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T B Reynolds

Publications and source records attributed to T B Reynolds.

At least 109 records · Page 6Linked to original sources
PubMed1969

Effective plasma volume in cirrhosis with ascites. Evidence that a decreased value does not account for renal sodium retention, a sponteneous reduction in glomerular filtration rate (GFR), and a fall in GFR during drug-induced diuresis.

A reduction in effective (nonportal) plasma volume is considered the basis for renal sodium retention, a spontaneous reduction in glomerular filtration rate (GFR), and a fall in GFR occurring during drug-induced diuresis in patients with cirrhosis and ascites. In the present study the concept of a reduced effective plasma volume in cirrhosis is challenged by two lines of evidence, even though effective plasma volume itself could not be measured. (a) Total plasma volume failed to rise in 10 patients with the spontaneous loss of ascites, the appearance of sodium in the urine, and a rise in GFR. Portal pressure remained constant in these patients as ascites left, suggesting that effective plasma volume had not increased while portal plasma volume decreased. (b) Reduction of GFR could not be prevented in five patients with cirrhosis and ascites while total plasma volume was prevented from falling with albumin infusions during drug-induced diuresis. Reduction of GFR during drug-induced diuresis in 15 patients with cirrhosis and ascites was completely reversed with saline infusion despite continued diuresis with the identical drugs, excluding drug nephrotoxicity as the cause for the reduced GFR. The ascites of cirrhosis might no longer be regarded as a cause of effective plasma volume contraction, stimulating renal sodium retention and a reduction in GFR. More likely, this form of ascites is a result of plasma volume expansion and sodium retention. The causes for renal sodium retention and a spontaneous reduction in GFR remain unknown. The cause for a fall in GFR during drug-induced diuresis also remains unknown, but effective plasma volume contraction and drug nephrotoxicity seem excluded.

Alcoholism↗
PubMed1967

Plasma volume in cirrhosis of the liver: its relation of portal hypertension, ascites, and renal failure.

Plasma volume was measured by using albumin-(131)I- and (51)Cr-labeled erythrocytes in 24 control subjects, 140 patients with hepatic cirrhosis, and 10 patients with various portal-systemic shunts for the relief of noncirrhotic portal hypertension. The cirrhotic patients included subgroups with ascites, functional renal failure, and portacaval anastomoses. Elevated values for plasma volume, by both methods, were found in each group of patients.The lymph space drained by the thoracic duct was measured by a radioisotopic technique in six patients with cirrhosis and ascites. The amount of radioactivity in this space was found to be negligible in accounting for the elevated plasma volume. Similar results were obtained when the degree of leakage of albumin-(131)I into the ascites was determined in 10 patients with cirrhosis.The plasma volume was unusually elevated in patients who had bled from esophageal varices, and paired comparisons before and after portacaval shunt normal values. There was a statistically significant correlation between normal values. There was a statistically significant correlation between plasma volume and wedged hepatic venous pressure measured in 36 patients.We concluded that the elevated values for plasma volume in cirrhosis are valid and are not artifacts due to leakage of albumin-(131)I from the circulation during mixing. We also concluded that portal hypertension is responsible for the plasma volume expansion; however, we were unable on this basis to explain the failure of portacaval shunting to return the plasma volume to normal, unless the shunt or some other factor keeps the plasma volume elevated.

Journal Article↗