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Biomedical subjects

M Hartleb

Publications and source records attributed to M Hartleb.

At least 37 records · Page 2Linked to original sources
PubMed1996

Role of sympathetic cardiovascular tone in control of arterial pressure in rats with cirrhosis.

Although an increase in sympathetic nervous activity has been recognized in cirrhosis, the contribution of this overactivity to the regulation of arterial pressure is unknown. The arterial pressure response to increasing doses of hexamethonium (0.05 to 3.2 mg.kg-1.min-1), a ganglionic blocker that decreases sympathetic cardiovascular tone, was explored in normal rats and in two models of portal hypertension, i.e., rats with cirrhosis and rats with portal vein stenosis. Changes in plasma norepinephrine concentrations were greater in rats with cirrhosis (356 +/- 50 vs 166 +/- 30 pg/ml, p = 0.04) than in normal rats (186 +/- 23 vs 86 +/- 31 pg/ml, p = 0.06) and rats with portal vein stenosis (103 +/- 37 vs 93 +/- 5 pg/ml, p = 0.10). The maximum decrease in arterial pressure was obtained at a dose of 1.6 mg.kg-1.min-1 in each group. However, the decrease in arterial pressure was significantly greater in rats with cirrhosis (-25 +/- 2%) than in normal rats (-11 +/- 1%) and in rats with portal vein stenosis (-13 +/- 2%) (p = 0.04). In conclusion, the results of this study suggest that the sympathetic cardiovascular tone is more important for the maintenance of arterial pressure in rats with cirrhosis than in normal rats and in rats with portal vein stenosis.

Animals↗
PubMed1995

Effect of propranolol on portosystemic collateral circulation estimated by per-rectal portal scintigraphy with technetium-99m pertechnetate.

BACKGROUND/AIMS: Propranolol is widely used in the prevention of variceal bleeding. However, in certain patients with cirrhosis, the portal hypotensive effect of propranolol cannot be obtained. An explanation for portal unresponsiveness to propranolol could be an increase in portocollateral vascular resistance mediated by this drug. METHODS: In 33 patients with cirrhosis the effect of chronic administration of propranolol on portocollateral blood flow from the inferior mesenteric vein was examined by means of per-rectal portal Tc-99m pertechnetate scintigraphy. RESULTS: Propranolol significantly reduced the shunt index by 15.3 +/- 4.2%. This reduction was observed only in patients with cirrhosis classified as Child-Pugh A and B groups, but not group C. Differences between groups in portosystemic shunt index changes after propranolol were significant (F = 3.4, p < 0.05). CONCLUSIONS: The data presented suggest that propranolol changes the distribution of blood between the portal and systemic circulation, which is probably due to the increase in vascular resistance of portocollateral vessels. The magnitude of the vascular response to propranolol depends on the severity of liver disease.

Adolescent↗
PubMed1995

Lack of vascular hyporesponsiveness to the L-type calcium channel activator, Bay K 8644, in rats with cirrhosis.

BACKGROUND/AIMS: In cirrhosis, the mechanism(s) for vascular hyporesponsiveness to vasoconstrictors such as, alpha 1-adrenoceptor agonists, vasopressin and angiotensin II, are unclear. Moreover, vascular reactivity to substances such as L-type calcium channel activators is unknown. METHODS: Thus, pressor dose-response curves to vasoconstrictors [phenylephrine (an alpha 1-agonist, 0.1-500 micrograms/kg) angiotensin II (10-500 ng/kg), vasopressin (0.01-5 IU/kg), and Bay K 8644 (an L-type calcium channel activator, 0.5-50 micrograms/kg)] were obtained in normal rats and in rats with secondary biliary cirrhosis. All experiments were performed in ganglionic-blocked animals to limit the influence of cardiovascular reflexes. Doses of vasoconstrictor necessary to obtain a 40 mmHg increase in arterial pressure (D40) were calculated. RESULTS: Compared to normal animals, rats with cirrhosis had significantly higher D40 values for angiotensin II (171 +/- 57 vs. 344 +/- 41 ng/kg), phenylephrine (2.6 +/- 0.2 vs. 26.4 +/- 10.7 micrograms/kg) and vasopressin (73 +/- 19 vs. 401 +/- 150 mU/kg). Pressor responses to Bay K 8644 did not differ between normal rats and rats with cirrhosis (8.8 +/- 0.9 vs. 10.5 +/- 2.1 micrograms/kg). CONCLUSIONS: In conclusion, this study shows that cirrhosis produces vascular hyporeactivity to phenylephrine, vasopressin and angiotensin II but not to Bay K 8644. Therefore, cirrhosis impairs certain constrictor mechanisms which are shared by phenylephrine, angiotensin II and vasopressin but which do not contribute to the vascular response to Bay K 8644.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Polyerga, a biological response modifier enhancing T-lymphocyte-dependent responses.

Cancer patients are often treated with biological response modifiers to enhance immunological functions. However, little is known about the actual mechanism of action of many of these substances. Therefore, we were interested in the effect of i.p. treatment with porcine low-molecular-weight spleen peptides, which are used during supportive cancer therapy, on lymphoid cell populations and function in mice. After treatment with 0.5 microgram peptides/kg body weight for 14 consecutive days, lymphokine secretion and the generation of cytotoxic T-cells were significantly enhanced as compared with controls. However, there was no effect on the number of cells or the percentage of cells expressing functional surface markers in secondary lymphoid organs.

Animals↗
PubMed1994

Vascular hyporesponsiveness to endothelin 1 in rats with cirrhosis.

BACKGROUND/AIMS: Because the vasodilator nitric oxide is overproduced in cirrhosis, this substance may decrease pressor responses to the vasoconstrictor endothelin 1. This study aimed to examine the effects of a NO synthesis inhibitor (NG-nitro-L-arginine methyl ester; L-NAME) on vascular responsiveness to endothelin 1 in normal and cirrhotic rats. METHODS: Pressor dose-response curves to endothelin 1 (0.5, 1, 3, 6, and 10 micrograms/kg intravenously) were obtained in animals with or without pretreatment with L-NAME. RESULTS: Pressor responses to endothelin 1 alone were significantly lower in cirrhotic than in normal rats. In cirrhotic animals, pressor responses to 3, 6, and 10 micrograms/kg of endothelin 1 were significantly higher in the presence than in the absence of L-NAME. The responses to the other doses of endothelin 1 were not affected by L-NAME. In normal rats, pressor responses to all doses of endothelin 1 were significantly higher in the presence than in the absence of L-NAME. In animals pretreated with L-NAME, pressor responses to 6 and 10 micrograms/kg of endothelin 1 did not differ between cirrhotic and normal rats, whereas responses to other doses remained lower in cirrhotic than in normal rats. CONCLUSIONS: In rats with cirrhosis, NO seems to contribute to vascular hyporeactivity to high doses but not to low doses of endothelin 1.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Blunted systemic, splanchnic, and renal hemodynamic responses to atrial natriuretic peptide in rats with cirrhosis.

Systemic, splanchnic and renal hemodynamic responses to saline, physiological (25 ng.kg-1.min-1) and pharmacological (100, 300 and 600 ng.kg-1.min-1) doses of alpha human atrial natriuretic peptide were measured in normal (n = 7 for saline and 7-8 for each dose of atrial natriuretic peptide) and cirrhotic (n = 7 for saline and 7-8 for each dose of atrial natriuretic peptide), conscious, unrestrained rats. In addition, plasma norepinephrine concentrations were measured in normal and cirrhotic rats, before and following a 300-ng.kg-1.min-1 dose of atrial natriuretic peptide. In cirrhotic rats, splanchnic, renal and systemic hemodynamics were not significantly affected by either physiological or pharmacological doses of atrial natriuretic peptide. In normal rats, a 300 ng.kg-1.min-1 dose of atrial natriuretic peptide significantly decreased cardiac index, portal tributary blood flow and renal blood flow, and significantly increased vascular resistance in the systemic, portal, and renal territories. The other doses of atrial natriuretic peptide did not significantly change regional and systemic hemodynamics. Atrial natriuretic peptide-induced changes in plasma norepinephrine concentrations were significantly higher in normal than in cirrhotic rats (1827 +/- 834 vs. 59 +/- 46 pg/ml, mean +/- S.E., respectively). In conclusion, this study shows that the normal cardiovascular response to a 300 ng.kg-1.min-1 atrial natriuretic peptide infusion is blunted in cirrhotic rats. Moreover, in cirrhotic rats, blunting of vasoconstriction following atrial natriuretic peptide administration seems to be due to a lack of increased sympathetic vascular tone.

Animals↗
PubMed1994

[Relationships between plasma concentrations of endothelin and the severity of liver cirrhosis].

OBJECTIVES: Results of studies on plasma endothelin concentrations in patients with cirrhosis are conflicting. Moreover, the relationships between plasma endothelin concentrations and the severity of cirrhosis have not yet been studied. The aim of this study was to measure plasma endothelin concentrations in controls and in patients with cirrhosis. In addition, this study examined the relationships between plasma endothelin concentrations, and the severity of liver disease, splanchnic and systemic hemodynamics. METHODS: Plasma endothelin concentrations (in the hepatic vein and the right atria), hepatic venous pressures, arterial pressure, cardiac output, pulmonary pressures and plasma concentrations of sodium and creatinine were measured in 7 controls and 28 patients with cirrhosis. RESULTS: Plasma endothelin concentrations in the hepatic vein and the right atria were significantly higher in patients with cirrhosis (18.9 +/- 2.9 and 20.2 +/- 3.1 pg/mL, respectively) than in controls (6.1 +/- 1.1 and 7.2 +/- 1.1 pg/mL, respectively). In these patients, hepatic venous plasma endothelin concentrations were significantly correlated with Pugh's score (r = 0.49), hepatic venous pressure gradient (r = -0.44), and plasma sodium concentrations (r = -0.46). No significant correlation was found between plasma endothelin concentrations and systemic hemodynamics. CONCLUSION: Plasma endothelin concentrations are increased in patients with cirrhosis. Moreover, this increase is more marked in patients with severe liver disease than in patients with no or moderate impairment of liver function.

Blood Chemical Analysis↗
PubMed1994

[Does hyperthyroidism promote drug hepatotoxicity].

Mechanisms and circumstances in which drugs injure hepatocytes are not clear. It is known that thyroid gland hormones sensitize the liver to hepatic toxins, but not to commonly used drugs. We report two cases of liver injury mediated by acetaminophen and oestrogens which occurred during hepatic exposure to increased plasma level of thyroid hormones. We suggest that hyperthyroidism might promote drug hepatotoxicity.

Acetaminophen↗
PubMed1994

[Cystic hepatic malignant tumors].

Non-parasitic hepatic cysts are common finding at abdominal sonography and in vast majority they are benign lesions. We report two cases of cystic liver neoplasms, namely the biliary cystadenocarcinoma and malignant hemangioendothelioma. In both cases, despite slow development of the tumour the presence of cyst considerably delayed diagnosis and hindered surgical treatment. We believe that more aggressive approach in "atypical" hepatic cysts could improve prognosis in such cases.

Adult↗
PubMed1994

[Per-rectal scintigraphy of the portal system with pertechnetate TC-99M: effect of propranolol on portosystemic collateral circulation in patients with cirrhosis. Part II].

Propranolol can reduce portal hypertension, therefore is recommended in prevention of variceal bleeding in patients with liver cirrhosis. However, in certain patients with cirrhosis portal hypotensive effect of propranolol cannot be obtained, and the reason of this finding is unknown. In 28 patients with cirrhosis the effect of seven days administration of propranolol on collateral blood flow from inferior mesenteric vein was examined by means of per-rectal portal scintigraphy. Portosystemic shunt index was significantly reduced by propranolol by 17.4 +/- 4.8%. This reduction was observed in cirrhotics classified to A and B, but not C Child-Pugh. These data suggest that propranolol increases vascular resistance in portosystemic circulation which depends on severity of liver failure. This mechanism opposes reduction of portal pressure.

Adult↗
PubMed1994

[Per-rectal scintigraphy of the portal system with pertechnetate TC-99M: clinically useful examination of patients with chronic liver disease.Part I].

Per-rectal portal scintigraphy with Tc-99m pertechnetate is a method to evaluate portosystemic shunting (shunt index) in inferior mesenteric vein. In this study the shunt index was estimated in patients with chronic liver disease in relation to the severity of liver injury, portal hypertension and incidence of oesophageal varices. Shunt index was elevated in patients with non-cirrhotic liver disease as compared with healthy normals (34 +/- 6% vs 8 +/- 2%; p < 0.0005). Moreover, patients with cirrhosis had the shunt index of 65 +/- 4% which was higher than in other groups. There was no correlation of the shunt index to the Child-Pugh classification, hepatic venous pressure gradient and varices size in the cirrhotic patients. Conversely, the shunt index differentiated variceal bleeders from non-bleeders (80 +/- 4% vx 59 +/- 6%; p < 0.005). These data show that peripheral collateral circulation develop in response to mild elevation of portal pressure, but its hemodynamic efficacy to alleviate portal hypertension seems to be unremarkable. High shunt index might reflect elevated risk of bleeding from varices.

Adult↗
PubMed1994

[Peak fibrinogen level as a prognostic indicator in acute biliary pancreatitis].

Early prediction of acute pancreatitis outcome is based on clinical classifications, but their complexity is limiting factor. The aim of this study was prospective, dynamic evaluation of plasma fibrinogen (Fb) concentration in acute pancreatitis and testing preselected, single Fb value as predictor of pancreatic and systemic complications. Serial measurement of Fb was done in 64 patients with acute biliary pancreatitis. Peak concentration of Fb was 5.93 +/- 1.08 g/L and was found 5-8 days following onset of the disease. The peak concentration differentiated patients with mild and complicated course of pancreatitis (5.68 +/- 1.00 g/L vs 6.31 +/- 1.10 g/L; p < 0.05), with the 67% sensitivity and 72% specificity. Similarly, Ranson's score distinguished mild from complicated form of pancreatitis (1.7 +/- 1.1 vs 2.6 +/- 1.3 points; p < 0.01), with the 58% sensitivity and 73% specificity. These data indicate that peak Fb concentration is useful as a single prognostic factor in acute biliary pancreatitis.

Acute Disease↗
PubMed1994

Portal shunting in inferior mesenteric vein in cirrhosis: correlation with hemorrhage from esophageal varices.

OBJECTIVE: Certain patients with portal hypertension develop large esophageal varices, whereas others have small varices, or none. Our objective in this study was to determine whether this variability depends upon the amount of blood derived by peripheral portosystemic collaterals. METHODS: Esophagogastroscopy to determine presence and size of esophageal varices, and pre-rectal portal scintigraphy to assess portosystemic shunt index (PSI) in inferior mesenteric vein were performed in 45 cirrhotics and 17 patients with pre-cirrhotic liver disease. RESULTS: Patients with cirrhosis had higher PSI than normal controls (67 +/- 4 vs. 8 +/- 2%; p < 0.0001) and pre-cirrhotic patients (vs. 34 +/- 6%; p < 0.0001). Neither variceal size nor PSI was correlated with Child-Pugh classification or hepatic venous pressure gradient. PSI was not related to the presence of varices or their size. On the other hand, patients with variceal hemorrhage had elevated PSI, compared with non-bleeders (80 +/- 4% vs. 59 +/- 6%; p < 0.005). CONCLUSIONS: This study shows that portosystemic collaterals in the inferior mesenteric vein do not prevent the formation of large varices. Furthermore, the magnitude of blood flow through peripheral collaterals might reflect the risk of variceal hemorrhage.

Adult↗
PubMed1993

[Isotope methods in diagnosis of portal vein occlusion].

The dynamic intravenous hepato-scintigraphy with pertechnetate Tc-99m enables a quantitative evaluation of portal and arterial blood flow in the liver. A case is presented of thrombotic occlusion of the portal vein with rapidly growing oesophageal varices in which hepato-scintigraphy showed the absence of portal blood flow in the liver, being the decisive diagnostic method. Using the dynamic transrectal porto-scintigraphy an evaluation was done of the degree of collateral circulation development in the area of the inferior mesenteric vein, obtaining indirect information about localization and duration of portal vein occlusion.

Adult↗
PubMed1993

[Focal nodular hyperplasia of the liver in doppler sonography--case report].

Current diagnostic capabilities of Doppler sonography in solid focal lesions were presented. Diagnostic difficulties were discussed in the case of focal liver lesion, wherein the diagnosis was not reached by sonography backed up by pulsed and color Doppler. The patient was submitted to surgical treatment. A histological specimen disclosed focal nodular hyperplasia. The analysis of the case in question proved that sonography even combined with Doppler method cannot differentiate between hepatocellular carcinoma and focal nodular hyperplasia.

Adult↗