狗肝硬化门脉高压症血浆儿茶酚胺浓度变化的实验研究

本研究通过结扎狗胆总管形成肝硬化门脉高压症的动物模型,对模型形成前后门静脉压力、肝静脉压力、门静脉血流量、肝动脉血流量、门静脉血管阻力,肝动脉血管阻力和门静脉、肝静脉、腹主动脉。下腔静脉四部位血浆儿茶酚胺浓度的变化进行了自身对照性对比研究。结果:①肝硬化形成后门脉压力明显增高,肝静脉嵌塞区也明显增高,门脉血流量减少而肝动脉血流量增加,门脉血管阻力增加而肝动脉血管阻力则下降。这些变化与人类肝硬化门脉高压症相同。②门静脉、肝静脉。腹主动脉和下腔静脉血浆去甲肾上腺素的含量均在门脉高压形成后明显增加。提示肝硬化时血浆去甲肾上腺素的增加可能参与门脉高压症的某些病理生理过程,并进一步支持用 a 受体阻滞剂降低门脉压力和门脉血管阻力,治疗肝硬化食道静脉曲张破裂出血或预防出血。     

狗肝硬化门脉高压症血浆儿茶酚胺浓度变化的实验研究

本研究通过结扎狗胆总管形成肝硬化门脉高压症的动物模型，对模型成前后门静脉压力、肝静脉压力、门静脉血流量、肝动脉血流量、门静脉血管阻力，肝动脉血管阻力和门静脉、肝静脉、脉主动脉。下腔静脉四部位血浆儿茶酚胺浓度的变化进行了自身对照性对比研究。结果：①肝硬化形成后门脉压力明显增高，肝静脉嵌塞压也明显增高，门脉血流量减少而肝动脉血流量增加，门脉血管阻力增加而肝动脉血管阻力则下降，这些变化与人类肝硬化门脉高压症相同。②门静脉、肝静脉。腹主动脉和下腔静脉血浆去甲肾上腺素的含量均在门脉高压形成后明显增加。提示肝硬化时血浆去甲肾上腺素的增加可能参与门脉高压症的某些病理生理过程，并进一步支持用a受体阻滞剂降低门脉压力和门脉血管阻力，治疗肝硬化食道静脉曲张破裂出血或预防出血。     

急性重症酒精性肝炎肝动脉缓冲效应研究进展*

目的 急性重症酒精性肝炎患者肝窦存在致密胶原沉积,阻力增加阻碍了血液流经肝窦,窦性压力增加,门静脉血流不畅,门静脉向肝窦的灌注显著减少,此时就启动了肝动脉缓冲效应,后者可以抵消肝脏灌注的两个主要血管肝动脉或门静脉中任何一个的流量减少,维持肝脏总血流量在一个生理范围内,使肝脏灌注(肝动脉和门静脉血流之和)恢复正常。双功能多普勒超声可以无创评估肝脏血流动力学和定量肝动脉缓冲效应。因此,肝动脉缓冲效应可能成为诊断急性重症酒精性肝炎的重要检测方法之一。     

门静脉高压药物治疗机制

近10年来,门静脉高压病理生理学的研究进展使药物治疗成为可能,现就药物治疗门静脉高压的病理生理学机制作一介绍。一、门静脉高压的血流动力学　根据Ｏｈｍ定律,血管系统某段血管的压力梯度=血流×阻力。可见门静脉压力梯度与其血流量和门静脉系统阻力成正比。临床上用肝静脉压力梯度(ＨＶＰＧ)代表门静脉压力梯度,门静脉系统的阻力包括门静脉阻力、肝内血管床阻力和侧支循环阻力,门静脉血流则受血容量等因素影响,因而可以通过降低血管阻力、减少门静脉血流和血容量等方法降低门静脉压力。二、调控肝内循环的药物许多血管扩张剂能降低肝内…     

超声弹性成像评估门静脉高压症

正门静脉高压症(PH)是一种常见的临床综合征。其血流动力学表现为流入肝脏的静脉压力梯度增加,可以通过对比门静脉流入量与肝静脉流出量计算得出~([1])。与其他血管系统一样,门静脉压力由两个独立因素决定的:血流阻力和流量,如欧姆定律所述:压力=阻力×流量。门静脉血流阻力增加是导致门静脉压力升高的初始因素。阻力可发生在肝前、肝内或肝后。在西方国家,约90%的PH     

超声门静脉血流动力学检测在老年肝硬化门静脉高压诊断中的意义

目的分析超声检测门静脉血流动力学在老年肝硬化门静脉高压诊断中的价值。方法选择老年肝硬化失代偿期的患者30例作为肝硬化失代偿组,老年肝硬化代偿期的患者30例作为肝硬化代偿组,同期体检的正常健康老年人30例作为正常对照组。彩色多普勒超声检测肝脏门静脉血流速度、肝脏门静脉内径和肝脏门静脉横截面积以及肝动脉阻力指数和脾动脉阻力指数,计算门静脉充血指数、门脉血流量和门脉高压指数,对3组患者的门静脉血流速度、肝脏门静脉内径、肝脏门静脉横截面积、肝动脉阻力指数、脾动脉阻力指数、门静脉充血指数、门脉血流量和门脉高压指数进行比较。结果肝硬化代偿组和肝硬化失代偿组的门静脉血流速度均低于正常对照组(P0.05),肝硬化失代偿组的门静脉血流速度低于肝硬化代偿组(P0.05);肝硬化代偿组和肝硬化失代偿组的门静脉内径、门静脉横截面积均高于正常对照组(P0.05),肝硬化失代偿组的门静脉内径、门静脉横截面积高于肝硬化代偿组(P0.05);肝硬化代偿组和肝硬化失代偿组的门脉充血指数均高于正常对照组(P0.05),肝硬化失代偿组的门脉充血指数高于肝硬化代偿组(P0.05);肝硬化代偿组的门脉血流量高于正常对照组(P0.05),肝硬化失代偿组的门脉血流量低于正常对照组和肝硬化失代偿组(P0.05);肝硬化代偿组和肝硬化失代偿组的肝动脉阻力指数、脾动脉阻力指数、门脉高压指数均高于正常对照组(P0.05),肝硬化失代偿组的肝动脉阻力指数、脾动脉阻力指数、门脉高压指数均高于肝硬化代偿组(P0.05)。结论超声检测门静脉血流动力学在老年肝硬化门静脉高压诊断中具有一定的诊断价值。     

对肝功能衰竭的猪行异位部分肝移植的效果评价

目的 探讨在猪急性缺血性肝功能衰竭时行辅助性异位部分肝移植的作用。 方法在缩窄门静脉8 5％以上的同时,对结扎及不结扎肝动脉的家猪体内配对开展辅助性异位部分肝移植,监测受体存活情况、肝功能、肝脏血流情况、病理及供肝胆汁分泌情况。 结果 在缩窄门静脉85％以上并结扎肝动脉的受体肝脏体积缩小,病理提示大片肝细胞坏死,在缩窄门静脉85％以上而未结扎肝动脉的受体肝脏色泽正常,病理肝细胞无明显异常;植入肝体积增大,病理提示肝细胞存活良好并有分裂增生。 结论 受体肝动脉结扎、门静脉缩窄可以造成急性肝功能衰竭模型;辅助性异位部分肝移植能纠正肝功能衰竭;保留受体肝脏动脉血供、减少门静脉血供对受体肝脏功能无严重影响。     

原发性肝癌患者肝动脉结扎加栓塞前后入肝血流量的变化

作者观察了41例原发性肝癌患者肝动脉结扎加栓塞前后的入肝血流量、肝功能和血中AFP浓度变化。结果:原发性肝癌患者的肝固有动脉和门静脉血流量均高于对照组;肝固有动脉结扎加栓塞后门静脉血流量明显增加,肝功能变化和AFP下降显著;一侧肝动脉结扎加栓塞后肝固有动脉血流量仅减少四分之一,门静脉血流量有所增加,对肝功能的影响不明显,AFP的下降也明显差于上组。提示了肝癌的血供特点和肝动脉阻断后经门静脉化疗的必要性。     

肝纤维化大鼠肝气郁结证与肝藏血关系的研究

目的:探讨中医藏象理论"肝藏血主疏泄"相关的肝脏生理病理生物学基础。方法:以四氯化碳皮下注射法建立肝纤维化肝气郁结证大鼠模型,采用肝脏超声检测和功能核磁灌注方法,检测肝气郁结证大鼠动态活体肝纤维化过程中脑部和肝脏血管血流速度、血管直径、血流量变化,同时进行大鼠大脑功能核磁分析。结果:在肝纤维化肝气郁结证病程中,大鼠肝动脉、肝静脉血管管径及血流量明显增加,海马及下丘脑脑区灌流量明显增加,且脑杏仁核异常激活。结论:脑部和肝脏血流变化与肝藏血理论之间具有相关性,肝藏血功能异常与肝脏和脑部血流动力学改变密切相关。     

门脉高压的药物治疗

门脉高压的药物治疗旨在减少门静脉的血流量和降低肝内血管阻力,因而临床上主要选用血管收缩剂和血管扩张剂。1.血管收缩剂:加压素对脾动脉和肠系膜动脉具有明显的收缩作用,可减少进入门脉系统的血流量,致使门脉压力下降。另外,该药还可减少静脉血流,有助于治疗食管静脉曲张出血。由于加压素对内脏血管床的作用远比其他部位强,故有人提出经动脉滴注加压素可以增加局部效应,减少对全身     

Portal Hemodynamics in Fulminant Hepatic Failure as Assessed by Duplex Doppler Ultrasonography

Portal hypertension usually occurs in patients with fulminant hepatic failure (FHF). There is, however, no information on portal venous hemodynamics in patients with FHF. Therefore, we studied the portal venous hemodynamics in patients with FHF using duplex Doppler ultrasonography. We measured the portal vein diameter, flow velocity, and volume flow with duplex Doppler ultrasonography in 29 patients with FHF and 15 patients with uncomplicated acute viral hepatitis. No significant difference was observed in the portal vein parameters in the two groups. Nineteen patients with FHF survived. No difference in portal flow velocity and flow rate was observed between survivors and nonsurvivors. A significantly lower portal flow velocity was observed in nine patients of FHF with ascites compared with those without ascites (12.29 ± 2.81 vs 16.26 ± 4.87 cm/sec; P < 0.01). Portal hemodynamics do not significantly change in fulminant hepatic failure; therefore, it has no prognostic significance.     

Portal venous hemodynamics in hepatocellular carcinoma. Effects of hepatic artery embolization

Portal hemodynamics were studied in 55 patients with hepatocellular carcinoma in comparison with 41 normal subjects, using the duplex system that consists of an electronic sector scanner and a pulsed Doppler velocitometer. Changes of portal hemodynamics after transcatheter hepatic artery embolization were also investigated in 15 of the patients with hepatocellular carcinoma. The duplex system showed that 9 of the 55 had no Doppler signal in the portal trunk, suggesting portal vein thrombosis, 2 had hepatofugal flow in the portal trunk indicative of arterioportal shunts, and 44 had hepatopetal flow in the portal trunk. One of the 9 patients with no significant portal venous flow showed hepatopetal flow in collateral veins at the porta hepatis, suggesting cavernous transformation of the portal vein. All of these ultrasound findings were confirmed by subsequent celiac-mesenteric angiography. In 44 of the 55 patients there was no tumor invasion in the portal trunk, and portal venous flow was found to be close to that of normal subjects regardless of the stage or size of tumor, and tumor invasion into relatively large portal branches. After transcatheter hepatic artery embolization, portal venous flow was increased, even on the next day, and it remained increased for at least 2 wk. Thus, the duplex system is useful to study qualitative and quantitative changes of portal hemodynamics in hepatocellular carcinoma. Our observations suggest that the portal venous flow is kept relatively constant by some homeostatic mechanism even in advanced hepatocellular carcinoma until the tumor invades into the portal trunk, and that it increases when hepatic arterial flow is occluded.     

Systemic, renal, and hepatic hemodynamic derangement in cirrhotic patients with spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis (SBP) is frequently associated with renal failure. This study assessed if systemic and hepatic hemodynamics are also affected by this condition. Standard laboratory tests, tumor necrosis factor alpha (TNF-alpha) in plasma and ascitic fluid, plasma renin activity (PRA) and norepinephrine (NE), and systemic and hepatic hemodynamics were determined in 23 patients with SBP at diagnosis and after resolution of infection. Eight patients developed renal failure during treatment. At diagnosis of infection, patients developing renal failure showed significantly higher values of TNF-alpha, blood urea nitrogen (BUN), PRA and NE, peripheral vascular resistance, and hepatic venous pressure gradient (HVPG) and lower cardiac output than patients not developing renal failure. During treatment, a significant reduction in cardiac output and arterial pressure and increase in PRA and NE, HVPG, and Child-Pugh score were observed in the first group but not in the second. Peripheral vascular resistance remained unmodified in both groups. Changes in PRA and NE correlated inversely with changes in arterial pressure and directly with changes in BUN, Child-Pugh score, and HVPG. Five patients in the renal failure group developed encephalopathy, and 6 died. In the group without renal failure, none of the patients developed encephalopathy or expired. In conclusion, patients with SBP frequently develop a rapidly progressive impairment in systemic hemodynamics, leading to severe renal and hepatic failure, aggravation of portal hypertension, encephalopathy, and death. This occurs despite rapid resolution of infection and is associated with an extremely poor prognosis.     

Effect of oral propranolol administration on azygos, renal and hepatic uptake and output of catecholamines in cirrhosis

Circulating catecholamines are increased in cirrhosis with portal hypertension, and increase further after propranolol. In 23 cirrhotic patients, plasma norepinephrine and epinephrine were determined in an artery, the azygos vein, the right renal vein and a hepatic vein before and after an oral 80-mg dose of propranolol. Baseline azygos and renal venous norepinephrine levels were significantly higher than arterial norepinephrine levels (+20%, p less than 0.005; and +28%, p less than 0.001, respectively). Hepatic venous norepinephrine and all venous epinephrine values were below the arterial values (all p less than 0.05). After propranolol intake, arterial norepinephrine and epinephrine increased (+16%, p less than 0.01; and +93%, p less than 0.001, respectively). Significant increases in norepinephrine and epinephrine were found in azygos and renal veins (all p less than 0.01), whereas hepatic venous norepinephrine and epinephrine remained unchanged. Azygos and hepatic blood flow decreased after propranolol intake (-27%, p less than 0.05; and -16%, p less than 0.01, respectively). Azygos spillover of norepinephrine (an estimate of locally released norepinephrine delivered to the circulation) and clearance of epinephrine remained unaltered. Hepatointestinal clearance showed no significant change for norepinephrine, but showed a borderline-significant decrease for epinephrine (-23%, p = 0.08). Our results show a net production of norepinephrine in the prehepatic splanchnic area drained through superior portalsystemic collaterals and in the kidneys. The increase in circulating catecholamines after propranolol intake is probably due to a combination of further enhancement of sympathetic activity and a decrease in catecholamine degradation.     

Effects of Propranolol on Portal Hemodynamics in Patients with Chronic Liver Disease

To elucidate the mechanism by which propranolol reportedly affects portal hemodynamics, we investigated the effect of propranolol on systemic and splanchnic hemodynamics in 15 patients with portal hypertension and esophageal varices by simultaneous catheterization of the portal vein and the right hepatic vein and measurement of portal venous flow using an ultrasound doppler system. Infusion of 5 mg of propranolol significantly decreased pulse rate (-12.6%), cardiac output (-24.5%), portal venous flow (-22.3%), portal venous pressure (-13.3%), and gradient between portal venous pressure and free hepatic venous pressure (-24.8%). Thus, propranolol seems to decrease portal venous pressure by reducing portal venous flow, at least in part, as a result of reduction of cardiac output due to its beta 1 adrenergic receptor blocking action.     

Hemodynamic study during transdermal application of nitroglycerin tape in patients with cirrhosis

We studied 14 patients with portal hypertension and cirrhosis using portal and hepatic vein catheterizations to determine the effects of transdermal application of nitroglycerin tape (containing 10 mg of nitroglycerin and capable of releasing 6 to 7 mg of nitroglycerin in 12 hr) on splanchnic hemodynamics. Patients randomly received nitroglycerin (n = 7) or a placebo (n = 7). No significant changes were observed after the administration of the placebo. In contrast, transdermal nitroglycerin caused a significant reduction in portal pressure, as evaluated by measurements of the portal venous pressure gradient (-22%, p less than 0.01). The reduction of portal pressure was due to a decrease in the portal venous pressure, with no changes in the free hepatic venous pressure. Despite the fall in portal pressure, the hepatic blood flow was maintained. These findings suggest that transdermal nitroglycerin could be potentially useful in the treatment of portal hypertension associated with cirrhosis.     

Effects of Cimetidine and Ranitidine on Splanchnic Hemodynamics in Patients with Chronic Liver Disease

Effects of two histamine H2 receptor antagonists, cimetidine and ranitidine, on systemic and splanchnic hemodynamics were studied in patients with chronic liver disease by simultaneous catheterization of the portal vein and the right hepatic vein and measurement of portal venous flow using the ultrasound doppler system or cineangiography. Neither infusion of 200 mg of cimetidine nor 50 mg of ranitidine reduced cardiac output, portal venous pressure, the gradient between wedged hepatic venous pressure and free hepatic venous pressure, hepatic blood flow, and portal venous flow. It is unlikely that histamine is an important modulator of flow via the H2 receptor.     

Effects of posture change on the hemodynamics of the liver

BACKGROUND/AIMS: According to our experience, blood flow in the portal vein may alter according to body posture. It is reported that decreased portal venous flow immediately gives rise to significantly increased blood flow in the hepatic artery. To gain further insight into blood flow changes affected by posture, we examined blood flows in the portal vein, hepatic artery and hepatic vein at different postures. METHODOLOGY: Using a Doppler ultrasound system, the hemodynamics of the portal vein, right hepatic artery, and hepatic vein were examined in 35 patients at supine and left decubitus positions. RESULTS: Portal vein blood flow volumes were significantly lower in the left decubitus position than in the supine. In the right hepatic artery, the left decubitus position gave significantly higher blood flow velocity values than the supine. CONCLUSIONS: Our results indicated that upon change of posture from the supine to left decubitus position, portal vein flow velocity was reduced and hepatic artery flow velocity increased. Changes in portal and hepatic arterial flows by changing posture may be explained by decreased portal flow as a direct result of changed posture, leading to increased hepatic arterial flow to maintain total hepatic blood inflow.     

Effect of propranolol on hepatic and systemic hemodynamics in dogs with chronic bile duct ligation

Propranolol has been reported to reduce portal and wedged hepatic vein pressures in man and may be useful for the prevention of variceal bleeding. However, its mechanism of action remains unclear. We have examined the effect of propranolol on the systemic and hepatic circulations in dogs with chronic bile duct ligation and secondary biliary cirrhosis. Under anesthesia, eight dogs received four increasing doses of propranolol as an i.v. bolus followed by continuous infusion. Systemic and hepatic hemodynamic parameters were measured in basal conditions and after a 30 min infusion for each dose. Portal vein and hepatic artery blood flows were measured with electromagnetic flow meters. All dogs had portal hypertension (portal venous pressure 15.3 +/- 0.8 mm Hg), a hyperdynamic circulation and severe liver disease resulting in a marked decrease of propranolol systemic clearance (8.75 ml per min per kg) and extraction (40%). The first dose of propranolol induced a decrease in heart rate (-27%) and in cardiac index (-21%), and an increase in systemic vascular resistance (+20%). With increasing doses, the systemic vascular resistance decreased with an increase in the cardiac index. Propranolol was not associated with significant modifications of hepatic hemodynamics: portal, wedged and free hepatic venous pressures and hepatic artery blood flow were stable, and portal blood flow decreased slightly at very high propranolol levels. In seven dogs studied without dissection of the hepatic vessels, there was a small decrease in portal pressure, but not in wedged and free hepatic venous pressures with increasing doses of propranolol. Thus, in dogs with intrahepatic portal hypertension, propranolol has significant effects on systemic hemodynamics, but only minimal effects on the hepatic circulation.     

PORTAL HAEMODYNAMICS AND HEPATIC BLOOD FLOW

Abstract Obstructive jaundice was produced in adult mongrel dogs by cholecystectomy and ligation of the common bile duct. Two weeks later 40% hepatectomy was performed during 10 min occlusion of hepatic inflow (group I). Liver tissue lipid peroxide levels increased significantly and superoxide dismutase activity decreased. The portal endotoxin (Et) concentration increased markedly after reperfusion and peripheral blood Et and serum β- N-acetyl hexosaminidase levels increased markedly, beginning 3 h after reperfusion. The phagocytic index increased transiently after reperfusion, but decreased markedly thereafter. Hepatocyte degeneration and necrosis became severe, intestinal villi were damaged and the 1 week survival rate was 23.1%; deaths were due to liver failure. These changes were prevented by construction of a portosystemic bypass and a 1 week survival rate of 70% (group II) was achieved. When the ischaemic time was prolonged to 20 min with the portosystemic bypass (group III), the pathological changes resembled those seen in group I, although no changes were observed in portal or peripheral blood Et levels. These findings suggest that major hepatectomy in the presence of severe jaundice should be carefully performed so that the ischaemic time is minimized during portosystemic bypass in an attempt not only to prevent production of Et in portal venous blood due to intestinal congestion, but also to reduce ischaemia-reperfusion injury.