Effect of metoclopramide on portal blood flow in patients with liver cirrhosis, measured by the pulsed Doppler system

The effect of metoclopramide on portal blood flow, the maximal diameter of the portal vein, and some cardiovascular haemodynamic variables was studied in 10 patients with cirrhosis of the liver and portal hypertension. Portal vein haemodynamics were studied by the pulsed Doppler system. Within 15 min of intravenous administration of 20 mg metoclopramide, portal blood velocity and portal blood flow decreased significantly, from 11.2 +/- 1.1 to 10.8 +/- 1.2 cm/sec and from 769.0 +/- 87.7 to 707.9 +/- 84.2 ml/min, respectively (p less than 0.001). Within about 30 min portal blood velocity and portal blood flow returned to basal values (p greater than 0.05). The maximal diameter of the portal vein, systolic and diastolic blood pressure, and heart rate remained unchanged. These results support the hypothesis that metoclopramide, which raises lower oesophageal sphincter pressure and reduces intravariceal blood flow, significantly decreases the portal blood flow in cirrhotic patients with portal hypertension.     

Portal venous blood flow while breath-holding after inspiration or expiration and during normal respiration in controls and cirrhotics

In this study, we used magnetic resonance (MR) imaging to measure portal blood flow in 12 healthy controls and 17 cirrhotics while they were breath-holding after inspiration and after expiration. We then compared the results with measurements made during normal respiration in the healthy controls and cirrhotics. Blood flow in the main portal vein under basal fasting conditions was quantitated using the cine phase-contrast MR velocity mapping method. Three measurements were made on one occasion, as follows: (1) throughout the cardiac cycle during normal respiration, (2) with the subject breath-holding after maximal inspiration, and (3) with the subject breath-holding after maximal expiration. During normal respiration, portal blood flow was 1.3 ± 0.2 l/min in controls vs 1.0 ± 0.1 l/min in cirrhotics (P < 0.0001); while subjects were breath-holding after inspiration, portal blood flow was 1.0 ± 0.2 l/min in controls vs 0.9 ± 0.1 l/min in cirrhotics; and while subjects were breath-holding after expiration, portal blood flow was 1.5 ± 0.2 l/min in controls vs 1.1 ± 0.2 l/min in cirrhotics (P < 0.0001). The differences were primarily due to changes in flow velocity. When the magnitude of these hemodynamic changes in the three respiratory conditions was compared in controls and cirrhotics, analysis of variance (ANOVA) showed a significant difference (P < 0.0001). In controls, portal blood flow decreased during maximal inspiration relative to flow during normal respiration (−24.6 ± 8.3%). Changes in portal blood flow in controls were greater than in cirrhotics (−13.5 ± 4.5%) (P < 0.0001); however, the difference in blood flow increase associated with maximal expiration between the two groups (+11.8 ± 9.4% vs +5.9 ± 11.5%) was not significant. We found that the respiration-induced hemodynamic variation in portal blood flow was less in cirrhotics than in the healthy controls. Portal blood flow measurements made during normal respiration using MR imaging closely reflect nearly physiologic conditions. Received: November 19, 1998 / Accepted: March 26, 1999     

A canine portal hypertension model induced by intra‐portal administration of Sephadex microsphere

Background and Aim: Big animal models of portal hypertension are important for the research into this disease. The aim of this study was to establish a canine portal hypertension model by intra‐portal administration of microspheres. Methods: Sixteen mongrel dogs were assigned to control group and experimental group randomly. The catheterization of portal vein was performed by laparotomy and the outer end of the catheter was fixed subcutaneously in the abdominal wall. The dogs of the experimental group were given intra‐portal injections of microspheres at a five‐day interval, six times in total. Portal hemodynamics, blood cell counting, liver and renal function test, portography, gastroscopy, liver, spleen and lung histological examination were taken to evaluate the model. Results: 1, 2, 3 and 4 months after initial injection of microspheres, portal venous pressure rose from baseline 8.7 ± 0.7 mmHg to 24.3 ± 1.6, 20.6 ± 2.1, 19.0 ± 1.8 and 17.7 ± 2.0 mmHg, respectively (P < 0.01). The diameter of portal vein increased from 7.6 ± 0.3 to 8.6 ± 0.3 mm, calculated portal resistance increased from 0.46 ± 0.06 to 1.06 ± 0.20 (mmHg/mL/min/kg body weight); velocity of portal blood flow decreased from 35.1 ± 1.7 to 26.1 ± 2.4 cm/s (P < 0.01, respectively). The animals of experimental group developed marked splenomegaly and profuse portosystemic collateral circulations with normal liver and renal function. Conclusion: Repeated intra‐portal administration of microspheres can induce stable and reproducible chronic portal hypertension in dogs with normal liver and renal functions. This model can meet multiple demands of both basic and clinical research of portal hypertension.     

Effect of metoclopramide on transmural oesophageal variceal pressure and portal blood flow in cirrhotic patients

This study was undertaken to evaluate the effect of metoclopramide on transmural oesophageal variceal pressure and portal blood flow in cirrhotic patients. Sixteen cirrhotics were randomly assigned to metoclopramide (10 mg i.v.) or saline. Metoclopramide significantly decreased transmural variceal pressure (15.7% decrease, p less than 0.05 vs. basal value). In order to evaluate if the metoclopramide-induced drop in transmural variceal pressure was due to an effect on portal haemodynamics, we also measured, by means of real time and pulsed Doppler ultrasonography, portal vein diameter, mean velocity of portal flow, and portal venous flow. No significant change was observed before and after metoclopramide. In conclusion, metoclopramide, which increases lower oesophageal sphincter pressure, significantly decreases transmural variceal pressure in cirrhotic patients. However, it does not have any effect on portal haemodynamics.     

Short- and long-term hemodynamic response to octreotide in portal hypertensive patients: a double-blind,controlled study

Abstract: This randomized, double-blind, placebo-controlled study on the hemodynamic effect of two different doses of octreotide administered subcutaneously was conducted among 20 cirrhotic portal hypertensive patients. The wedged hepatic venous pressure, the hepatic venous pressure gradient, the mean portal venous flow velocity, the resistive index of the superior mesenteric artery, the heart rate and the mean arterial pressure were simultaneously evaluated by hepatic vein catheterization and Doppler flowmetry at baseline, 30 and 45 min after a subcutaneous injection of octreotide [0.10 mg (7 patients), 0.05 mg (7 patients)] and of a placebo (6 patients). The portal blood flow velocity, the resistive index of the superior mesenteric artery, the heart rate and the mean arterial pressure were also measured 2, 4, 6 and 8 h after the injection. The hemodynamic changes observed 30 min after the injection did not differ from those at 45 min and the changes at 2, 4, and 6 h were similar to those at 8 h. A statistically significant decrease, in comparison to the placebo group, was observed 45 min after the injection of the two doses of octreotide in the wedged hepatic venous pressure (cumulative median decrease: —10%, p<0.005), in the hepatic venous pressure gradient (cumulative median decrease: —10%, p<0.005) and in the mean portal flow velocity (cumulative median decrease: —11%, p<0.005). A significant increase in the resistive index of the superior mesenteric artery was observed 45 min after the injection of the two doses of octreotide (cumulative median increase: + 10%, p<0.005). Lower, but significant changes in the mean portal flow velocity and in the resistive index of the superior mesenteric artery persisted until 8 h after the injection of the two doses of octreotide (cumulative median decrease of mean portal flow velocity: —7%, p<0.005 and cumulative median increase of resistive index of the superior mesenteric artery: +4%, p<0.005). Changes in the wedged hepatic venous pressure, the hepatic venous pressure gradient, the mean portal flow velocity and the resistive index of the superior mesenteric artery showed a great variability among patients. These changes were more pronounced in patients injected with the lower dose with no relationship with the plasma drug concentrations. Responder patients showed a significant higher baseline mean portal flow velocity in comparison with nonresponders (15.2±1.7 cm/s vs 11.3 ±1.3 cm/s; p<0.005).     

非侵入法对高血压早期血管内皮功能障碍的评价

为了评估高血压 1 2级无心血管危险因素病人是否存在内皮依赖性血管内皮功能的损害 ,并探讨高血压对内皮功能的影响 ,我们应用非侵入方法研究了高血压病人和正常人各 2 5例。用高分辨二维超声方法检测反应性充血前后肱动脉直径和血流 ,比较两组的肱动脉直径变化率、血流以及它们与血压之间的关系。结果发现 ,高血压病人血流介导的肱动脉舒张明显低于对照组 (9.8%± 6 .7%比 14 .7%± 6 .8% ,P <0 .0 1) ;血流介导的肱动脉血流亦较对照组明显减少 (5 2 9± 114mL min比 6 4 2± 16 0mL min ,P <0 .0 1) ;相关分析发现 ,血流介导的肱动脉舒张分别与收缩压 (r=- 0 .4 73,P <0 .0 1)、舒张压 (r=- 0 .30 8,P <0 .0 5 )呈负相关 ;血流介导的肱动脉血流与收缩压呈负相关 (r=- 0 .35 5 ,P <0 .0 1) ,而与舒张压无关。此结果提示 ,高血压病早期虽无明显动脉硬化 ,但已存在血管内皮功能的损伤。     

Azygos venous blood flow while fasting, postprandially, and after endoscopic variceal ligation, measured by magnetic resonance imaging

Using cine phase-contrast magnetic resonance (MR) imaging, we measured fasting and postprandial azygos blood flow in 15 cirrhotic patients with portal hypertension and 11 healthy controls. In 10 of the cirrhotics, measurements were made before and after prophylactic endoscopic variceal ligation therapy (EVL). Flow volume was measured in the azygos vein at the level of the midthoracic vertebra. Azygos blood flow was measured under basal fasting conditions and 30–40 min after ingestion of a 500 Kcal meal. Fasting azygos blood flow was 139 ± 43 ml/min in controls vs 519 ± 249 ml/min in cirrhotics (P < 0.01). Eating significantly increased azygos blood flow, by 38% in controls (P < 0.02) and by 27% in cirrhotics (P < 0.02), compared with fasting conditions. EVL markedly decreased azygos blood flow, by 25% compared with pre-EVL (P < 0.03). The cine phase-contrast MR velocity mapping method measured flow volume in the azygos veins. Azygos blood flow was markedly greater in the cirrhotics than in the controls. In the cirrhotics and controls, blood flow volume increased after eating. Azygos blood flow was significantly reduced by successful EVL. Received: July 28, 1998/Accepted: December 18, 1998     

硝酸异山梨酯气雾剂对门静脉血流动力学的影响

探讨硝酸异山梨酯以气雾剂的形式应用对门静脉血流动力学的影响。于1999年2月—1999年11月选择肝硬化门脉高压患者31例，利用无创伤自身对照的方法，用彩色超声多普勒检测患者的门静脉直径、血流速度、血流量，脾静脉直径、血流速度及血流量，然后向患者口腔内喷入硝酸异山梨酯气雾剂(商品名：欣舒气雾剂，山东省医药工业研究所制药厂生产)4喷(约含药量2．5mg)，于用药后1分钟、10分钟、30分钟再分别检测以上项目，并进行统计学处理。用硝酸异山梨酯气雾剂后可缩小肝硬化门脉高压患者的门静脉直径、降低门脉血流速度、减少门脉血流量(P＜0．01)，因而可降低门脉压力，对患者的血压和脉搏无显著影响(P＞0．05)其它副作用轻微，并且在1分钟内起效，持续半小时以上。提示：硝酸异山梨能气雾剂可快速降低门静脉压力，从而提出将硝酸异山梨酯以气雾剂的形式用于预防和治疗肝硬化门静脉高压引起的上消化道出血。     

Effect of release‐controlled nifedipine on portal hemodynamics in cirrhotic patients

OBJECTIVE : To evaluate the therapeutic effect of release‐controlled nifedipine on portal hypertension. METHODS : Thirty‐two cirrhotic patients were enrolled to investigate, by using duplex Doppler ultrasonography, differences in portal hemodynamics before and after treatment with release‐controlled nifedipine (30 mg once per day). RESULTS : After taking nifedipine, the diameter, blood velocity and blood flow of the portal vein decreased, but only the change in velocity was statistically significant. After treatment, the congestion index increased, and the blood velocity and blood flow of the splenic vein significantly decreased. The resistance and pulsatile indices of the right hepatic and splenic arteries also decreased markedly. The total hepatic blood flow was elevated slightly and there were no significant changes in mean arterial pressure and heart rate. CONCLUSIONS : The resistance and pulsatile indices of the hepatic and splenic arteries are representative indices of portal resistance. Release‐controlled nifedipine may decrease portal pressure by the following mechanisms: (i) decrease of systemic blood pressure triggers the sympathetic reflex, leading to splanchnic artery constriction and portal blood flow reduction; (ii) dilatation of the portal vein and sinusoids leads to decrease portal resistance; and (iii) dilatation of the collateral veins. Nifedipine has no significant effect on systemic circulation in normotensive cirrhotic patients, therefore it has good prospects as a drug for clinical use in portal hypertension.     

Systemic and splanchnic hemodynamic changes in patients with hepatic schistosomiasis

Abstract: Although hepatic schistosomiasis is a common cause of portal hypertension, only a few hemodynamic studies, in humans, have been published on this subject. The aim of this study was to determine the systemic and splanchnic hemodynamic changes in hepatic schistosomiasis and to evaluate the influence of liver fibrosis on these changes. A retrospective analysis of a series of 13 patients with hepatic schistosomiasis who had undergone hemodynamic studies was performed. Portal or perisinusoidal fibrosis was present at liver biopsy in 8 patients. The control group included 22 patients with chronic hepatitis and normal hepatic venous pressure gradients. Patients with schistosomiasis exhibited high cardiac index (4.11±1.15 1 · min^-1 · m^-2 vs 2.99±0.85 1 · min^-1 · m^-2; p<0.05) and low systemic vascular resistance (1039±316 dyn · s · cm^-5 vs 1334±336 dyn · cm^-5; p<0.05). The hepatic venous pressure gradient and hepatic blood flow were normal. Azygos blood flow was markedly increased (0.90±0.66 1 · min^-1 vs 0.13±0.04 1 · min^-1; p<0.05). Hemodynamic values were not significantly different between patients with liver fibrosis and those without fibrosis at liver biopsy. In conclusion, patients with hepatic schistosomiasis had a hyperkinetic systemic and splanchnic circulation. In patients with esophageal varices, a normal hepatic venous pressure gradient confirmed presinusoidal portal hypertension. The presence of portal or perisinusoidal fibrosis did not influence hyperdynamic splanchnic state.     

EFFECT OF NITRIC OXIDE INHIBITION ON KIDNEY FUNCTION IN EXPERIMENTAL RENOVASCULAR HYPERTENSION

We examined the effect of acute systemic blockade of nitric oxide (N0) synthesis on blood pressure and renal function in rats with angiotensin II dependent two-kidney, one-clip Goldblatt hypertension. Hypertensive animals had significantly higher blood pressures, plasma NO metabolite concentrations and urinary NO metabolite excretion rates than control rats. Intravenous administration of N^G-nitro-L-arginine methylester (L-NAME) (10 mg/kg) increased mean arterial pressure in both hypertensive and control animals with the magnitude of increase being greater in hypertensive than control rats (32±3 vs. 20±2 mmHg,p< 0.05). L-NAME did not affect glomerular filtration rates of normal and clipped kidneys but significantly decreased non-clipped kidney glomerular filtration rate (1.1±0.1 vs. 0.7±0.1 ml/min per g kidney wt, p< 0.05). Blood flow to normal and non-clipped kidneys fell in response to L-NAME. Percent reduction in renal blood flow produced by L-NAME was significantly greater in non-clipped than normal kidneys (38±3 vs. 24±2%,p< 0.05). In contrast, clipped kidney blood flow increased after L-NAME (3.3±0.2 vs. 4.0±0.2 ml/min per g kidney wt,p< 0.05). An identical improvement in clipped kidney blood flow occurred when arterial pressure was raised with aortic constriction indicating that the systemic pressor effect of L-NAME was responsible for this finding. These results indicate that NO plays an important role in systemic and non-clipped kidney hemodynamics in renovascular hypertension. Because NO has little influence on stenotic kidney function, the stimulus for increased NO system activity in this disease appears to be vascular shear stress rather than elevated circulating or intrarenal angiotensin II concentrations.     

部分脾动脉栓塞术对肝硬化门静脉高压症血流动力学的影响

目的探讨部分脾动脉栓塞术（PSE）治疗肝硬化门静脉高压症的临床疗效及应用价值。方法 23例不同原因肝硬化门静脉高压患者行PSE治疗,PSE术前及术后1周、1、3、6个月彩色多普勒分别检测患者门静脉和脾静脉的内径、血流速度,计算血流量,并与PSE术前配对分析。结果术后各期患者脾静脉、门静脉血流速度及血流量较术前降低（P〈0.05）;脾静脉内径术后各期与术前相比明显缩小（P〈0.05）;而门静脉主干内径术后6个月内缩小不明显（P〉0.05）。结论 PSE能有效的降低门静脉压力。     

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.     

Chronic Portal Venous Hypertension: The Effect on Liver Blood Flow and Liver Function and the Development of Esophageal Varices

Portal venous hypertension was induced in Göttingen minipigs by banding the portal vein. The pigs were checked repeatedly during the following 24 weeks. Portal pressure increased immediately on banding, from 8.4 ± 0.7 mm Hg to 19.4 ± 0.7 mm Hg, and remained constant throughout the observation period. Within 5 weeks all pigs developed esophageal varices, as demonstrated by portal angiography and endoscopy. The experimentally induced portal hypertension was accompanied by a 65% decrease in hepatic blood flow, most probably caused by almost complete shunting of portal venous blood. The hepatic arterial flow appeared to be within normal limits and sufficient to cover the oxygen demand of the liver; to judge from the splanchnic elimination rate of galactose, the hemodynamic changes did not affect the functional capacity of the liver.     

A simple deep breathing test reveals altered cerebral autoregulation in type 2 diabetic patients

Aims/hypothesis Patients with diabetes mellitus have an increased risk of stroke and other cerebrovascular complications. The purpose of this study was to evaluate the autoregulation of cerebral blood flow in diabetic patients using a simple method that could easily be applied to the clinical routine screening of diabetic patients. Methods We studied ten patients with type 2 diabetes mellitus and 11 healthy volunteer control participants. Continuous and non-invasive measurements of blood pressure and cerebral blood flow velocity were performed during deep breathing at 0.1 Hz (six breaths per minute). Cerebral autoregulation was assessed from the phase shift angle between breathing-induced 0.1 Hz oscillations in mean blood pressure and cerebral blood flow velocity. Results The controls and patients all showed positive phase shift angles between breathing-induced 0.1 Hz blood pressure and cerebral blood flow velocity oscillations. However, the phase shift angle was significantly reduced (p < 0.05) in the patients (48 ± 9°) compared with the controls (80 ± 12°). The gain between 0.1 Hz oscillations in blood pressure and cerebral blood flow velocity did not differ significantly between the patients and controls. Conclusions/interpretation The reduced phase shift angle between oscillations in mean blood pressure and cerebral blood flow velocity during deep breathing suggests altered cerebral autoregulation in patients with diabetes and might contribute to an increased risk of cerebrovascular disorders.     

Intractable Hepatic Encephalopathy After Tips with Polytetrafluoroethylene-covered Stent-Graft

Abstract

Objective. The objective of this study is to analyze the changes in portal hemodynamics that occurs in portal hypertension before and after transjugular intrahepatic portosystemic shunt (TIPS), to investigate the relationship between these changes and portal pressure (PP) and to determine the significance of sonographic parameters in measuring PP. Methods. Ultrasonography of the portal and splenic veins and direct measurement of the PP were performed in 92 patients before and after TIPS. The differences observed in the portal and splenic vein diameters, the blood flow velocity in the portal and splenic veins and the PP were measured, and the correlations between PP and the other parameters were assessed using the SPSS 13 (SPSS Inc., Chicago, IL, USA). P < 0.05 was considered statistically significant. Results. We observed a significant decrease in the PP and the diameters of the portal and splenic veins compared to preoperative conditions (p < 0.001). The velocity of blood flow in the portal and splenic veins was significantly increased after TIPS (p < 0.001). The PP correlated with the diameter and velocity of blood flow in portal (r = 0.46, p = 0.020; r = 0.47, p = 0.017) and splenic vein (r = 0.57, p = 0.003; r = 0.33, p = 0.003) only in Child's A and was absent in Child's B cirrhosis patients. Conclusion. The PP is influenced by the complex interaction between intrahepatic vascular resistance, collaterals and the amount of portal blood flow, which varies considerably between individuals. Once a certain pressure threshold is reached, collaterals form, and the correlation between the ultrasonographic parameters and PP becomes limited.     

Influence of the degree of liver failure on portal blood flow in patients with liver cirrhosis

Portal vein haemodynamics as demonstrated by the pulsed Doppler system were studied in 37 patients with cirrhosis who had been classified in three groups (A, B, and C) in accordance with the degree of liver failure. Maximal inner diameter of the portal vein was significantly lower in patients who were considered to be in good condition (group A) than in patients with moderate and severe liver failure (group B and group C) (p less than 0.001). A significant difference was also found between group A and group B and between group A and group C with regard to the portal blood velocity and portal blood flow (p less than 0.001). In accordance with the presence and size of the oesophageal varices, in patients with large varices the portal blood velocity and portal blood flow were significantly lower than in patients without varices (p less than 0.001), whereas maximal inner portal vein diameter was significantly higher (p less than 0.001). This study demonstrated that in patients with cirrhosis circulatory alterations in the portal vascular bed may be, at least in part, an indicator of the stage of liver disease.     

Mechanical pumping of portal blood to the liver: hemodynamic effects of a new experimental treatment for portal hypertension

Background/Aims: It has been suggested that mechanical pumping of portal blood to the liver may correct portal hypertension while increasing portal flow to the liver, which may enhance liver function in cirrhosis. However, the hemodynamic effects of this procedure are unknown. The present study investigated these issues in rats with portal hypertension due to portal vein stenosis.Methods: Mechanical pumping of portal blood to the liver was established by an extracorporeal shunt bypassing the portal vein stenosis, connected to a continuous withdrawal/infusion pump. Portal pressure, portal-systemic shunting (mesenteric injection of Cr-51 microspheres, n=10), mesenteric artery blood flow (perivascular Transonic flowmeter, n=7) and systemic hemodynamics and regional blood flows (left ventricle injection of Ce-141 microspheres, n=15), were measured at pumping rates of 0, 3 and 6 ml·min⁻¹.Results: Mechanical pumping of portal blood to the liver caused a marked decrease in portal pressure (from 17±1 to 12.6±1 and 9.4±.9 mmHg at pumping rates of 0, 3 and 6 ml·min⁻¹) and portal-systemic shunting (from 97±4 to 70±4 and 51±6% respectively) (p<0.001). However, there were no significant changes in mesenteric artery flow (5.5±3 vs 5.6±3 ml·min⁻¹·100 g⁻¹), suggesting that all blood pumped to the liver was withdrawn from that circulating through the collaterals. Moreover, there were no changes in mean arterial pressure, cardiac index, peripheral resistance and splanchnic arteriolar resistance.Conclusions: The short-term mechanical pumping of portal blood to the liver effectively decreases portal pressure and portal-systemic shunting and has no significant effects on systemic and splanchnic hemodynamics in portal hypertensive rats.     

Cardiac effects of prolonged and intense exercise training in patients with coronary artery disease

The effects of intense and prolonged exercise training on the heart were studied with echocardiography in eight men with coronary artery disease with a mean age ( ±standard error of the mean) of 52 ± 3 years. Training consisted of endurance exercise 3 times/week at 50 to 60 percent of the measured maximal oxygen uptake for 3 months followed by exercise 4 to 5 days/week at 70 to 80 percent of maximal oxygen uptake for 9 months. Maximal oxygen uptake capacity increased by 42 percent (26 ± 1 versus 37 ± 2 ml/kg per min; p < 0.001). Heart rate at rest and sub-maximal heart rate and systolic blood pressure at a given work rate were significantly lower after training. Systolic blood pressure at the time of maximal exercise increased (145 ± 9 before versus 166 ± 8 mm Hg after training; probability [p] < 0.01). Left ventricular end-diastolic diameter was increased after 12 months of training (from 47 ± 1 to 51 ± 1 mm; p < 0.01). Left ventricular fractional shortening and mean velocity of circumferential shortening decreased progressively in response to graded isometric handgrip exercise before training but not after training. At comparable levels of blood pressure during static exercise, mean velocity of circumferential shortening was significantly higher after training (0.76 ± 0.04 versus 0.98 ± 0.07 diameter/sec, p < 0.01). No improvement in echocardiographic or exercise variables was observed over a 12 month period in another group of five patients who did not exercise. Thus the data suggest that prolonged and vigorous exercise training in selected patients with coronary artery disease can elicit cardiac adaptations.     

Different hemodynamic patterns of alcoholic and viral endstage cirrhosis: Analysis of explanted liver weight,degree of fibrosis and splanchnic Doppler parameters

Objective. In cirrhosis, portal hemodynamics is usually considered independently of the disease etiology. The objective of this study was to investigate the role of the etiology of liver disease on the relationship between liver blood flow and liver pathology in endstage cirrhosis. Material and methods. Portal blood velocity and volume, congestion index of the portal vein, and hepatic and splenic pulsatility indices were evaluated with echo-Doppler in cirrhotic patients immediately before liver transplantation. When a patent paraumbilical vein was present, its blood flow was measured and effective portal liver perfusion was calculated as portal blood flow minus paraumbilical blood flow. The hemodynamic parameters were correlated with liver weight and the pattern of the liver fibrosis morphometrically assessed in explanted livers. A total of 131 patients with alcoholic or viral cirrhosis were included in the study. Results. In alcoholic cirrhosis, liver weight was higher than that in viral disease (1246±295 g versus 1070±254 g, p=0.001), portal liver perfusion per gram of liver tissue was lower (0.49±0.36 ml g^?1 min^?1 versus 0.85±0.56 ml g^?1 min^?1, p=0.004) and hepatic pulsatility indices were higher (1.45±0.31 versus 1.26±0.30, p=0.018). The degree of liver fibrosis was similar in alcoholic and viral cirrhosis (11.7±5.5% versus 11.0±4.4%, p=NS). An inverse relationship between liver weight and Child-Pugh score was disclosed in viral (p<0.001) but not in alcoholic disease. Conclusions. A different hemodynamic pattern characterizes the advanced stage of cirrhosis of alcoholic and viral origin. A more severe alteration of intrahepatic portal perfusion, probably coexisting with a more severe hepatocyte dysfunction, and a higher liver weight can be detected in alcoholic cirrhosis.