1. The effect of cross-circulation on hepatic encephalopathy (evaluated by electroencephalography; EEG) induced by hepatectomy in the rat was examined.2. Systemiosystemic cross-circulation induced improvement of the altered EEG in only two out of seven liverless rats when the exchange-flow rate was 6.4 ml min-' kg body wt.-', and in all seven liverless rats when the exchange-flow rate was 14.0 ml min-kg body wt.-; the difference is statistically significant (P = 0.01 1). Systemioportal cross-circulation (systemic blood from the liverless rat beinginfused into the portal vein of the normal rat) induced improvement of the altered EEG in all seven liverless rats although the exchange-flow rate was only 6.4 ml min-' kg body wt.-' 4. It is concluded (a) that a certain level of exchange-flow rate is required for cross-circulation to be efficient, and (b) that, for the same exchange-flow rate, systemio portal cross-circulation is more efficient than systemiosystemic cross-circulation.
1. The present work was carried out to compare the electroencephalographic changes in liverless rats and eviscerated rats and to determine whether substances released from the intestine, in particular ammonia, play a major part in the mechanism of hepatic encephalopathy.2. The animals were prepared according to a three-stage procedure: ligation of inferior vena cava; 3 weeks later, end-to-side portacaval shunt ; 2 days later, removal of the liver (liverless rats) or removal of the liver, spleen, stomach, intestine and pancreas (eviscerated rats).3. In liverless rats, the electroencephalographic changes began 4-8 h after hepatectomy with a predominance of 'slow' sleep pattern followed by increasing changes, which consisted successively of (a) alteration of, then disappearance of, spindles of high-voltage waves; (b) predominance of slow waves; (c) depression in voltage and finally flat tracing. The mean duration of survival was 18.4 h. Mean plasma ammonia concentration 15 h after hepatectomy was 353 ymolll.4. In eviscerated rats, the electroencephalographic changes were similar. The mean duration of survival was 21-3 h, which is not statistically different from that of liverless rats. Mean plasma ammonia concentration 15 h after evisceration was 148 pmolll, a value significantly lower than that of liverless rats.5. These results suggest that ammonia, and substances released from the intestine in general, play no part or at most a minor role in the mechanism of hepatic encephalopathy of the liverless rat. F 599 SVEDBERG, A., MADDOCK, S. & DRURY, D.D. (1938) The effect of total removal of the liver in the rabbit.
Oestrogen stimulation of plasma renin substrate (PRS) was studied in men with alcoholic cirrhosis. PRS values, before and 1, 2, 4 and 6 days after a single oral administration of 100 microgram of an oestrogen derivative, 11beta-methoxy-17-ethynyl-1,3,5(10)-estratriene-3,17beta-diol (Moxestrol), were measured by radioimmunoassay of generated angiotensin I in five men with normal liver function and five men with alcoholic cirrhosis. Basal PRS was 0.93 +/- 0.22 nmol/ml (mean +/- 1 SD) in the normal men and significantly lower (P less than 0.01) in the men with cirrhosis (0.33 +/- 0.14 nmol/ml). Two days after administration of Moxestrol, PRS rose significantly but transiently (P less than 0.05) to 1.41 +/- 0.42 nmol/ml in the normal men and to 0.47 +/- 0.15 in the cirrhotic men, the relative increase (approximately 50%) being similar in both groups. A study of the plasma kinetics and urinary excretion of Moxestrol was also performed to evaluate its metabolic clearance rate and absorption. Since the intestinal absorption of [14C] Moxestrol was not depressed in cirrhotic men, the low PRS values recorded are probably the consequence of hepatocyte dysfunction.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.