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Biomedical subjects

E Sikuler

Publications and source records attributed to E Sikuler.

62 records · Page 4Linked to original sources
PubMed1986

Interaction of flow and resistance in maintenance of portal hypertension in a rat model.

To clarify the roles that portocollateral resistance ("backward-flow" theory) and portal flow ("forward-flow" theory) play in maintaining chronic portal hypertension, we studied, in a rat model with prehepatic portal hypertension, the hemodynamic changes that occur when portocollateral resistance is reduced and high portal venous inflow is maintained. In 30 portal-hypertensive rats the constriction around the portal vein was removed 4 days after induction of portal hypertension, 30 rats were used as portal vein-constricted controls, and 30 additional rats were subjected to a sham operation. The removal of the ligature constricting the portal vein was followed by an immediate decrease in portal pressure (from 16.3 +/- 0.8 to 9.6 +/- 0.8 mmHg, P less than 0.001). Two days after the ligature removal, hyperdynamic circulation was still evident and was characterized by a decreased splanchnic arteriolar resistance and an increased portal venous inflow. The coexistence of high portal venous inflow and normal portal pressure indicates that high portal venous inflow per se is not sufficient to produce an increase in portal pressure when it faces a low-resistance vascular bed. We conclude that portal hypertension is induced by the interaction of an abnormally high portal venous inflow and high resistance offered to the flow by the portocollateral vessels. Neither the forward-flow theory nor the backward-flow theory can be applied solely to explain the increased portal pressure.

Animals↗
PubMed1985

Hemodynamic studies in a parabiotic model of portal hypertension.

Splanchnic and systemic hemodynamic studies were performed in a rat model of parabiosis and portal hypertension. A portal hypertensive and a normal rat were surgically united side to side. A hyperdynamic circulation, characterized by increased cardiac index (413 +/- 26 vs 318 +/- 23 ml X min-1 X kg-1; p less than 0.05) and portal venous inflow (9.61 +/- 1.29 vs 6.33 +/- 0.36 ml X min-1 X 100 g b.wt-1; p less than 0.05), was found in all the portal hypertensive rats but not in the normal parabiotic partners. These results do not support the existence of a transferable humoral factor mediating the hyperdynamic circulatory state of chronic portal hypertension.

Animals↗
PubMed1985

Evolution of portal hypertension and mechanisms involved in its maintenance in a rat model.

In rats with portal hypertension induced by partial ligation of the portal vein, we have recently demonstrated an increased portal venous inflow that becomes an important factor in the maintenance of portal hypertension. The sequence of events that leads into this circulatory disarray is unknown. We evaluated chronologically the chain of hemodynamic changes that occurred after portal hypertension was induced by partial ligation of the portal vein. In this model it is possible to follow, from the initiation of the portal-hypertensive state, the interaction between blood flow and resistance in the portal system as well as the relation between the development of portal-systemic shunting and the elevated portal venous inflow. The study was performed in 45 portal-hypertensive rats and in 29 sham-operated rats. Blood flow and portal-systemic shunting were measured by radioactive microsphere techniques. The constriction of the portal vein was immediately followed by a resistance-induced portal hypertension characterized by increased portal resistance (9.78 +/- 0.89 vs. 4.18 +/- 0.71 dyn X s X cm-5 X 10(4), mean +/- SE, P less than 0.01), increased portal pressure (17.7 +/- 0.9 vs. 9.5 +/- 0.6 mmHg, P less than 0.001), and decreased portal venous inflow (3.93 +/- 0.26 vs. 6.82 +/- 0.49 ml X min-1 X 100 g body wt-1, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Detection and persistence of specific IgA antibodies in serum of patients with hepatitis A by capture radioimmunoassay.

The serum immunoglobulin A (IgA) response to hepatitis A virus (HAV) was investigated with a sensitive capture radioimmunoassay. In serial serum samples drawn from 15 patients with viral hepatitis A, IgA anti-HAV antibodies reached their highest titer between 1-2 weeks after onset and peak titers ranged from 10,000-20,000. Serum samples were available from six patients 30-32 months after onset of illness. These samples were all positive for IgA anti-HAV and some had titers similar to peak titers during illness. However, the height of the titration curves, expressed as the binding ratio (BR) at a dilution of 1/1000, was in all cases significantly lower at 30-32 months than during acute illness and early convalescence. The significance of the persistence of the IgA anti-HAV and possible reasons for the change in the BR are discussed.

Antibodies, Viral↗
PubMed1978

Hepatitis B antigen and antibody among staff members of an Israeli hospital and a kibbutz population.

Until recently, hepatitis type B was thought to be transmitted parenterally. However, much evidence has appeared regarding non-parenteral transmission. Hospital personnel are exposed both ways to this disease. We compared the incidence of hepatitis B surface antigen (HBsAg) and antibody (anti-HBs) among 388 workers at a major medical center in Israel with 203 kibbutz residents, using radioimmunoassay procedures. Of the hospital personnel, 1.8% were found to carry the antigen and 23.9% the antibody. In contrast, 0.5% of kibbutz personnel were antigen-positive and 11.8% carried the antibody. The highest incidence of antibody was found among people born in middle-eastern countries outside of Israel. These results show a significant increase in the exposure of hospital personnel to hepatitis B virus. A marked increase in the frequency of sera positive for anti-HBs occurred after the first year of hospital work.

Age Factors↗
PubMedDate not supplied

Hemodynamic studies in long- and short-term portal hypertensive rats: the relation to systemic glucagon levels.

It is not known whether the hyperdynamic state which has been observed in several experimental models and in patients with portal hypertension reflects a temporary phase during the evolution of the portal hypertensive syndrome or is an expression of a permanent steady state. A hemodynamic study was performed in a group of rats with long-standing portal hypertension induced by portal vein constriction performed 6.2 +/- 0.1 months earlier. A group of rats matched by age and weight with short-term (20.7 +/- 0.9 days) portal hypertension and a group of long-term (6.2 +/- 0.1 months) sham-operated rats were used as controls. Cardiac output and regional blood flows were measured using a radioactive microsphere technique. Arterial blood levels of glucagon, a known vasodilator that was implicated in the etiology of the hyperdynamic circulation, were also measured. Portal pressure in long- and short-term portal hypertensive groups (12.3 +/- 0.4 and 13.7 +/- 0.4 mm Hg; not statistically significant) was higher than in the sham group (9.0 +/- 0.3 mm Hg; p less than 0.01). Cardiac output in the long-term portal hypertensive rats was similar to the sham-operated group and lower than in the short-term portal hypertensive group (19.4 +/- 1.0 and 20.6 +/- 1.5 vs. 32.7 +/- 2.0 ml X min-1 X 100 gm body weight-1; p less than 0.01). Portal venous inflow in the long-term portal hypertensive group was also similar to the sham group and lower than in the short-term portal hypertensive group (4.51 +/- 0.36 and 4.58 +/- 0.39 vs. 6.72 +/- 0.48 ml X min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Prevalence of specific IgA and IgM anti-HBc antibodies compared with HBV DNA in the sera of HBsAg chronic carriers.

OBJECTIVE: We evaluated the significance of IgA antibodies directed against the hepatitis B virus core antigen (IgA anti-HBc) as a marker for viral replication. STUDY DESIGN/METHODS: Serum samples of 143 hepatitis B surface antigen (HBsAg) carriers and 189 HBsAg-negative subjects were studied. Hepatitis B virus (HBV) DNA was detected by polymerase chain reaction. IgA anti-HBc was determined by a capture enzyme-linked immunosorbent assay developed in our laboratory. The results were compared with those for IgM anti-HBc, which were determined by a commercially available method. RESULTS: IgA anti-HBc was detected in 57 (40%) and HBV DNA in 38 (27%) of the HBsAg carriers. Among the HBsAg-negative subjects, IgA anti-HBc and HBV DNA were detected simultaneously in four samples. All 42 HBV DNA-positive samples were IgA anti-HBc positive. IgM anti-HBc was detected in 27 (64%) of them. CONCLUSIONS: IgA anti-HBc is a sensitive marker for HBV replication, and its absence may exclude HBV replication. The role of IgA anti-HBc in monitoring response to therapy and predicting clinical course is being evaluated.

Biomarkers↗