous flow, and portal venous flow were significantly increased in patients with liver cirrhosis but not in patients with chronic active hepatitis compared with normal subjects. Portal venous flow (control value 10.5 +/- 2.3 ml/min/kg body weight) minus the sum of superior mesenteric venous flow and splenic venous flow was 0.8 +/- 2.1 ml/min/kg body weight in the control, (0.1 +/- 1.9) in chronic active hepatitis, and (-2.2 +/- 4.3) in liver cirrhosis; the difference was significant between the control and cirrhosis groups. These results indicate that in patients with liver cirrhosis a hyperdynamic state occurs in the splanchnic circulation of the intestine and spleen and that some portion of splanchnic blood flow bypasses the liver into the systemic circulation.     

The hepatic hemodynamic response to intra-arterial infusion of vasoactive agents--Part 1. Blood flow measurements in dogs

The common hepatic arterial (CHA), portal venous (PV) and liver tissue (LT) blood flows were measured during continuous infusion of vasoactive agents to the celiac axis under the observation of systemic circulation. The infusions of Angiotensin II (AT) (0.05 microgram/kg/min) and Prostaglandin F2 alpha (PGF) (0.025-0.05 microgram/kg/min) reduced CHA and LT blood flow, but caused no remarkable change of PV blood flow. The infusions of AT (0.5 microgram/kg/min) and PGF (0.5 microgram/kg/min) caused a biphasic response in CHA blood flow: an initial decrease in CHA blood flow was followed by a marked increase in this parameter (p less than 0.05), while PV blood flow decreased, but LT blood flow remained unchanged. The infusion of PGF (1.0 microgram/kg/min) reduced all parameters of CHA, PV and LT blood flows. The infusion of Dibutyryl cyclic AMP (DBcAMP) (2.0 mg/kg/hr) increased all parameters of CHA, PV and LT blood flows. Preinfusion of DBcAMP weakened the primary effects of PGF (1.0 microgram/kg/min) infusion.     

Hepatic arterial and portal flow in cardiogenic and hemorrhagic shock in awake dogs

The changes in liver blood flow produced by experimental cardiogenic and hemorrhagic shock are relatively unexplored. Fifteen unanesthetized dogs in which electromagnetic blood flow transducers had been implanted on the common hepatic artery and portal vein were subjected to acute myocardial infarction by mercury embolization of the circumflex coronary artery. Another group of ten dogs were bled to an arterial pressure of 40 mmHg and maintained at that level for 2 hours before reinfusion. Six additional dogs in which blood flow transducers had been implanted on the superior mesenteric artery and portal vein also were subjected to hemorrhage. In three of the six, phenoxybenzamine was infused directly into the superior mesenteric artery 45 minutes prior to bleed-out. During cardiogenic shock, both hepatic arterial and protal venous flow fell. However, whereas protal flow continued to fall, eventually stabilizing at values 36 +/- 3% of control, hepatic arterial flow subsequently rose, reaching values 93 +/- 9% above control. Total liver blood flow, after an initial decline to 53 +/- 4% of control levels rose as a result of the increased hepatic arterial flow to 73 +/- 4% of control values. During hemorrhage, both hepatic arterial and protal venous flows decreased as aortic pressure fell. Within 5 minutes of reinfusion, hepatic arterial flow surpassed its control values. Portal flow also increased but, on a percentage basis, not to so great an extent. Flow in hepatic artery remained high for 40 minutes after reinfusion, whereas portal flow rapidly decreased to levels seen at the end of hemorrhage. In hemorrhage without alpha-adrenergic receptor blockade the superior mesenteric bed constricted, thereby supporting systemic pressure. With alpha-adrenergic blockade, however, mesenteric flow became pressure-dependent and no longer acted as a homeostatic mechanism.     

Effects of vasopressin on left gastric venous flow in cirrhotic patients with esophageal varices

To assess vasopressin control of esophageal variceal bleeding, we investigated the effect of vasopressin on the left gastric venous flow, portal venous flow, superior mesenteric venous flow, and splenic venous flow in seven cirrhotic patients with esophageal varices, using a duplex system consisting of a real-time ultrasonograph and an echo-Doppler flowmeter. Infusion of vasopressin (0.3 U/min) significantly decreased the blood flow in the left gastric vein (-56%), portal trunk (-54%), superior mesenteric vein (-54%), and splenic vein (-56%) as a result of decrease of blood velocity in these vessels. Thus, vasopressin seems to control esophageal variceal bleeding, in part, by reducing blood velocity and blood flow in the left gastric vein following reduction of blood velocity and blood flow in the superior mesenteric vein and splenic vein.     

Hemodynamic effects of calibrated stenosis of the superior mesenteric artery in conscious rats with portal vein stenosis.

Because superior mesenteric arterial blood flow is increased in portal hypertension and plays a role in elevated portal pressure, mechanical reduction of artery diameter should induce decreases in portal pressure and superior mesenteric arterial blood flow. In this study, calibrated superior mesenteric artery stenosis (induced with a 22-gauge needle) was performed in rats simultaneously with portal vein stenosis or 2 wk after creation of portal vein stenosis. Hemodynamic studies were performed 3 wk after induction of portal vein stenosis in conscious, unrestrained rats. At that time, neither weight loss nor digestive tract alterations were observed in rats with arterial stenosis. In neither group of rats with arterial stenosis was portal tributary blood flow significantly different from that of normal rats; nor was it significantly lower than in rats with portal vein stenosis without arterial stenosis. In both groups of rats with arterial stenosis, portal pressure was significantly lower (12.1 +/- 1.6 mm Hg and 12.5 +/- 1.8 mm Hg, respectively) than in rats subjected to portal vein stenosis (15.4 +/- 1.5 mm Hg) but significantly higher than in controls (7.2 +/- 1.0 mm Hg). In rats with arterial stenosis, cardiac index was also significantly lower than that in rats with portal vein stenosis but higher than that in controls. In conclusion, this study shows that both early and late superior mesenteric artery stenosis significantly reduce the degree of portal hypertension and the hyperkinetic state of rats with extrahepatic portal hypertension. Thus we can speculate that superior mesenteric artery stenosis might provide a new therapeutic approach for portal hypertension.     

Interrelationship between splenic and superior mesenteric venous circulation manifested by transient splenic arterial occlusion using a balloon catheter

We examined the hemodynamic changes induced by transient splenic arterial occlusion using a balloon catheter to investigate the hemodynamic effect of transcatheter splenic arterial embolization--a procedure that has been used since its introduction in 1973 as therapy for hypersplenism and more recently for portal hypertension. The blood flow volume was measured in 20 patients with liver disease using an ultrasonic duplex system (Toshiba SAL50A/SDL-01A). The portal venous pressure was also measured via a 3F catheter using a transducer. The catheter was placed in position by substituting it for a 25-gauge needle that had been inserted into the portal vein under ultrasonic guidance percutaneously and transhepatically. Splenic arterial occlusion caused a drop in splenic venous blood flow from 708 +/- 487 to 241 +/- 155 ml per min, in portal venous blood flow from 993 +/- 439 to 807 +/- 419 ml per min and in portal venous pressure from 17.4 +/- 7.2 to 14.4 +/- 6.1 mm Hg. The latter two reductions were less than expected from the decrease in the splenic venous blood flow volume. This phenomenon was caused by an increase in the mesenteric venous blood flow from 475 +/- 126 to 630 +/- 270 mm per min. This increase may be due to a compensatory mechanism under the control of a regulatory loop in the liver or portal vein, and there seems to be a relationship between splenic and intestinal circulation in portal hypertension that maintains hepatic circulation.     

Effect of ethanol on splanchnic hemodynamics in awake and unrestrained rats with portal hypertension

Alcoholic liver disease is frequently accompanied by portal hypertension. We have previously shown that alcohol intake in awake, unrestrained rats is followed by an increase in portal tributary blood flow. In this study, the effect of ethanol on splanchnic hemodynamics in rats with portal hypertension was analyzed. Portal hypertension was induced by partial ligation of the portal vein. This procedure resulted in an increase in portal tributary and hepatic arterial blood flows compared to sham-operated animals. Ethanol (2 gm per kg, oral) increased portal tributary blood flow in both sham-operated and portal vein-ligated rats (sham + water = 37.6 +/- 1.4; sham + ethanol = 63.1 +/- 1.9; p less than 0.01; partial portal vein stenosis + water = 53.2 +/- 3.3; partial portal vein stenosis + ethanol = 69.5 +/- 2.2 ml.kg-1.min-1; p less than 0.01). In sham-operated rats, hepatic artery blood flow was unchanged following ethanol (sham + water = 6.6 +/- 0.7; sham + ethanol = 7.1 +/- 1.0 ml.kg-1.min-1), whereas in portal vein-ligated rats, flow was increased (partial portal vein stenosis + water = 13.7 +/- 1.4; partial portal vein stenosis + ethanol = 19.8 +/- 1.1 ml.kg-1.min-1; p less than 0.025). The adenosine receptor blocker 8-phenyltheophylline suppressed only the ethanol-induced increase in both portal tributary and hepatic artery blood flows in portal vein-ligated rats. The increases in hepatic artery and portal tributary blood flows observed in portal vein-ligated rats without ethanol were not influenced by 8-phenyltheophylline.(ABSTRACT TRUNCATED AT 250 WORDS)     

Splanchnic Hemodynamics in Idiopathic Portal Hypertension: Comparison with Chronic Persistent Hepatitis

A comparative study of splanchnic hemodynamics was made in 12 patients with idiopathic portal hypertension and in eight patients with chronic persistent hepatitis, but without portal hypertension, who served as the control. Venous pressures were measured by portal and hepatic vein catheterizations, blood flow by the pulsed Doppler flowmeter, and organ volume by computed tomography. Splenic artery blood flow was 788 +/- 242 ml/min in idiopathic portal hypertension and about four times that in chronic persistent hepatitis (215 +/- 42 ml/min), whereas there was no difference in superior mesenteric artery blood flow between the former and the latter (408 +/- 142 vs. 389 +/- 32 ml/min). Spleen volume in idiopathic portal hypertension was six times that in chronic persistent hepatitis, and splenic artery blood flow showed a significant linear correlation with spleen volume in idiopathic portal hypertension (r = 0.71, p less than 0.02). The sum of splenic artery blood flow and superior mesenteric artery blood flow in idiopathic portal hypertension was 1195 +/- 294 ml/min, twice that in chronic persistent hepatitis (603 +/- 109 ml/min). Portal vascular resistance and intrahepatic portal vascular resistance were three times and four times those in chronic persistent hepatitis, respectively. These results indicate that both increased intrahepatic portal vascular resistance and increased splenic artery blood flow may play roles in the development of portal hypertension in idiopathic portal hypertension.     

Effect of synthetic porcine neuropeptide Y (NPY) on splanchnic blood flows and Exocrine pancreatic secretion in dogs

This study examined the effect of synthetic porcine neuropeptide Y on the splanchnic blood flows and the exocrine pancreatic secretion in dogs. Graded doses of neuropeptide Y (0.1–5 g/kg, intravenous) caused dose-dependent reduction of the secretin-stimulated exocrine pancreatic secretion and of the blood flows in the superior mesenteric artery, the portal vein, and the pancreatic tissue. Neuropeptide Y at 5 g/kg reduced the blood flows to 45.9±13.3% (superior mesenteric artery), 63.0±10.5% (portal vein), and 77.9±4.8% (pancreatic tissue), respectively. This dose also reduced secretin-stimulated pancreatic juice volume and CCK-8 plus secretin-stimulated protein output to 65.2±9.3 and 63.3±14.0%, respectively. This study shows a potent vasoconstrictor effect of neuropeptide Y on splanchnic vessels. Neuropeptide Y also inhibited exocrine pancreatic secretion in a significant correlation with the reduction in pancreatic tissue blood flow, which suggests that reduction in the blood flow may be one of the possible mechanisms of the inhibitory action of neuropeptide Y on exocrine secretion.This work was supported by a grant from the Ministry of Education, Japan (A-61440060).     

Myocardial function and transmural blood flow during coronary venous retroperfusion in pigs.

BACKGROUND. The degree of recovery of regional myocardial contraction during coronary venous retroperfusion has not been well established, particularly in the absence of coronary collateral channels. Therefore, the maximal functional benefit attainable with coronary venous retroperfusion was assessed in pigs by means of using selective pump retroperfusion of the left anterior descending vein, with venting of the left anterior descending artery to zero pressure. METHODS AND RESULTS. In eight anesthetized open-chest pigs during selective left anterior descending venous retroperfusion over a range of retroperfusion flows, regional myocardial function (percent systolic wall thickening by sonomicrometry) increased progressively to an average of 62% of control values at a retroperfusion flow rate 200% of control arterial flow. Progressive thickening of the end-diastolic dimension of the anterior wall was observed with increasing retroperfusion flow (from 8.7 +/- 0.9 to 10.7 +/- 2.3 mm, p less than 0.001). Perfusion pressures within the left anterior descending vein increased linearly with increased retroperfusion flow rates (up to 132 +/- 57 mm Hg with retroperfusion flow 200% of control). A gradual increase of retrograde left anterior descending arterial outflow was observed with increasing retroperfusion flows; however, the absolute amount (maximum, 8.3 +/- 4.1 ml/min) was much too low to explain the extent of functional recovery. Transmural myocardial capillary blood flows in the anterior wall with retroperfusion flows of 100% and 200% of control arterial flow were 0.22 and 0.42 ml/min/g with corresponding subendocardial blood flows of 0.14 and 0.29 ml/min/g; ratios of endocardium to epicardium were 0.51 and 0.61, respectively. Thus, capillary blood flows during selective retroperfusion were relatively low despite considerable restoration of regional systolic wall thickening, and a significant difference was noted in the slopes of the relations between regional systolic wall thickening and myocardial blood flow during retroperfusion and anterograde arterial perfusion (p less than 0.05). With retrograde injection of silicone elastomer at different retroperfusion pressures (50, 75, and 100 mm Hg) in three pigs, capillaries were well visualized, and profuse intramyocardial venous anastomotic connections were seen at the highest retroperfusion pressure (100 mm Hg), whereas there was filling of small venules but little capillary filling at the lowest retroperfusion pressure (50 mm Hg). CONCLUSIONS. Considerable recovery of regional myocardial function with low regional capillary blood flows were observed during acute venous retroperfusion with high retroperfusion flows with arterial blood. These findings together with low levels of retrograde arterial outflow and visualization of retrograde capillary filling with a rich venous network provide evidence for possible oxygen delivery via the intramyocardial venous plexus.     

Validation of Doppler arterial flow in humans]

A method of measuring volumetric flow in human arteries with pulsed Doppler technique was developed. Doppler flowmetry was assessed in 11 adult patients whose admission-diagnoses included aneurysm of the aorta or dissections. During surgery, regional blood flows of the left common carotid artery, terminal aorta, common iliac artery, external iliac artery or common femoral artery were measured by Doppler method and electromagnetic flowmeter. Eighty four arterial flow determinations were obtained from the 11 patients studied. On comparison of simultaneous electromagnetic and Doppler measurements of blood flow, an excellent correlation (r = 0.93) was found between the two methods. The slope of the regression line was 0.587. Regional blood flow was measured with Doppler flowmetry in another 9 patients. The values of the left common carotid, celiac, superior mesenteric and terminal aortic flows were 251 +/- 62, 608 +/- 399, 687 +/- 381, 783 +/- 324 ml.min-1, respectively. This method provides an easy, reliable way of measuring regional blood flow.     

Initial evaluation of systemic and regional pCO2 gradients as markers of mesenteric hypoperfusion

BACKGROUND: Mesenteric ischemia is a life-threatening emergency with a mortality rates still ranging between 60% and 100%. AIM: To evaluate the systemic and regional pCO2 gradients changes induced by mesenteric ischemia-reperfusion injury. In addition, we sought to determine if other systemic marker of splanchnic hypoperfusion could detect the initial changes in intestinal mucosal microcirculation after superior mesenteric artery occlusion. METHODS: Seven pentobarbital anesthetized mongrel dogs (20.6 +/- 1.1 kg) were subjected to superior mesenteric artery occlusion for 45 minutes, and followed for an additional 120 minutes. Systemic hemodynamic was evaluated through a Swan-Ganz and arterial catheters, while gastrointestinal tract perfusion by superior mesenteric vein and jejunal serosal blood flows (ultrasonic flowprobe). Intestinal oxygen delivery, extraction and consumption (DO2intest, ERO2intest and VO2intest, respectively), intramucosal pH (gas tonometry), and mesenteric-arterial and mucosal arterial pCO2 gradients (D(vm-a)pCO2 and D(t-a)pCO2, respectively) were calculated. RESULTS: Superior mesenteric artery occlusion was not associated with significant changes on systemic hemodynamics parameters. A significant increase of D(vm-a)pCO2 (1.7 +/- 0.5 to 5.7 +/- 1.8 mm Hg) and D(t-a)pCO2 (8.2 +/- 4.8 to 48.7 +/- 4.6 mm Hg) were detected. During the reperfusion period a significant decrease on DO2intest (67.7 +/- 9.9 to 38.8 +/- 5.3 mL/min) and a compensatory increase on ERO2intest from 5.0 +/- 1.1% to 12.4 +/- 2.7% was observed. CONCLUSION: We conclude that gas tonometry can detect the mesenteric blood flow disturbances sooner than other analyzed parameters. Additionally, we demonstrated that changes on systemic or regional pCO2 gradients are not able to detect the magnitude of intestinal mucosal blood flow reduction after mesenteric ischemia-reperfusion injury.     

Regional hemodynamic effects of prostaglandin A1 in the conscious dog

Prostaglandin A₁ (PGA₁) administered intravenously in a dosage range of 0.01 to 1.0 μg per kilogram of body weight to unsedated, conscious dogs previously instrumented with Doppler ultrasonic or electromagnetic flow transducers caused dose-dependent decreases in arterial pressure and total systemic resistance and elevations in cardiac output and heart rate. PGA₁ caused increases in blood flow and decreases in resistance in the left circumflex coronary, superior mesenteric, renal, and external iliac vascular beds. At the maximum dose of 1.0 μg per kilogram of body weight, when marked arterial hypotension had occurred, left circumflex coronary flow increased 74 per cent and mesenteric flow increased 76 per cent above control values while renal and iliac flows increased by only 14 per cent and 44 per cent, respectively. Thus PGA₁, in doses tolerated by conscious dogs, increased cardiac output and blood flow to the left coronary, mesenteric, renal, and external iliac beds. At the dose of 1.0 μg per kilogram of body weight, which produced prominent arterial hypotension, the greatest relative increases in flow were observed in the coronary and superior mesenteric beds, while flow increased less in the iliac bed and least in the renal bed.     

Effects of ethanol and wine on hepatic arterial and portal venous flows in conscious dogs.

The effects of ethanol and wine on hepatic arterial and portal venous flows were examined in conscious dogs. Ethanol was given intravenously or intragastrically, and red wine (ethanol: 14%) was given intragastrically over 30 min. Intravenous ethanol (0.8 g/kg) and intragastric ethanol (14% vol/vol) increased hepatic arterial flow, which remained elevated for 60 min after the cessation of ethanol administration. Ethanol also increased portal venous flow. Portal venous flow returned gradually toward basal levels after the cessation of intravenous ethanol infusion, whereas it remained elevated even after the cessation of intragastric ethanol. Intragastric wine increased hepatic arterial and portal venous flows. In contrast to intragastric ethanol, hepatic arterial flow continued to rise after the cessation of intragastric wine infusion, while portal venous flow returned toward basal levels. We conclude that, though both ethanol and wine increase hepatic blood flow, the responses of hepatic arterial and portal venous flows differ substantially among intravenous ethanol, intragastric ethanol and intragastric wine.     

Circulatory changes induced by portal venous diversion and mesenteric hypertension in rats.

We studied the hemodynamics in four groups of rats with combinations of mesenteric hypertension and portal diversion. Operations created three groups with mesenteric hypertension and different degrees of portal venous diversion: mesenteric vein stenosis, portal vein stenosis and end-to-side portacaval anastomosis with mesenteric vein stenosis, the fourth group had only portacaval anastomosis. A control group had sham operations. Cardiac output, splanchnic blood flows and portosystemic shunt indices were measured with radioactive microspheres. Mesenteric venous pressures in the mesenteric-stenosed, portal-stenosed, portacaval-shunted and end-to-side portacaval anastomosis with mesenteric vein stenosis rats were, respectively, 13.5 +/- 0.6, 15.3 +/- 0.7, 4.3 +/- 0.5 and 13.0 +/- 0.9 mm Hg, which were all significantly different from controls: 8.3 +/- 0.3 mm Hg. Portosystemic shunt indices were also significantly different from each other: controls, 0.4% +/- 0.02%; mesenteric-stenosed, 5.9% +/- 2.3%; and portal-stenosed, 52.1% +/- 4.9%. Cardiac output and splanchnic visceral blood flows were significantly increased in the portal-stenosed rats and the two groups with portacaval anastomoses, with the latter two groups having the highest values. The addition of mesenteric stenosis did not change the blood flows because mesenteric-stenosed rats did not differ from controls and end-to-side portacaval anastomosis with mesenteric vein stenosis rats did not differ from rats with portacaval anastomosis alone. These results suggest that mesenteric venous hypertension per se does not affect hemodynamics but that diversion of portal venous blood from the liver is a critical factor in the development of hyperkinetic circulation in portal hypertension.     

Effects of synthetic human gastric inhibitory polypeptide on splanchnic circulation in dogs

Changes in blood flow in the celiac artery, superior mesenteric artery, and pancreas in response to an intravenous injection of synthetic human gastric inhibitory polypeptide (GIP) were determined simultaneously and continuously in anesthetized dogs, using a transit-time ultrasonic flowmeter and a laser-Doppler flowmeter. Injection of GIP significantly increased superior mesenteric arterial flow in a dose-related manner (by 9%, 43%, and 139% at 30 s after an injection at the doses of 3, 50, and 800 pmol/kg, respectively). In contrast, celiac arterial flow was not significantly altered by GIP at any of the three doses. Calculated vascular resistance in the superior mesenteric artery decreased after GIP infusion, whereas that in the celiac artery was not changed by GIP. Pancreatic blood flow decreased significantly after GIP injection at the doses of 50 and 800 pmol/kg (by 11% and 17%, respectively). Our data indicate that there is a substantial difference in the hemodynamic responses to GIP among splanchnic organs, and suggest that GIP acts specifically on the mesenteric vasculature.     

Acute effect of propranolol on splanchnic circulation in normal and portal hypertensive rats

Propranolol decreases portal venous pressure in patients with cirrhosis but no method is available in man to study the effect of this beta-blocker on splanchnic organ blood flow. Because in rats, the microsphere method allows evaluation of regional blood flow, the acute effect of propranolol on both splanchnic and systemic circulations was studied in normal rats and in rats with portal hypertension due to portal vein stenosis. Portal venous pressure significantly decreased during propranolol administration in normal (5.6 +/- 1.0-4.7 +/- 1.1 mm Hg; mean +/- SD) as well as in portal hypertensive rats (11.7 +/- 2.3-10.3 +/- 1.8 mm Hg). Propranolol slightly decreased cardiac output and arterial pressure in all rats. Portal tributary blood flow was significantly reduced by propranolol in normal rats (17.4 +/- 3.0-11.3 +/- 2.2 ml/min) and in portal hypertensive rats (23.7 +/- 5.0-16.6 +/- 3.3 ml/min). Accordingly vascular resistance of the different organs in the portal venous territory increased in these rats receiving propranolol. The percentage of the decrease in portal tributary blood flow was significantly more marked than the percentage of reduction in cardiac output in portal hypertensive rats but, in normal rats, these percentages were parallel. Hepatic arterial blood flow did not change or slightly increased and, consequently, hepatic arterial vascular resistance decreased. These findings further clarify the marked effects of propranolol on splanchnic circulation.