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PubMedDate not supplied

Beta blockers in portal hypertension--current status.

Pharmacotherapy of portal hypertension started with the use of intravenous vasopressin in the 1960s. However, the short half life of the drug and the non-availability of an oral preparation limited its use to acute variceal bleeding. It was two decades later that propranolol, a beta blocker was shown to decrease portal pressure. However, the usefulness of beta blockers in the treatment of recurrent variceal bleeding remains controversial with controlled trials showing both benefit and lack of benefit. This review is aimed to bring into perspective, current knowledge of the effect of beta blockers on the splanchnic circulation in man and animals, its clinical usefulness in portal hypertension and its place in the therapeutic armamentarium against portal hypertension.

Adrenergic beta-Antagonists↗
PubMed2000

Splanchnic metabolism of fuel substrates in acute liver failure.

BACKGROUND/AIMS: This study aimed to characterize the exchange of fuel substrates in the splanchnic circulation in acute liver failure. METHODS: Liver vein catheterization was used in 22 patients with acute liver failure after development of hepatic encephalopathy grade III-IV Healthy controls, patients with cirrhosis and patients with acute on chronic liver disease were also studied. RESULTS: In acute liver failure there was splanchnic removal of glucose (0.21+/-0.44 mmol/min), release of lactate (0.34+/-0.37 mmol/min), pyruvate (0.08+/-0.06 mmol/min) and ketone bodies (0.04+/-0.02 mmol/min), while extraction of amino acids and free fatty acids was insignificant. In the acute liver failure group, a normal hepatic venous oxygen saturation (0.69+/-0.12) and normal pyruvate/lactate ratio suggested absence of hypoxia even though the acetoacetate/beta-hydroxybutyrate ratio was decreased. Only in the acute liver failure group did the measured splanchnic oxygen content difference exceed what could be accounted for even by hypothesizing complete oxidation of all extracted blood-borne fuel substrates; oxidation of endogenous substrates may be quantitatively important in this condition. CONCLUSION: Acute liver failure was associated with a state of accelerated glycolysis in the splanchnic region, leading to release of lactate in the absence of splanchnic hypoxia.

3-Hydroxybutyric Acid↗
PubMed1993

Superior mesenteric artery blood flow in celiac disease.

Measurements of the hemodynamic parameters of the superior mesenteric artery were performed in 18 patients with celiac disease. Ten were studied at the time of diagnosis, when a small bowel biopsy showed a flat mucosa. The remaining eight patients were studied after complete clinical and histological recovery induced by a gluten-free diet. Doppler ultrasound flowmetry was used to measure blood flow in physiological and fasting conditions and after a mixed liquid test meal (Ensure-Plus). The results were compared with those of healthy subjects (N = 7). Mean basal flow was 50% higher in untreated celiac disease patients than in healthy controls and patients with chronic pancreatitis (P = NS). Postprandial mesenteric blood flow was significantly increased (P < 0.002) and delayed in time (P < 0.005) in celiac disease as compared to controls. Successful treatment reduced the mesenteric blood flow in celiac disease to normal values. Our study demonstrates that pathophysiological changes in the small bowel mucosa during the active clinical phase of celiac disease induce an abnormal splanchnic circulation.

Adult↗
PubMed1996

Dose-dependent effects of a nitric oxide biosynthesis inhibitor on hyperdynamic circulation in two models of portal hypertension in conscious rats.

The role of nitric oxide (NO) in the hyperkinetic circulation in portal hypertension has not been clearly elucidated. Different doses of NO inhibitors, haemodynamic values and experimental conditions might explain the discrepant results. The aim of the present study was to investigate the acute effects of a specific biosynthesis inhibitor of NO, Nomega-nitro-L-arginine (L-NNA), on the systemic and splanchnic circulation in normal conscious rats and rats with portal hypertension due to either partial portal vein stenosis or secondary biliary cirrhosis. The administration of L-NNA (15 to 960 micrograms.kg-1.min-1) induced a significant dose dependent increase in arterial pressure which was not different among the three groups of rats. Following an acute and maximal vasopressive dose of L-NNA (1 mg.kg-1.min-1) cardiac index decreased more in portal vein stenosed and cirrhotic rats (-45 +/- 3% and -45 +/- 2%, respectively) than in normal rats (-31 +/- 2%), and systemic vascular resistance increased more in the two groups of portal hypertensive rats than in normals (+ 161 +/- 13% and + 154 +/- 10% vs + 85 +/- 6%, respectively). L-NNA caused a greater decrease in portal tributary blood flow in portal vein stenosed and cirrhotic rats (-63 +/- 4% and -55 +/- 4%, respectively) than in normal rats (-45 +/- 6%). Similarly, the increase in portal territory vascular resistance was significantly more marked in portal vein stenosed and cirrhotic rats (+ 337 +/- 62% and + 214 +/- 24%, respectively) than in normal rats (+ 153 +/- 23%). Portal pressure did not change. Following the acute administration of L-NNA, no significant difference in splanchnic and systemic haemodynamics were noted between portal vein stenosed and normal rats, except for portal pressure. In cirrhotic rats, splanchnic and systemic values remained different from normal rats. This study confirms that NO plays a role in the haemodynamic changes in portal hypertension, and shows that NO inhibitors have a dose-dependent effect in conscious portal hypertensive rats.

Animals↗
PubMed2004

Splanchnic and peripheral vascular resistance during lower body negative pressure (LBNP) and tilt.

We tested the hypothesis that vasoconstriction in response to LBNP or head up tilt would be reflected in a reduction in splanchnic (portal vein) blood flow (PVF) and increases in forearm and total peripheral vascular resistance (TPR). Changes in vascular resistance indicators were obtained from measurement of PVF from portal vein cross-sectional area and blood velocity by Doppler ultrasound, from forearm vascular resistance (FVR, by Doppler) and total peripheral resistance (TPR, by impedance cardiography). 21 subjects were tested during LBNP (0, -10, -20 and -30 mmHg) and 9 subjects during tilt (0, 45 and 70 degrees). During progressive LBNP, PVF decreased approximately linearly with LBNP (-30, -48 and -64% at -10, -20 and -30 mmHg) and with tilt angle (-39 and -58% at 45 and 70 degrees). The increase in FVR approximately mirrored these changes during LBNP (20.1, 44.7 and 55.3%) and tilt (45.6 and 63.6%). However, the changes in TPR during LBNP (12.0, 16.9 and 26.4%) and tilt (25.2 and 29.2%) were markedly less. This observation of different percent changes in forearm versus total peripheral resistance might reflect true physiological differences in the forearm (and splanchnic) circulations compared with the whole body, or the data might suggest that impedance cardiography did not provide a reliable indicator of cardiac output and therefore TPR under these conditions. The primary observation in this study was that Doppler ultrasound measurement of portal vein blood flow provided a non-invasive estimate of splanchnic vascular resistance during postural or LBNP challenge and that using the reduction in portal vein flow as an index of increased vasoconstriction paralleled the change in forearm vascular resistance.

Arm↗
PubMed1996

[Hemodynamic management of septic shock. From a global approach to a gastrointestinal approach].

Oxygen uptake and increased metabolic requirements are characteristic of the acute state resulting from septic shock. One therapeutic approach to improving hemodynamics is to increase oxygen delivery in an attempt to overcome tissue oxygen debt. Recent randomized trials have suggested that systematically increasing oxygen supply is not necessarily the ideal strategy. It might be better, for each patient, to reach an optimal oxygen supply. This requires identification of parameters capable of indicating the optimal level, a rather difficult task. Currently, focus has been placed on the importance of the splanchnic circulation in severe septic shock. Hypoxia resulting from hypoperfusion of the intestinal mucosa occurs early in sepsis and could, via intermediary bacterial and/or endotoxinic translocation, maintain the septic syndrome and favor development of multiple organ failure. Since the drugs used to restore hemodynamics have vasoactive properties, measuring their effect on relevant indicators of splanchnic perfusion and oxygenation such as PCO2 or pH within the gastric mucosa using tonometric gastric probes might be a means of determining optimal oxygen level. With this approach, it would be possible to avoid sacrifying the perfusion of the gastrointestinal mucosa by using drugs which appear to favor the microcirculation in this territory.

Digestive System↗
PubMed2003

Dopexamine reverses colonic but not gastric mucosal perfusion defects in lethal endotoxin shock.

BACKGROUND: Whilst dopexamine appears to increase overall splanchnic blood flow in postoperative and septic patients, the effects on gastric mucosal perfusion are controversial and based on concomitantly increasing mucosal to arterial PCO(2) gradients (PdCO(2)). We hypothesized that dopexamine alters splanchnic blood flow distribution and metabolism during experimental endotoxin shock and modifies the inflammatory response induced by endotoxin. METHODS: In an experiment with anaesthetized normovolaemic, normoventilated pigs, 21 animals were randomized into: (i). subacute lethal endotoxin shock for 14 h (n=7 at baseline); (ii). endotoxin shock with dopexamine infusion (aiming to exceed baseline cardiac output, n=7); or (iii). controls (n=7). Regional blood flow and metabolism were monitored. RESULTS: Endotoxin produced a hypodynamic phase followed by a normo/hyperdynamic, hypotensive phase. Despite increasing systemic blood flow in response to dopexamine, proportional splanchnic blood flow decreased during the hypodynamic phase. Dopexamine gradually decreased fractional coeliac trunk flow, while fractional superior mesenteric arterial flow increased. Dopexamine induced early arterial hyperlactataemia and augmented the gastric PdCO(2) gradient while colonic luminal lactate release and colonic PdCO(2) gradient were reversed. Dopexamine did not modify the inflammatory response as evaluated by arterial IL-1beta and IL-6 concentrations. CONCLUSIONS: Dopexamine protects colonic, but not gastric mucosal epithelium in experimental endotoxin shock. This may be related to redistribution of blood flow within the splanchnic circulation.

Animals↗
PubMed2006

Therapy insight: Management of hepatorenal syndrome.

Hepatorenal syndrome (HRS), a feared complication of advanced cirrhosis, is characterized by functional renal failure, secondary to renal vasoconstriction in the absence of underlying kidney pathology. Extreme underfilling of the arterial circulation, caused by arterial vasodilation of the splanchnic circulation, activates vasoconstrictor systems, which lead to intense renal vasoconstriction and HRS. Factors predictive for the development of HRS include intense urinary sodium retention, dilutional hyponatremia, low blood pressure, decreased cardiac output, and increased activity of systemic vasoconstrictors. The prognosis for patients with HRS is extremely poor, especially for those with the acute, progressive (type 1) form. Liver transplantation is the best treatment for suitable candidates and should always be the management option considered first. Pharmacologic therapies are aimed at improving renal function to enable patients to survive until transplantation is possible. These therapies are based on plasma expansion with albumin, combined with the use of either vasopressin analogs or alpha-adrenergic agonists. Other nonpharmacologic therapies, such as transjugular intrahepatic portosystemic shunts and albumin dialysis show promise, but experience with these treatments is limited. For prevention of HRS, albumin infusion is recommended in patients with spontaneous bacterial peritonitis, and pentoxifylline treatment is recommended in patients with acute alcoholic hepatitis.

Adrenergic alpha-Agonists↗
PubMed2006

Tissue production of cortisol by 11beta-hydroxysteroid dehydrogenase type 1 and metabolic disease.

Activation of intracellular glucocorticoid receptors is determined not only by the plasma concentrations of cortisol, under the influence of the hypothalamic-pituitary-adrenal (HPA) axis, but also by 11HSD enzymes within the target cell which interconvert cortisol with its inert metabolite cortisone. Data from cells in culture, isolated tissues, and transgenic mouse models have established that 11HSD type 1 regenerates glucocorticoids and amplifies glucocorticoid receptor activation. In humans, the rate of cortisol regeneration in peripheral tissues is of similar magnitude to adrenal secretion of cortisol at most times of day, and occurs principally in the splanchnic circulation. Approximately two-thirds of the splanchnic activity appears to reside in visceral adipose tissue, sufficient to allow visceral adipose tissue to "deliver" cortisol to the liver via the portal vein. In obesity, 11HSD1 activity in subcutaneous adipose tissue is increased, putatively explaining the link between obesity and other features of the metabolic syndrome. The regulation of 11HSD1, and the basis for its upregulation in obesity, are now being explored. Against this background, inhibition of 11HSD1 has become a major therapeutic target in metabolic syndrome. Preclinical results with novel selective 11HSD1 inhibitors are encouraging, and clinical proof of principle has been achieved with the nonselective inhibitor carbenoxolone. Although the parallels between metabolic syndrome and Cushing's syndrome were originally drawn with reference to patients with elevated plasma cortisol concentrations, it now appears that manipulating tissue concentrations of cortisol will allow the subtle level of control required for long-term therapy to reduce the risks of cardiovascular disease.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2005

Propranolol-exacerbated mesenteric ischemia in a patient with hyperthyroidism.

OBJECTIVE: To report a case of acute mesenteric ischemia associated with the use of oral propranolol. CASE SUMMARY: A 59-year-old white man was admitted to the hospital with chronic diarrhea and weight loss. The patient was diagnosed as having hyperthyroidism. Therapy with propylthiouracil 100 mg 3 times daily and propranolol 20 mg twice daily was initiated on an outpatient basis. The following day, the patient was readmitted to our hospital with increased abdominal pain and bloody diarrhea. Angiography revealed superior mesenteric artery occlusion. Antegrade aorta-mesenteric bypass surgery was performed for revascularization, and the patient was discharged 10 days after the surgery. The patient was well both clinically and endoscopically at a follow-up visit 8 months later. DISCUSSION: Although mesenteric ischemia is a devastating illness of varied causes, drug-associated mesenteric ischemia is rarely seen. By decreasing cardiac output and selective vasodilatory receptor inhibition in the splanchnic circulation, propranolol can cause a decline in splanchnic blood flow. An objective causality assessment indicated that propranolol was the possible cause of the arterial occlusion. CONCLUSIONS: Propranolol may rarely be associated with mesenteric ischemia. In cases of newly developed acute abdomen undergoing propranolol therapy, physicians should be aware of this rare and serious adverse reaction to this drug.

Adrenergic beta-Antagonists↗
PubMed2001

[Role of the monocye-lymphocye system and of endogenous mediators in the severity of acute pancreatitis and in development of its septic complications].

The activity of monocyte/lymphocyte system and the splanchnic circulation was investigated in acute pancreatitis. The splanchnic blood flow was characterised indirectly by gastric intramucosal pH changes, which strongly correlated with APACHE-II score, and predicted the bad prognosis. The high CD14/HLA-DR and CD14/CD16 coexpression, the low TNF-alpha production proved to be unfavourable prognostic factor in the early phase of the disease. The expression of IL-2, IL-10 and moderately of IL-4 was elevated, but the expression of INF gamma did not show significant alteration. The thrombocyte aggregation decreased in the early phase. There are bad prognostic signs if its level remains constantly low and ATP-release increases. The activity and index of phagocytosis were higher in comparison with controls, but these parameters were not increasable with higher cell concentration. The ROI production increased, and the increase in the fMLP and o'zymosan indicated LDCL seems to be unfavourable prognostic sign, which well correlated with the APACHE-II score.

Acute Disease↗
PubMed2000

Interleukin-1beta alters the oxygen delivery-oxygen consumption relationship in rabbits by increasing the slope of the supply-independent line.

When systemic oxygen delivery (DO2) is reduced, oxygen consumption (VO2) is maintained until a critical level is reached (DO2crit). Sepsis is thought to shift DO2crit to the right and lengthen the supply-dependent portion. We tested the effect of interleukin (IL)-1beta, which is one of the key cytokines related to sepsis, on the DO2-VO2 relationship. Fifteen rabbits were subjected to stepwise cardiac tamponade to reduce DO2 to 10% by inflating a handmade balloon placed into the pericardial sac. Seven rabbits were given 10 microg/kg of IL-1beta intravenously (IL-1beta group) prior to the graded cardiac tamponade. The remainder received saline alone (control group). The DO2-VO2 relationship was analyzed by the dual-line method. IL-1beta significantly decreased mean arterial pressure (65 +/- 11 mmHg from baseline 85 +/- 7 mmHg) without altering cardiac output. The IL-1beta group showed significantly steeper supply-independent line slopes than did the control group (0.19 +/- 0.02 vs. 0.11 +/- 0.02, respectively), which resulted in a DO2crit shift to the left (IL-1beta group, 8.7 +/- 1.7 ml/kg x min vs. control, 11.7 +/- 0.7 ml/kg x min). The IL-1beta group also showed greater PO2 and plasma lactate levels in the portal vein than did the control group. These results indicate that IL-1beta impairs systemic oxygen uptake even before VO2 becomes supply-dependent, presumably due to maldistribution of the blood flow including the splanchnic circulation.

Animals↗
PubMed1999

Acute mesenteric ischemia and reperfusion: protective effects of recombinant soluble P-selectin glycoprotein ligand-1.

The effects of recombinant soluble P-selectin glycoprotein ligand-1 (rsPSGL.Ig) were studied after 120 min of splanchnic artery occlusion and 120 min of reperfusion (SAO/R). SAO/R rats administered a low-affinity mutant form of rsPSGL.Ig exhibited signs of severe circulatory collapse with marked hypotension, a survival time of only 37+/-16 min, and significant increases in intestinal myeloperoxidase (MPO) activity (P<0.01). In addition, SAO/R rats given rsPSGL.Ig low-affinity mutant showed severe endothelial dysfunction characterized by a blunted vasorelaxation to the endothelium-dependent vasodilator acetylcholine in comparison to sham-operated controls (30+/-9% vs. 97+/-3%). Administration of rsPSGL.Ig (0.5 mg/kg) significantly improved mean arterial blood pressure and increased survival time to 107+/-13 min (P <0.01). rsPSGL.Ig treatment also resulted in a significant attenuation in both intestinal MPO activity as well as the SAO/R-induced decline in endothelium-dependent vasorelaxation of superior mesenteric artery rings (P<0.01). In addition, rsPSGL.Ig attenuated in vitro neutrophil adherence to thrombin-stimulated superior mesenteric artery endothelium to a comparable degree as a P-selectin monoclonal antibody. These data suggest that rsPSGL.Ig provides beneficial effects by preserving endothelial function and attenuating neutrophil-endothelial cell interactions in the splanchnic circulation following ischemia-reperfusion.

Acute Disease↗
PubMed2006

Oral carbohydrate solution ameliorates endotoxemia-induced splanchnic ischemia.

The purpose of this study was to investigate the effect of oral administration of a simple carbohydrate solution on splanchnic circulation and bacterial translocation in endotoxemia. Group 1 was sham control; group 2 was starved for 24 hours; in group 3, endotoxin was administrated at the end of starvation; in group 4, carbohydrate solution was administrated via orogastric route for 24 hours; and in group 5, carbohydrate solution was given and endotoxin was administrated at the end of 24 hours. Splanchnic blood flows were recorded and tissue samples were collected for microbiological analyses. There was a significant increase (P<.05) in the incidence of bacterial translocation in starvation. Endotoxemia decreased distal (P=.021) and midmesenteric (P=.046) flow in starved animals. Oral carbohydrate significantly increased ileal blood flow in starvation (P=.036) and endotoxemia (P=.008). In conclusion, oral carbohydrate solution prevents bacterial translocation during starvation and endotoxemia. The possible mechanism is the improvement in the mesenteric blood flow.

Animals↗
PubMed2001

Cellular and molecular basis of portal hypertension.

The molecular basis of the vascular wall abnormalities that contribute to development of portal hypertension are an area of active investigation. Studies to date suggest that diminution in eNOS-derived NO production in liver contributes to this process by causing increased intrahepatic resistance. This process seems to be mediated through inhibitory posttranslational regulatory mechanisms of eNOS. Endothelin-1 signaling is also increased in the intrahepatic vasculature. The mechanisms responsible for increased ET-1 signaling include increased ET-1 production and increased ET-A receptor expression, particularly within hepatic stellate cells, although the stimulus responsible for activation of the ET-1 system remains uncertain. In the splanchnic circulation, increases in eNOS-derived NO contribute to increased portal venous inflow through transcriptional and posttranslational regulation of eNOS. Development of the porto-systemic collateral circulation characteristic of portal hypertension occurs through a combination of NO-dependent dilation of preexisting vessels and through growth factor-mediated angiogenesis and neovascularization (Fig. 3). Further studies in vascular wall biology are continuing to elucidate more clearly the molecular mechanisms of portal hypertension. The [figure: see text] mechanism by which eNOS-derived NO production is increased in the splanchnic arteriolar endothelial cell but decreased in the liver endothelial cell and the role of specific ET receptor subtypes in the mechanism of activation of the ET-1 system and its effect on contractile cells in liver cirrhosis are areas that require further investigation. Further studies are needed to determine the intrahepatic site of pressure and perfusion regulation, be it the hepatic sinusoid and its unique, specialized cell types or the endothelial and smooth muscle cells in the hepatic and portal venules. The role of more recently delineated vasoactive pathways such as urotensin-II/GPR 14 and anandamide/CB1 receptor in portal hypertension must be examined. Most importantly, future studies must focus on novel experimental therapies, using pharmacologic and genetic approaches to modulate these vascular biologic systems and thereby to ameliorate complications and symptoms relating to portal hypertension in patients with cirrhosis.

Animals↗
PubMed1986

Effect of extradural analgesia on glucose metabolism and gluconeogenesis. Studies in association with upper abdominal surgery.

Concentrations of glucose and gluconeogenic substrates across the splanchnic circulation were studied in 20 patients undergoing cholecystectomy with general anaesthesia. In 10 patients, general anaesthesia was administered alone, and in 10 general anaesthesia was combined with thoracic extradural analgesia. All patients received a constant i.v. infusion of glucose. Blood glucose concentration increased markedly in the general anaesthesia group in contrast to a moderate and shortlived increase in the patients given extradural analgesia, in whom the splanchnic release of glucose tended to be lower. The splanchnic uptake of glycerol was lower in the patients given extradural analgesia, while the uptake of lactate and the increase in alanine uptake was similar in both groups. Plasma catecholamine and serum cortisol concentrations were higher in the group receiving general anaesthesia alone, while serum growth hormone concentration was higher after surgery in the extradural group. The addition of extradural blockade to general anaesthesia suppresses the increase in blood glucose concentration--and this may be related to a reduced splanchnic release of glucose combined with an increased peripheral uptake.

Abdomen↗
PubMed2004

Bladder mucosa pH and Pco2 as a minimally invasive monitor of hemorrhagic shock and resuscitation.

BACKGROUND: Continuous monitoring of pH, Pco2, and Po2 using fiberoptic sensor technology has been proposed recently as a clinical monitor of the severity of shock and impaired tissue perfusion. Surrogates of gut tissue perfusion such as gastric tonometry, although cumbersome, have been used to indirectly quantify the degree of gut ischemia. The purpose of this study was to demonstrate the feasibility of monitoring bladder mucosa (BM) and to compare urinary bladder mucosa and proximal jejunum mucosa interstitial pH and Pco2 during hemorrhagic shock and resuscitation. METHODS: Eleven male miniature swine (25-35 kg) (control, n = 4; shock, n = 7) underwent jejunal tonometry and cystostomy. A multisensor probe was placed adjacent to the BM. Urine was diverted. Normocarbia was maintained. Animals were hemorrhaged and kept at a mean arterial pressure of 40 mm Hg. When a constant infusion was required to maintain the mean arterial pressure at 40 mm Hg (decompensation), animals were resuscitated with shed blood plus two times the shed volume in lactated Ringer's solution (20 minutes) and observed for 2 hours. RESULTS: During decompensation, BM pH values decreased significantly from 7.33 +/- 0.08 to 7.01 +/- 0.2 (p < 0.01) and recovered to 7.11 +/- 0.19 at 120 minutes after completion of resuscitation. During decompensation, BM Pco2 values increased significantly compared with baseline (from 49 +/- 6 mm Hg to 71 +/- 19 mm Hg, p < 0.05) and returned to baseline with resuscitation. Jejunum mucosa and BM interstitial Pco2 correlated throughout shock and resuscitation (r = 0.49). Bland-Altman analysis demonstrated significant differences between jejunum mucosa (intramucosal pH) and BM interstitial pH. CONCLUSION: Shock-induced changes in the Pco2 of the BM are comparable to tonometric changes in the gut. These data suggest that continuous fiberoptic multisensor probe monitoring of the BM could potentially provide a minimally invasive method for the assessment of impaired tissue perfusion of the splanchnic circulation during shock and resuscitation.

Analysis of Variance↗
PubMed1997

Nitric oxide and pancreatic islet blood flow after induced portal hypertension in rats.

Portal hypertension (PH) is associated with a hyperdynamic splanchnic circulation, partially mediated by nitric oxide-dependent mechanisms. The aim of the present study was to evaluate the influence of PH and nitric oxide on pancreatic islet blood flow. PH was induced by a calibrated stenosis of the portal vein in male Sprague-Dawley rats. Control were sham-operated. Ten days later pancreatic, duodenal, colonic, and arterial hepatic blood flows were measured with microspheres. All splanchnic blood flow values were markedly increased in the PH rats. The fraction of whole pancreatic blood flow diverted through the islets increased from approximately 5 to 15%. Intravenous administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine (25 mg/kg body weight) in rats with PH 10 min before blood flow measurements decreased pancreatic, duodenal, colonic, and arterial hepatic blood flow to control values. Pancreatic islet blood flow was also decreased, but more markedly than that of the whole pancreas. Pancreatic islet morphology was normal, and the rate of islet cell replication was not influenced. PH induced a preferential increase in pancreatic islet blood flow, which is likely to be associated with an increased production of nitric oxide.

Animals↗