Effects of glucagon on the splanchnic and the systemic circulation

1.

1. Dogs were treated with an intravenous injection of 2 mg of glucagon. Hepatic, celiac, and superior mesenteric arterial blood flows and concomitant cardiac output rates were measured. Local and total peripheral resistance was calculated. Heart rate, systemic arterial pressure, central venous pressure, and portal venous pressure were measured. Also, blood sugar, potassium, and blood gases were determined.     

Effects of hypocapnia and hypercapnia on splanchnic circulation and hepatic function in the beagle

The effects of mild hypocapnia (PaCO2 22 mm Hg) and hypercapnia (PaCO2 59 mm Hg) on the splanchnic circulation and hepatic function were studied in six pentobarbital anesthetized, laparotomized, mechanically ventilated beagles. Tidal volume and respiratory frequency were held constant throughout the measurements. Hepatic artery blood flow (HABF) and portal vein blood flow (PVBF) were measured by electromagnetic flowmeters. Hepatic function was assessed by indocyanine green (ICG) elimination kinetic analysis after intravenous injection of the dye. Hypocapnia caused a decrease in HABF without affecting the systemic circulation. Hypercapnia, on the other hand, caused a significant increase in cardiac output without changing mean arterial pressure. There was a significant increase in PVBF and total hepatic blood flow (THBF = PVBF + HABF). Despite the increases in PVBF and THBF, the half-life of ICG was significantly longer during hypercapnia (9.09 +/- 0.79 min) than during hypocapnia (7.16 +/- 0.37 min), and plasma ICG clearance was smaller during hypercapnia (4.79 +/- 0.44 ml.min-1) than during hypocapnia (5.44 +/- 0.33 ml.min-1) or normocapnia (5.27 +/- 0.50 ml.min-1), indicating the depressed hepatic function during hypercapnia. We conclude that mild hypocapnia decreases HABF without affecting hepatic function and that mild hypercapnia is associated with a depression of hepatic function in spite of the increases in PVBF and THBF.     

Anatomy of the splanchnic circulation.

The blood supply to the intestines is a complex one, including branches of the three main splanchnic arteries as well as a vast collateral circulation. The variant anatomy and collateral pathways are described, based on anatomic dissections and angiographic studies, to focus attention on anatomically based explanations for clinical entities.     

Effects of positive end-expiratory pressure on splanchnic circulation and function in experimental peritonitis

Splanchnic and central hemodynamic effects of positive end-expiratory pressure (PEEP) were studied in anesthetized pigs using mechanical ventilatory assistance, with or without sepsis (fecal peritonitis). One hour after sepsis, PEEP (10 cm H2O) was applied (n = 6). Another group (n = 6) had sepsis without PEEP. In one group (n = 6) without sepsis, PEEP was applied after 1 hour, while a fourth group (n = 5), without sepsis or PEEP, served as a control. The group with PEEP and sepsis had reduced cardiac index, portal venous blood flow, and liver surface blood flow. The group with PEEP alone had reduced splanchnic circulation by increasing gastrointestinal vascular resistance, while the group with sepsis alone had increased portal vascular resistance. In a separate series with sepsis, intermittent PEEP, and vigorous fluid resuscitation, it was demonstrated that avoiding hypovolemia did not seem to protect from the PEEP effects on the splanchnic circulation. The combination of sepsis and PEEP was not additive on portal blood flow reduction but reduced bile production.     

胃酸调节肽C端8肽对胰腺炎大鼠胰腺外分泌的影响

目的探讨胃酸调节肽C端8肽(KA-8肽)对蛙皮素诱导的急性水肿性胰腺炎胰腺外分泌影响。方法采用Wistar大鼠蛙皮素皮下注射诱导急性水肿性胰腺炎,收集胰液计量,并检测蛋白和碳酸氢盐的含量;胰腺干湿比、Evans blue漏出率、胰腺组织蛋白/DNA评价胰腺水肿情况。结果KA-8肽和生长抑素对蛙皮素所致的胰腺外分泌功能的升高有明显的抑制作用(59.7±19.5比89.8±18.9;37.5±7.8比89.8±18.9,单位:μl/30min),但并不能影响胰液中蛋白的含量(0.50±0.16比0.47±0.19;0.53±0.19比0.47±0.19,单位:mg/30min);两种多肽可明显降低胰腺组织水肿(干湿比:0.20±0.08比0.15±0.08;0.19±0.09比0.15±0.08)。结论KA-8肽对蛙皮素诱导的急性水肿性胰腺炎有一定的保护作用。     

Interactions of vasoactive intestinal polypeptide and cholecystokinin octapeptide on the control of gallbladder contraction

The gallbladder is supplied by three types of vagal fibers: cholinergic, cholecystokinin (CCK)-ergic, and vasoactive intestinal polypeptide (VIP)-ergic. Most previous studies on the interaction of VIP and CCK on gallbladder contraction have been in vitro. In this study we evaluate this interaction more fully in vivo using six dogs with chronic bile fistula. Dose-response curves were constructed to CCK-8 alone and to VIP alone. The effect of graded doses of VIP on maximal response to CCK-8 was also studied. CCK-8 caused the expected dose-related stimulation of gallbladder contraction, while graded doses of VIP had the opposite effect. VIP also caused a dose-related inhibition of the maximal response to CCK-8, decreasing bilirubin output from 39 +/- 8 to 15 +/- 3 mg/hr (p less than 0.05). The corollary to these findings is that gallbladder tone and contraction is regulated by the interplay of stimulatory cholinergic-CCK-ergic and inhibitory VIP-ergic fibers. Further, a plausible explanation for the variable effects of vagotomy on gallbladder contraction is that variable proportions of these opposing fibers are cut.     

蛋白激酶B参与门静脉高压症高动力循环的研究

目的 探讨蛋白激酶B （AKT）与肝硬化门静脉高压症（portal hypertension,PHT）高动力循环的关系,特别是AKT与肝门静脉高压症内脏血管收缩反应性降低的关系.方法 将SD大鼠随机分为4组：正常对照组（N组,n=7）、四氯化碳诱导的肝硬化门静脉高压组（PHT组,n=7）,经AKT特异性阻滞剂LY294002处理的门静脉高压组（LY组,n=7）和注射二甲基亚枫（DMOS）的门静脉高压组（DMOS组,n=7）,分别测量门静脉压力（portal vein pressure,PP）,离体肠系膜分支动脉对缩血管物质去甲肾上腺素（norepinephrine,NE）的反应性,应用LY294002对离体微动脉收缩反应性的影响以及肠系膜动脉内皮细胞内AKT、内皮一氧化氮合酶（eNOS）的蛋白表达变化.结果 ①与N组相比,PHT组PP明显增高（P＜0.01）,应用LY294002后,PP无明显降低（P＞0.05）;②PHT组肠系膜微动脉对NE的反应性较N组明显降低（P＜0.01）,LY294002可改善这种低反应性（P＜ 0.01）;③AKT在PHT肠系膜动脉内皮中的表达明显上调（P＜0.05）,eNOS的表达PHT组和N组无明显差别（P＞ 0.05）,但p-eNOS的表达在PHT组动脉内皮中明显增高（P＜ 0.05）.结论 肝硬化门静脉高压症的内脏动脉中,AKT的表达上调,通过促进eNOS的活化和降低血管收缩反应性,参与内脏高动力循环的形成.     

Effect of pentagastrin on cholecystokinin and secretin choleresis in the dog

Dogs were prepared with cholecystectomy, ligation of the lesser pancreatic duct, an Heidenhain pouch, and gastric and duodenal fistulae. Bile was collected by cannulation of the common duct. The enterohepatic circulation was artifically maintained with intravenous bile salt while the effects of CCK, secretin and pentagastrin on biliary and gastric acid secretions were studied. Pentagastrin stimulated gastric acid secretion but did not significantly alter bile flow or composition. CCK and secretin increased bile volume and the concentration and output of bicarbonate and chloride in bile. The biliary responses to CCK and secretin were unaltered by the concurrent administration of pentagastrin, but the acid secretory responses seen with pentagastrin were inhibited. The study suggests that pentagastrin is not active as a hormone in the biliary system of dogs.     

Study on splanchnic circulation: measurement of the liver blood flow

In anesthetized patients during abdominal surgery, hepatic artery and portal vein flows were measured simultaneously utilizing an ultrasonic transit-time volume flowmeter. The total hepatic blood flow was 994.6 +/- 52.4 ml/min. The hepatic artery flow and the portal vein flow were 260.0 +/- 23.8 ml/min and 730.8 +/- 41.3 ml/min, respectively. The ratio of hepatic artery flow to portal vein flow was 0.37 +/- 0.04. A significant increase in hepatic artery flow (p less than 0.01) followed portal vein occlusion, whereas no significant change was observed in portal vein flow after hepatic artery occlusion. Common hepatic artery occlusion resulted in a significant decrease in hepatic artery flow (p less than 0.05), but no significant change was observed in portal vein flow. The present study firstly demonstrated that ultrasonic transit-time volume flowmeter is a device to quantitatively assess hepatic artery and portal vein flows with good reproducibility and stability in human subjects. This easy and simple technique seemed to have wide clinical application to abdominal surgery and would have a promising in studying splanchnic blood flows in various situations such as in cases of hepatectomy and portal hypertension.     

Effects of sevoflurane and isoflurane on hepatic circulation in the chronically instrumented dog.

To compare the effects of sevoflurane and isoflurane on hepatic circulation, eighteen dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic and portal blood flows. Each animal was studied while awake and during 1.2 and 2 MAC of either isoflurane or sevoflurane. Both anesthetics induced tachycardia and a dose-dependent decrease in mean aortic blood pressure (isoflurane -27% and -39%; sevoflurane -22% and -37%). Cardiac output decreased only at the highest concentration (isoflurane -10%; sevoflurane -21%). During sevoflurane, portal blood flow decreased at both 1.2 and 2 MAC (-14 and -33%, respectively), whereas an increase in hepatic arterial blood flow was recorded at 2 MAC (+33%). During isoflurane, the only significant change was a decrease in portal blood flow (-16%) at 1.2 MAC. Neither anesthetic significantly changed renal blood flow. Therefore, both anesthetics led to similar systemic and hepatic vasodilation.     

Temporary extracorporeal perfusion of the splanchnic circulation dependent on the Riolan anastomosis

A thorough investigation of a hypertensive 25 year old male was undertaken due to the finding of an absent right radial pulse. This work-up revealed widespread, largely asymptomatic arterial disease characterised by a combination of multiple sites of stenosis and occlusion, aneurysmal dilatation and extensive vessel wall calcification. The findings included a right renal artery stenosis, an abdominal aortic aneurysm and a splanchnic vasculature completely supplied by the inferior mesenteric artery. Consequently it was thought that a prolonged clamping time during the aortic repair would possibly result in ischemic injury. Therefore, the splanchnic organs were perfused by a paediatric oxygenator and pump during the aortic cross-clamping. This case report discusses the etiology of the disease and the technical aspects of splanchnic perfusion.