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Biomedical subjects

J Bosch

Publications and source records attributed to J Bosch.

At least 145 records · Page 8Linked to original sources

Time profile of the haemodynamic effects of terlipressin in portal hypertension.

BACKGROUND/AIMS: Terlipressin is a long-acting vasopressin analogue that has been proved useful in the treatment of variceal haemorrhage. This study investigates the time profile of the haemodynamic effects of terlipressin on portal hypertension as well as the efficacy in decreasing portal-pressure and collateral blood flow of reduced doses, suitable for longer therapy to prevent early rebleeding. METHODS: Splanchnic and systemic haemodynamics were measured in 23 patients with cirrhosis and portal hypertension in baseline conditions and at 30 min, 1, 2, 3 and/or 4 h after the double-blind administration of a single intravenous injection of 1 mg (n=8) or 2 mg (n=8) of terlipressin, or placebo (n=7). RESULTS: Placebo caused no significant effects. At 30 min of terlipressin administration, the hepatic venous pressure gradient (1 mg: -16+/-9%, 2 mg: -21+/-11%; p<0.01) and azygos blood flow (1 mg: -19+/-13%, 2 mg: -25+/-17%; p<0.05) were significantly reduced. These effects were still significant at 4 h (2 mg) or 3 h (1 mg). Both doses moderately increased arterial pressure at 1 h. At 4 h, neither arterial pressure nor peripheral vascular resistance was significantly modified by either dose of terlipressin. Terlipressin caused no significant changes in hepatic blood flow. CONCLUSIONS: In patients with cirrhosis, a single injection of 2 mg of terlipressin significantly and markedly reduces portal pressure and azygos blood flow for up to 4 h. The effects of a reduced dose (1 mg) were almost as pronounced and prolonged, suggesting that after the initial control of variceal bleeding, terlipressin therapy could be maintained for several days at low dosage to reduce the risk of early rebleeding.

Adult↗

Pharmacological prevention of variceal bleeding. New developments.

The introduction of pharmacological therapy has been one of the major advances in the treatment of the complications of portal hypertension. Many drugs have been shown to reduce portal hypertension in patients with cirrhosis. However, the most widely used drugs and the only ones for which there is sufficient evidence, are the beta-blockers. These drugs have been, up to now, the only accepted prophylactic therapy for oesophageal variceal bleeding and are also an alternative treatment to sclerotherapy or surgery to prevent variceal rebleeding. A reduction in portal pressure gradient by beta-blockers below 12 mmHg or by more than 20% of baseline values is associated with almost a total protection from oesophageal bleeding. Such a marked response in portal pressure is only achieved in some patients receiving propranolol. New pharmacological approaches with a greater portal pressure reducing effect may improve the beneficial effect of drugs in preventing variceal bleeding. The more promising approach is the combined administration of beta-blockers and isosorbide-5-mononitrate, which has been shown to potentiate the reduction in portal pressure and to be highly effective in initial randomized clinical trials.

Adrenergic beta-Antagonists↗

Anemia worsens hyperdynamic circulation of patients with cirrhosis and portal hypertension.

This retrospective cohort study was aimed at investigating the effects of anemia on the hemodynamic disturbances associated with portal hypertension. In all, 202 consecutive nontreated portal-hypertensive patients referred for evaluation to our Hepatic Hemodynamic Laboratory were included. Compared to the nonanemic patients, anemic cirrhotic patients had an increased cardiac output (7.9 +/- 1.9 vs 7.1 +/- 2 liters/min, P < 0.01), and a decreased mean arterial blood pressure (82 +/- 11 vs 94 +/- 13 mm Hg, P < 0.0001) and systemic vascular resistance (838 +/- 235 vs 1102 +/- 356 dyn/sec/cm5, P < 0.0001). Similar results were obtained when Child A or Child B-C patients were analyzed separately. Multivariate logistic regression disclosed that hemoglobin concentration, in addition to age, sex azygos blood flow, and albumin concentration, was an independent factor influencing the degree of systemic vasodilation in cirrhotic portal-hypertensive patients. This study discloses that anemia worsens the hyperdynamic circulation associated with portal hypertension. Since hemoglobin concentration may change with time, this parameter should be taken into account when evaluating hemodynamics in portal-hypertensive patients.

Aldosterone↗

The portal pressure response to beta-blockade is greater in cirrhotic patients without varices than in those with varices.

BACKGROUND & AIMS: Nonselective beta-blockers are effective in reducing portal pressure in cirrhotic patients. However, this beneficial effect is highly variable and may depend on the extent of portal system collateralization. The aim of this study was to compare portal pressure response with timolol, a nonselective beta-blocker, in cirrhotic patients with and without varices. METHODS: Portal and systemic hemodynamics were measured before and after a single oral dose of 10 mg of timolol in 50 patients with cirrhosis and portal hypertension, 15 with and 35 without esophageal varices. RESULTS: Timolol significantly decreased portal pressure in all patients (mean reduction, 20% +/- 13%; P < 0.0001). The reduction in hepatic venous pressure gradient was greater in patients without varices (-24% +/- 14%) than in those with varices (-12% +/- 8%) (P < 0.01). A decrease in the hepatic venous pressure gradient of <12 mm Hg was achieved in 7 of 12 (58%) patients without varices and a baseline pressure gradient of <12 mm Hg, but only in 3 of 15 patients with varices (20%) (P < 0.01). CONCLUSIONS: Timolol is effective in reducing portal pressure in cirrhotic patients, more so in patients without varices, suggesting that nonselective beta-blockers will be more effective in the treatment of portal hypertension when administered at early stages, before the development of varices.

Aged↗

Endoscopic assessment of variceal volume and wall tension in cirrhotic patients: effects of pharmacological therapy.

BACKGROUND & AIMS: Variceal rupture is believed to occur when variceal wall tension is excessive. The combined use of endosonography, allowing the objective measurement of variceal radius, and endoscopic measurement of transmural variceal pressure may enable assessment of this important parameter. The aim of this study was to assess the effects on variceal hemodynamics of drugs acting through different mechanisms: decreasing portocollateral blood flow (propranolol) or resistance (isosorbide-5-mononitrate [ISMN]). METHODS: Repeated measurements of variceal radius, volume (by endosonography), and transmural pressure (using endoscopic gauge) were performed in 27 cirrhotic patients at baseline and 40 minutes after double-blind administration of placebo (n = 9), propranolol (n = 9), or ISMN (n = 9). RESULTS: Placebo had no effect. Propranolol significantly reduced variceal volume (-32% +/- 26%; P = 0.01), radius (-12% +/- 9%; P < 0.005), and pressure (-26% +/- 10%; P < 0.0001). The resulting decrease in wall tension (-34% +/- 13%; P < 0.0005) exceeded that in transmural pressure (P < 0.01). ISMN reduced transmural variceal pressure (-26% +/- 21%; P < 0.005), but not radius (-3% +/-14%; NS) and volume (-9% +/- 31%; NS). CONCLUSIONS: The combination of endosonography and endoscopic measurement of transmural variceal pressure allows quantitative estimation of variceal wall tension. Propranolol and ISMN reduce similarly transmural variceal pressure. Propranolol, but not ISMN, reduces variceal volume and radius. Therefore, despite similar decreases in variceal wall tension, propranolol may offer a greater therapeutic effect than ISMN in portal hypertension.

Adrenergic beta-Antagonists↗

Constitutive NOS isoforms account for gastric mucosal NO overproduction in uremic rats.

To study whether renal failure enhances gastric mucosal nitric oxide (NO) formation in the rat, we measured 1) in vivo NO concentration and 2) NO synthase (NOS) activity, content, and mRNA expression in gastric mucosal homogenates of uremic and sham-operated anesthetized rats. Gastric mucosal NO release was measured by an electrochemical technique. NOS content was analyzed by Western immunoblots, using specific monoclonal antibodies. Constitutive (Ca2+ dependent; cNOS) and inducible (Ca2+ independent; iNOS) NOS activities were assayed by following the conversion of L-[U-14C]arginine to [U-14C]citrulline. mRNA expression for the constitutive neuronal (ncNOS), endothelial (ecNOS), and iNOS isoforms was determined by reverse transcription-polymerase chain reaction. Under basal conditions, gastric mucosal NO concentration was significantly greater in uremic compared with control rats. This was accompanied by significantly greater gastric mucosal cNOS activity in uremic rats than in control rats, whereas no differences were observed in iNOS activity between both groups of animals. Moreover, total enzyme content and the levels of gastric mucosal mRNA expression for ncNOS, ecNOS, and iNOS showed no significant differences between uremic and sham-operated rats. These data confirm that, in uremic rats, enhanced Ca2+-dependent NOS activity is responsible for gastric mucosal NO overproduction and suggest that the main regulatory mechanism is not transcriptional but translational and/or posttranslational in nature.

Animals↗

Role of medical conditions in the exacerbation of self-injurious behavior: an exploratory study.

Self-injurious behavior (SIB) is common among people with severe mental retardation who may also have multiple complex medical problems coupled with communication difficulties. This combination of factors sometimes makes it difficult to obtain accurate and detailed medical histories. In this exploratory descriptive study of 25 patients with SIB, 28% had previously undiagnosed medical conditions that could be expected to cause pain or discomfort. Six of the 7 patients experienced decreased SIB with treatment of their medical conditions. In patients with SIB, impaired communication skills, and complex medical histories, medical conditions that may be associated with pain or discomfort must be a consideration in determining the etiology of the SIB.

Adolescent↗

[Effects of percutaneous intrahepatic portosystemic shunt on splanchnic and systemic hemodynamics in patients with portal hypertension].

Transjugular intrahepatic portosystemic shunt (TIPS) is a calibrated shunt directed at reducing the portal pressure gradient with a low incidence of hepatic encephalopathy and deterioration of hepatocellular function. The present study investigated the effects of TIPS on splanchnic and systemic hemodynamics on liver function and on the development of encephalopathy. A group of 30 patients treated with TIPS were included in the study: 26 patients with hepatic cirrhosis for an hemorrhagic episode by esophageal varices not controlled by medical treatment and sclerotherapy and in 4 cases with the Budd-Chiari syndrome for ascites refractory to medical treatment. Before, at 24 hours and 2 months after TIPS, the portal pressure gradient, cardiopulmonary pressure and cardiac output, blood flow of the azygos vein, and hepatic clearance of indocyanine green as indexes of liver function were determined. TIPS significantly decreased the portal pressures gradient and azygos blood flow. This was associated with a significant increase in cardiac output and a significant decrease in peripheral vascular resistance and hepatic clearance of indocyanine green. Portal flow deviated by TIPS was greater in the 9 patients (30%) who developed hepatic encephalopathy during follow up. In conclusion, TIPS effectively reduces portal hypertension. Nonetheless, it is associated with an increase in hyperdynamic circulation, a high incidence of encephalopathy and a deterioration in liver function.

Adolescent↗

[Budd-Chiari syndrome associated with chronic myeloproliferative syndromes: analysis of 6 cases].

The chronic myeloproliferative disorders (CMPD) are considered the main etiology of Budd-Chiari syndrome in Western countries. Moreover, an occult CMPD has been recently identified in most patients with idiopathic hepatic vein thrombosis. In order to determine the frequency of the association between the above entities and to analyze the clinical and hematologic features of such patients, fourteen cases of Budd-Chiari syndrome diagnosed at a single institution over a five year period were reviewed. In 6 patients a CMPD was identified, with this being the first cause of the syndrome. Median age of the later six patients was 32 years (range: 14-54), and 4 were females. In all cases the CMPD was suspected due to the presence of hematological abnormalities, including a high hematocrit (5 cases), leucocytosis (4 cases) and thrombocytosis (3 cases). Five patients had polycythemia vera (PV) and one idiopathic myelofibrosis. In an additional Budd-Chiari patient with polycythemia, PV was ruled out on the basis of high serum erythropoietin and the absence of endogenous growth of erythroid colonies in the hematopoietic progenitor culture. The CMPD treatment included phlebotomies and hydroxiurea, whereas the Budd-Chiari syndrome was treated in most patients with transjugular intrahepatic portosystemic stent-shunt. One patient died from a gastrointestinal hemorrhage at 48 months from Budd-Chiari diagnosis, and the remaining five are alive after a median follow-up of 28 months.

Adolescent↗

[The applicability and diagnostic effectiveness of transjugular liver biopsy].

BACKGROUND: The aim of this study was to evaluate the applicability, the diagnostic profitability and the incidence of complications associated with tranjugular liver biopsy associated with the measurement of the hepatic venous pressure gradient (HVPG). PATIENTS AND METHODS: The clinical histories of 829 consecutive patients in whom transjugular liver biopsy was performed from 1982 to 1993 were reviewed. The diagnostic value of the sample obtained was evaluated in all the patients and the HVPG determined. Moreover, the size of the greatest fragment obtained during biopsy was also determined. RESULTS: Material for histologic study was obtained in 95% of the cases. In 70% the biopsy was diagnostic, in 11% it provided data contributing to diagnosis and in 19% it was not useful. Potentially severe complications were presented in 0.8% of cases being fatal in one (0.1%). The obtention of a fragment of small size was significantly associated with the presence of disease with marked fibrosis and high HVPG. A HVPG > 10 mmHg in patients with a suspicion of liver disease had a sensibility of 92% and a specificity of 63% for the diagnosis of hepatic cirrhosis. In 83% of patients with a GPVH > 10 mmHg in whom the biopsy was not useful, the diagnosis of hepatic cirrhosis was performed by other methods. CONCLUSIONS: Transjugular biopsy in a safe, effective diagnostic method in patients with severe coagulation disorders. The appearance of the material obtained and the HVPG provide useful information for diagnosis although the biopsy is not diagnostic.

Biopsy, Needle↗

Anatomical differences in responsiveness to vasoconstrictors in the mesenteric veins from normal and portal hypertensive rats.

The present study evaluates the effects of pre-hepatic portal hypertension, induced in rats by partial portal vein ligation, on the responsiveness of rostral (proximal) and caudal (distal) rings from the mesenteric vein. The anatomical origin of the sample influenced the response to vasoconstrictors in sham-operated animals, and this pattern of reactivity was specifically modified in portal-ligated rats. In veins from sham-operated rats, contraction induced by a submaximal concentration of KCl (60 mM) was greater in proximal than in distal rings. Vasopressin and 5-hydroxytryptamine contracted mainly distal rings, methoxamine showed a greater effect on proximal rings, and endothelin-1 and angiotensin-II contracted vein rings independently of their anatomical origin. In veins from portal hypertensive rats, response to KCl (60 mM) were increased in distal rings, and all rings exhibited enhanced reactivity to vasopressin and 5-hydroxyptyptamine as well as attenuation of the response to methoxamine. Responses to endothelin-1 were decreased in proximal vein rings from portal hypertensive rats whereas responses to angiotensin-II were not influenced by the anatomical origin. Incubation with atropine, propranolol or indomethacin, did not modify the responses to vasopressin and 5-hydroxytryptamine in tissues from either sham-operated or portal hypertensive animals. Likewise, the hyporeactivity to methoxamine and endothelin-1 in rings from portal hypertensive rats persisted in the presence of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester. These results suggest the physiological existence of anatomical differences in the responsiveness to vasoconstrictors throughout the mesenteric vein and that changes in the responsiveness of the mesenteric vein induced by portal hypertension are specific for each agonist and possibly result from individual variations at a receptor or post-receptor level.

Animals↗

Visually induced gamma-band responses in human electroencephalographic activity--a link to animal studies.

Visual presentation of an object produces firing patterns in cell assemblies representing the features of the object. Based on theoretical considerations and animal experiments, it has been suggested that the binding of neuronal representations of the various features is achieved through synchronization of the oscillatory firing patterns. The present study demonstrates that stimulus-induced gamma-band responses can be recorded non-invasively from human subjects attending to a single moving bar. This finding indicates the synchronization of oscillatory activity in a large group of cortical neurons. Gamma-band responses were not as apparent in the presence of two independently moving stimuli, suggesting that the neuronal activity patterns of different objects are not synchronized. These results open a new paradigm for investigating the mechanisms of feature binding and association building in relation to subjective perception.

Animals↗

Surgical resection of hepatocellular carcinoma in cirrhotic patients: prognostic value of preoperative portal pressure.

BACKGROUND & AIMS: Although resection of hepatocellular carcinoma complicating cirrhosis is restricted to patients with preserved liver function, postoperative hepatic decompensation develops in some patients. The aim of this study was to determine the value of increased portal pressure in the development of postoperative hepatic decompensation. METHODS: Twenty-nine cirrhotic patients with Child-Pugh's class A disease and hepatocellular carcinoma (all except one < 5 cm) scheduled to undergo resection were evaluated by conventional criteria and by a systemic and hepatic hemodynamic study. Predictors of decompensation were assessed among a series of 44 clinical, analytical, tumoral, and hemodynamic parameters. RESULTS: Eleven patients had unresolved decompensation 3 months after surgery. Bilirubin and blood ureic nitrogen levels, platelet count, wedged hepatic venous pressure, hepatic venous pressure gradient, and indocyanine green intrinsic clearance were significantly associated with unresolved decompensation, but only hepatic venous pressure gradient was significant, in the multivariate analysis (P = 0.0001; odds ratio, 1.90; 95% confidence interval, 1.12-3.22). The preoperative gradient of patients with unresolved decompensation was higher than that of patients without it (13.9 +/- 2.4 and 7.4 +/- 3.5 mm Hg, respectively; P < 0.001). CONCLUSIONS: Cirrhotics with increased portal pressure are at high risk of hepatic decompensation after resection of hepatocellular carcinoma. Surgical resection should therefore be restricted to patients without portal hypertension.

Aged↗

Effects of isosorbide-5-mononitrate on variceal pressure and systemic and splanchnic haemodynamics in patients with cirrhosis.

BACKGROUND: Isosorbide-5-mononitrate is a long-acting nitrovasodilator which was introduced for the treatment of portal hypertension because of its capacity to reduce portal pressure. In contrast to vasoconstrictors, isosorbide-5-mononitrate acts primarily by decreasing portal-collateral resistance without deleterious effects on liver function, although at high doses, a reflex splanchnic vasoconstriction elicited by the fall in arterial pressure may further decrease portal pressure. However, there is no information on the effects of isosorbide-5-mononitrate on variceal pressure, which is thought to be a major determinant of variceal haemorrhage. METHODS: We investigated the effects of isosorbide-5-mononitrate (40 mg, orally; n = 12) or placebo (n = 10) on variceal pressure (non-invasive endoscopic gauge) and hepatic haemodynamics in 22 patients with cirrhosis. RESULTS: Placebo administration had no significant effects. In contrast, isosorbide-5-mononitrate significantly reduced variceal pressure (from 13.5 +/- 3.6 to 9.8 +/- 3.2 mmHg, p < 0.005). This was associated with a fall in wedged hepatic venous pressure (from 28 +/- 5.8 to 25.9 +/- 6.2 mmHg, p < 0.005), hepatic venous pressure gradient (from 20 +/- 4 to 18 +/- 4.7 mmHg, p < 0.005) and azygos blood flow (from 668 +/- 197 to 597 +/- 160 ml/min, p < 0.05), suggesting that the decrease in variceal pressure caused by isosorbide-5-mononitrate could be caused by both reductions in collateral resistance and collateral blood flow. Isosorbide-5-mononitrate moderately reduced mean arterial pressure (-13 +/- 16%; p < 0.005), its fall being directly related to the fall in hepatic venous pressure gradient (r = 0.6, p < 0.01). CONCLUSIONS: The results of this study show that isosorbide-5-mononitrate markedly and significantly reduces variceal pressure in patients with cirrhosis and provide further support for its clinical use in the pharmacological treatment of portal hypertension.

Aged↗

Propranolol plus molsidomine vs propranolol alone in the treatment of portal hypertension in patients with cirrhosis.

BACKGROUND/AIMS: Effective protection from the risk of variceal bleeding is achieved when the hepatic venous pressure gradient is reduced to 12 mmHg or at least by 20% of baseline values. Such a marked decrease is rarely achieved with propranolol, and new agents or combinations of them are now being explored. The present randomized study investigated whether chronic treatment with the combination of propranolol plus molsidomine, a preferential venous dialator that reduces hepatic venous pressure gradient and does not cause pharmacological tolerance, achieves greater reduction in hepatic venous pressure gradient than propranolol alone. METHODS: A hemodynamic study was performed in 34 patients with cirrhosis with portal hypertension in baseline conditions and after 3 months of chronic oral treatment with propranolol alone (n = 19) or propranolol plus molsidomine (n = 15). RESULTS: Propranolol produced a significant reduction in hepatic venous pressure gradient (-16%, p < 0.01). Propranolol plus molsidomine also caused a slight but significant decrease in hepatic venous pressure gradient (-9%, p < 0.05). Hepatic blood flow and the hepatic and intrinsic clearance of indocyanine green were significantly reduced by propranolol. The combined administration of propranolol+molsidomine significantly reduced hepatic blood flow but not hepatic and intrinsic clearance of indocyanine green. Both treatment groups produced similar reduction in azygos blood flow, heart rate and cardiac output. However, contrary to propranolol alone, propranolol plus molsidomine did not increase cardiopulmonary pressures. CONCLUSIONS: The current study shows that although the combined administration of propranolol plus molsidomine prevents some of the adverse effects of propranolol on liver function and cardiopulmonary pressures, it does not achieve a greater reduction in hepatic venous pressure gradient than propranolol alone and therefore, does not support the use of this combined therapy for the pharmacological treatment of portal hypertension.

Adult↗

Measurement of variceal pressure with an endoscopic pressure sensitive gauge: validation and effect of propranolol therapy in chronic conditions.

AIM/METHODS: Variceal pressure was measured at endoscopy in 98 patients with a non-invasive, pressure-sensitive gauge technique. RESULTS: In nine patients undergoing sclerotherapy, the values obtained correlated closely with those determined by fine-needle puncture of the varices (r = 0.95, p < 0.001). In 15 patients receiving placebo as part of a double-blind, placebo-controlled prospective evaluation of prophylactic treatment with propranolol, variceal pressure did not change significantly over a 1-year period: 16.5 +/- 3.2 mmHg at onset: 16.7 +/- 3.4 after 3 months and 15.9 +/- 3.5 after 12 months. In contrast, propranolol therapy given to 15 patients decreased the pressure from 16.2 +/- 3.0 mmHg before therapy to 13.5 +/- 2.0 after 3 months (p < 0.001) and to 13.1 +/- 4.1 after 12 months (p < 0.05). Patients with a recent bleeding episode had higher pressures than those who had not yet experienced any haemorrhage (19.3 +/- 3.5 mmHg, n = 17 vs 13.9 +/- 3.3, n = 62) (p < 0.001). This was confirmed in a prospective study: the last variceal pressure in bleeders and non-bleeders was respectively 17.2 +/- 1.7 mmHg (n = 4) and 14.8 +/- 4.1 mmHg (n = 26) (p < 0.01). Overall, variceal pressure measurements correlated with the size of varices, the presence of red colour signs and with the North Italian Endoscopic Club score. CONCLUSIONS: This study has shown that the non-invasive pressure gauge Varipress represents a reproducible method to regularly assess variceal pressure, an important parameter related to the risk of bleeding, and to assess the effects of pharmacological therapy with propranolol.

Adrenergic beta-Antagonists↗

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.

Animals↗