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Biomedical subjects

W G Rector

Publications and source records attributed to W G Rector.

At least 37 records · Page 2Linked to original sources
PubMed1989

Pseudo-Budd-Chiari syndrome: extrinsic deformity of the intrahepatic inferior vena cava mimicking membranous obstruction.

Budd-Chiari syndrome secondary to membranous obstruction of the intrahepatic inferior vena cava is a treatable form of chronic liver disease. I report a patient with portal hypertension in whom distortion of the inferior vena cava by cirrhosis and increased intraabdominal pressure initially suggested this condition. The correct diagnosis was made by obtaining lateral views during inferior vena cavography, which demonstrated a tapered, rather than membranous, obstruction, along with normal hepatic venous anatomy and pressure and markedly increased portal vein pressure during transhepatic puncture with a thin needle. That extrinsic deformity of the inferior vena cava may mimic membranous obstruction has not been emphasized recently. This distinction is important as surgical membranotomy is not indicated in patients with cirrhosis and secondary deformity of the inferior vena cava.

Aged↗
PubMed1988

Intravascular volume in cirrhosis. Reassessment using improved methodology.

Previous studies of blood volume (BV) in cirrhosis have either not adjusted BV properly for body size; determined plasma volume from the dilution of labeled albumin 10-20 min postinjection, when some extravascular redistribution has already occurred; and/or not used the correct whole body-peripheral hematocrit ratio (0.82) in calculating whole BV from plasma volume and the peripheral hematocrit. We measured BV with attention to these considerations in 19 patients with cirrhosis and reexamined the determinants of vascular volume and the relationship between vascular volume and sodium retention. BV was calculated as plasma volume (determined from extrapolated plasma activity of intravenously injected [131I]+albumin at time 0) divided by (peripheral hematocrit X 0.82). The result was expressed per kilogram "dry" body weight, determined by subtracting the mass of ascites (measured by isotope dilution; 1 liter = 1 kg) from the actual body weight of nonedematous patients. Measured and expressed in this way, BV correlated strongly with esophageal variceal size (r = 0.87, P less than 0.05), although not with net portal, right atrial, inferior vena caval, or arterial pressure, and was significantly greater in patients with sodium retention as compared to patients without sodium retention. The principal modifier of vascular volume in cirrhosis is vascular capacity, which is probably mainly determined by the extent of the portasystemic collateral circulation. Increased vascular volume in patients with sodium retention as compared to patients without sodium retention supports the "overflow" theory of ascites formation.

Adult↗
PubMed1988

Pathogenesis of sodium retention complicating cirrhosis: is there room for diminished "effective" arterial blood volume?

We measured total blood volume (125I-albumin), cardiac dimensions and function (echocardiography with Doppler), systemic hemodynamics (blood pressure and pulse), and plasma renin activity and norepinephrine levels in cirrhotic patients with and without ascites to assess the likelihood that either diminished central or arterial filling is the stimulus to sodium retention. Patients with ascites (n = 9) had significantly increased total blood volume, cardiac output, pulse rate, plasma renin activity, and plasma norepinephrine concentration, as well as decreased systemic vascular resistance and arterial blood pressure compared with patients without ascites (n = 8). Left atrial size was similar in the two groups but significantly larger than in normal control subjects. Right and left atrial pressures were also similar in retrospectively studied patients with and without ascites. Sodium retention in cirrhosis is probably not triggered by diminished central filling. Increased blood volume is compatible with either a primary hepatorenal stimulus to sodium retention or a signal arising from a region of underfilling within an otherwise expanded circulation. If the latter model is correct, a "hyperdynamic" systemic circulation and increased plasma neurohormone concentrations may indicate "effective" arterial underfilling in patients with ascites.

Adult↗
PubMed1988

Splanchnic and hepatic renin metabolism in alcoholic cirrhosis. Lack of evidence of a splanchnic source of production or of significantly impaired hepatic clearance.

Cirrhosis is frequently associated with increased arterial plasma renin activity. This could be the result of increased renin production or diminished renin clearance. We measured plasma renin activity in simultaneous portal, hepatic vein, and femoral artery blood samples in 7 patients with clinically stable alcoholic cirrhosis to determine whether hepatic extraction of renin is reduced and whether, as has been suggested, there is a splanchnic source of plasma renin activity in this condition. Plasma renin activity (mean +/- S.E. in ng/ml/min) was similar in portal, arterial, and hepatic venous samples (portal: 8.0 +/- 3.7; arterial: 7.6 +/- 3.1; hepatic vein: 6.4 +/- 2.3). Hepatic extraction of plasma renin activity, calculated as [arterial-hepatic vein)/arterial) X 100, was 14 +/- 6%, not significantly different from reported normal values (26 +/- 3%, n = 46). The intrinsic hepatic clearance of plasma renin activity (235 +/- 89 ml/min) and the hepatic renin extraction rate (1.801 +/- 1.032 micrograms/min) were also similar to estimated normal values. The intrinsic clearance and extraction rates of renin correlated with arterial plasma renin activity (r = 0.93, P less than 0.01 and r = 0.79, P less than 0.05). These data indicate that in clinically stable patients with alcoholic cirrhosis: (1) hepatic renin clearance is not significantly impaired; and (2) there is not a splanchnic source of plasma renin activity. Therefore, increased peripheral plasma renin activity in this condition is due solely to increased renal renin production.

Female↗
PubMed1988

Ascites kinetics in cirrhosis: effects of rapid volume expansion and diuretic administration.

I examined whether the rate of ascites formation in cirrhosis is increased by volume expansion and whether this rate is related to the intensity of renal sodium retention, and I examined the mechanisms by which ascites is mobilized during diuresis. The plasma-ascites filtration rate (PFR) of intravenously injected iodine 125-labeled albumin (the rate of ascites formation by the liver) after volume expansion with normal saline solution in seven patients was similar to that observed in 14 patients who had not received infusions (0.010 +/- 0.003 vs. 0.013 +/- 0.006 L/hr/m2) and was unrelated to natriuresis both before and after intravenous administration of 80 mg furosemide the previous day (r = 0.04 and -0.36). Diuresis of seven patients who had not received infusions reduced PFR (from 0.679 +/- 0.267 to 0.411 +/- 0.198 L/day, P less than 0.05) and total ascites formation rate (from 3.029 +/- 1.620 to 1.465 +/- 1.053 L/day, P less than 0.02) but not plasma volume (from 3.464 +/- 0.646 to 3.391 +/- 0.775 L). Increases occurred in ascites albumin concentration (from 7 +/- 4 to 9 +/- 4 gm/L, P less than 0.05) and in the ascites/serum albumin ratio (from 0.26 +/- 0.12 to 0.35 +/- 0.13, P less than 0.05) but not in the serum-ascites albumin gradient (portal pressure). Fractional changes in ascites volume and albumin concentration were unrelated (r = 0.20). The calculated rate of ascites reabsorption decreased in five patients during diuresis, indicating that ascites was mobilized by decreased formation. Ascites reabsorption increased in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1988

Hepatic inflammation, hepatitis B replication, and cellular immune function in homosexual males with chronic hepatitis B and antibody to human immunodeficiency virus.

We measured serum aspartate transaminase (AST) concentration and serum hepatitis B virus (HBV) DNA concentration in homosexual men with chronic HBV infection and a spectrum of immune deficiency as a result of exposure to human immunodeficiency virus (HIV). Serum AST and HBV DNA concentrations were similar in patients with varying immune function as indicated by in vivo criteria (diagnosis and skin tests reactivity) and in vitro criteria (lymphocyte transformation responses to mitogens and Candida and tetanus antigens) and were unrelated to the number of circulating T cells, suppressor/cytotoxic cells, helper cells, natural killer cells, and the helper:suppressor ratio. Serum AST concentration and indices of cellular immune function were similar in patients with varying HBV replicative activity (high and low HBV DNA concentrations). The observed lack of relationship between serum AST concentration and indices of cellular immune function and HBV replication suggests either that other factors determine the severity of hepatic inflammation in chronic HBV infection, or that currently available tests of cellular immune function and HBV replicative activity do not accurately reflect processes in the liver.

Adult↗
PubMed1988

Delta hepatitis in Denver.

The prevalence of hepatitis D virus (HDV) infection in patients with hepatitis B virus (HBV) infection in the mid-United States is not well defined. We tested 65 patients seen between 1983 and 1986 with HBV infection in Denver for evidence of coexisting HDV infection. Five patients had anti-delta (delta) antibody. The prevalence of HDV infection was higher in patients with chronic hepatitis B (4/37) than in patients with acute hepatitis B (1/28). The prevalence of HDV infection in male homosexuals (3/32) was similar to reported figures, but the incidence of delta-infection in intravenous drug users in Denver was usually low (1/16). In comparison to Los Angeles, New York, southern Italy, and Sweden, Denver appears to have a low incidence of HDV infection, which probably reflects its low prevalence in the drug-using population.

Acute Disease↗
PubMed1987

Urinary prostaglandin E2 excretion, sodium retention, and diuretic responsiveness in patients with chronic liver disease.

It has been postulated that diminished renal prostaglandin E2 (PGE2) production, whether basal or in response to stimulation by diuretic treatment, determines the intensity of sodium retention in cirrhosis. Urinary PGE2 excretion (as an index of renal PGE2 production) as well as urine volume, urinary sodium and potassium excretion, and creatinine clearance were examined in 19 patients with cirrhosis and either no ascites, diuretic-responsive ascites, or diuretic-resistant ascites. Measurements were made both before (all patients) and after (ascitic patients) stimulation of renal PGE2 synthesis by 80 mg of furosemide intravenously. Urinary PGE2 excretion was similar in the three groups both before and after furosemide. Baseline urine volume and creatinine clearance were similar in all groups but were significantly less after furosemide in patients with diuretic-resistant ascites as compared to the other two groups. The natriuretic response to intravenous furosemide was significantly less in patients with diuretic-resistant ascites. Insertion of the peritoneovenous shunt to aid in the management of diuretic-resistant ascites resulted in a marked, immediate increase in urine volume and urinary PGE2 excretion in the four patients who were serially evaluated, but natriuresis occurred in only two. Overall, urinary PGE2 excretion correlated with urine volume but not with sodium excretion or creatinine clearance. Diminished renal PGE2 production, as reflected by urinary PGE2 excretion, does not appear to be a determinant of the severity of renal sodium retention in cirrhosis.

Chronic Disease↗
PubMed1987

Observations on the mechanism and location of ascites reabsorption in man.

Animal data indicate that ascites is reabsorbed by a lymphatic mechanism and that these vessels are subdiaphragmatic in location. We evaluated the relative role of lymphatics in ascites reabsorption in man by comparing the ascites clearance and plasma appearance rates of intraperitoneally injected radiolabeled albumin to those of intraperitoneally injected labeled autologous red blood cells, which require, owing to their large size, lymphatic removal, in patients with cirrhosis and ascites. To evaluate the location of reabsorption, we repeated these measurements after replacing ascites in the subdiaphragmatic region with 500-1000 ml of intraperitoneally injected air, reasoning that this maneuver should slow or eliminate ascites reabsorption occurring at this site. We found that the transfer rates of albumin and red cells out of ascites were similar and that creation of pneumoperitoneum did not influence these rates. These data confirm that ascites protein reabsorption occurs via a lymphatic mechanism in man. They suggest, however, that these vessels may not be subdiaphragmatic in location.

Absorption↗
PubMed1986

Portal hypertension: a permissive factor only in the development of ascites and variceal bleeding.

It is controversial whether the occurrence of ascites and gastrointestinal bleeding in cirrhosis is related to the severity of portal hypertension. Portal pressure was examined in 124 unselected patients with portal hypertension due to chronic liver disease to evaluate this issue. Portal pressure was less in patients without complications of chronic liver disease (11.7 +/- 3.0 mmHg, n = 16) as compared to patients who had bled from varices or erosive gastritis (16.6 +/- 3.4 mmHg, p less than 0.001, n = 49), who had ascites (16.2 +/- 3.0 mmHg, p less than 0.001, n = 78) or both (16.5 +/- 3.0 mmHg, p less than 0.001, n = 19). Portal pressure was similar in patients bleeding from varices and erosive gastritis (16.7 +/- 3.4 mmHg, n = 43; vs 16.2 +/- 4.0 mmHg, n = 6, respectively) and in patients with refractory and nonrefractory ascites (16.2 +/- 3.5, n = 21; vs 16.2 +/- 3.5 mmHg, n = 57). The lowest portal pressure recorded in a patient with variceal bleeding was 9.0 mmHg. The lowest portal pressure recorded in a patient with ascites was 8.0 mmHg. Esophageal varices (graded 0-4 at endoscopy) were larger in patients with a history of bleeding from esophageal varices as compared to patients without such a history (3.2 +/- 0.7 vs 2.0 +/- 0.9, p less than 0.001). Serum albumin concentration was greater in patients without ascites as compared to patients with ascites (33 +/- 5 vs 26 +/- 5 g/l p less than 0.001) but was similar in patients with refractory and nonrefractory ascites (25 +/- 7 vs 26 +/- 5 g/l, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Drug therapy for portal hypertension.

Drugs used to treat portal hypertension cause constriction of mesenteric arterioles, reducing inflow to the portal venous system, portal pressure, and flow through portasystemic collaterals (such as esophageal varices). Vasopressin and somatostatin are direct vasoconstrictors. Propranolol acts by blocking vasodilatory beta 1 receptors and reducing cardiac output. A major side effect of vasopressin therapy is impaired cardiac performance secondary to coronary vasoconstriction and increased work against high arterial pressure. Infusion of vasopressin together with a cardiac inotrope or a vasodilator, and administration of vasopressin as an inactive "hormonogen" which is slowly released in vivo, may lessen adverse effects. Somatostatin appears to act selectively in the mesenteric circulation. Controlled trials indicate that vasopressin may be useful for controlling hemorrhage from esophageal varices and that somatostatin works at least as well as vasopressin. Propranolol treatment has been used to prevent variceal bleeding; however, controlled trials of its effectiveness have produced conflicting results.

Animals↗
PubMed1986

Ascites kinetics in cirrhosis: relationship to plasma-ascites hydrostatic-oncotic balance and intensity of renal sodium retention.

The factors controlling ascites formation and reabsorption, as well as the relationship of ascites dynamics to renal sodium retention complicating cirrhosis, are not defined. We measured, using labeled albumin, the ascites albumin clearance rate, the plasma-ascites and ascites-plasma albumin filtration rates, the ascites albumin exit rate, and the plasma-ascites and ascites-plasma albumin transfer rates in seven patients with cirrhosis and ascites. Wedged hepatic vein pressure (WHVP), right atrial pressure (RAP), ascites pressure (AP), and serum and ascites oncotic pressure (SOP, AOP) were used to calculate the net hydrostatic (WHVP - AP), oncotic (SOP - AOP) and hydrostatic-oncotic pressure, or "transfer" pressure, favoring ascites formation [(WHVP - AP) - (SOP - AOP)], and the net hydrostatic pressure favoring ascites reabsorption (AP - RAP). Over 4 hours: the ascites albumin exit rate greater than the plasma-ascites albumin transfer rate greater than the ascites-plasma albumin transfer rate (P less than 0.05), and the ascites albumin clearance rate greater than the plasma-ascites and ascites-plasma albumin filtration rates (P less than 0.05). The ascites-plasma albumin filtration rate was inversely related to ascites volume (r = 0.91, P less than 0.01). Calculating the ascites-plasma albumin transfer rate from the extrapolated ascites-plasma albumin filtration rate at an ascites volume of 0 (0.031 L/hr/m2) produced values similar to the mean plasma-ascites albumin transfer rate (0.20 + 0.11 gm/hr/m2 vs. 0.24 + 0.13 gm/hr/m2, not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1986

'Diuretic-resistant' ascites. Observations on pathogenesis.

Hepatic sinusoidal hydrostatic-oncotic balance was measured in 25 patients with alcoholic liver disease and varying severity of sodium retention. Eight patients had diuretic-responsive ascites and 17 patients had diuretic-resistant ascites. Net "transfer pressure," the force theoretically favoring fluid transudation across the hepatic sinusoids, was similar in the diuretic-responsive and diuretic-resistant groups and was unrelated to the fractional excretion of sodium after intravenous administration of furosemide. Fractional sodium excretion was significantly less in resistant than in responsive patients, but kaliuresis after furosemide was similar. Baseline creatinine clearance was similar in the two groups, but maximal oral diuretic therapy caused a significantly steeper rise in serum creatinine concentration in resistant than in responsive patients, despite less weight loss. More marked hepatic sinusoidal hydrostatic-oncotic imbalance was not present in patients with diuretic-resistant ascites. Similar kaliuretic response despite reduced natriuretic response to furosemide suggested that the proximal tubule is the site of enhanced sodium resorption in these patients. Renal insufficiency developing during long-term diuretic treatment is an important factor limiting natriuresis in patients with diuretic-resistant ascites.

Ascites↗
PubMed1985

Propranolol for portal hypertension. Evaluation of therapeutic response by direct measurement of portal vein pressure.

Portal vein pressure was measured before and after a week of oral propranolol hydrochloride therapy in 27 patients with alcoholic liver disease. Mean net portal pressure fell (14.5 +/- 3.3 to 12.5 +/- 4.5 mm Hg), but there was wide variation in individual response to the drug. Simultaneous transhepatic portal vein pressure and wedged hepatic vein pressure were similar before and one hour after a single oral dose of 40 mg of propranolol hydrochloride in six additional patients. Arterial, portal, and hepatic vein oxygen content did not change significantly. Propranolol hydrochloride appears not to dissociate portal and wedged hepatic vein pressure or to impair liver oxygenation. Because of variability of response, the portal hypotensive effect of propranolol should be documented before beginning therapy with the drug.

Blood Pressure↗