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C H Sloop

Publications and source records attributed to C H Sloop.

26 records · Page 2Linked to original sources
PubMed1981

Mesenteric lymph apolipoproteins in control and ethinyl estradiol-treated rats: a model for studying apolipoproteins of intestinal origin.

Rat mesenteric lymph contains all serum apolipoproteins. However, it is uncertain whether some of these apolipoproteins are derived from intestinal synthesis or are transferred from plasma. We compared lymph apolipoprotein composition, concentrations, and transport rates in normal rats and in rats treated with pharmacologic doses of ethinyl estradiol which have negligible concentrations of serum lipids and apolipoproteins. Lymph apolipoproteins were examined before and after duodenal lipid infusion. Lymph d less than 1.006 and 1.006-1.21 g/ml lipoproteins were isolated and SDS-electrophoresis was performed using 10 and 3.5% polyacrylamide. During lipid absorption, lymph flow increased in control but not in treated rats. Control lymph contained all major apolipoproteins, but lymph from ethinyl estradiol-treated rats contained only apoB, A-I, and A-IV. Two apoB bands were noted on 3.5% gels in control lymph, but only the lower molecular weight protein was found in lymph from ethinyl estradiol-treated rats. In control rats, transport rates for apoA-I, A-IV, E, and C proteins increased during lipid absorption, but only in the case of A-IV was this a reflection of increased apolipoprotein concentration and not the enhanced lymph flow. In ethinyl estradiol-treated rats only the A-IV transport rate increased due to lipid infusion. It is concluded that in the ethinyl estradiol-treated rat 1) the intestine does not synthesize apoE, C, or the high molecular weight apoB; 2) lymphatic output of A-IV is predominantly increased during lipid absorption; and 3) since plasma apolipoprotein concentrations are negligible, lymph lipoproteins from ethinyl estradiol-treated rats may represent a close approximation to nascent particles of intestinal origin.

Animals↗
PubMed1976

Renin response and angiotensinogen control during graded hemorrhage and shock in the dog.

Hemorrhage and hemorrhagic hypotension have been shown to be potent stimulators of renin release. However, the relationship between angiotensinogen consumption and angiotensinogen production has yet to be completely defined during this type of circulatory stress. Peripheral renin activity increased progressively as the blood pressure was decreased stepwise by hemorrhage to 50 mmHg and remained elevated throughout the shock phase of the experiment. Angiotensinogen did not change from control (809 ng/ml) throughout hemorrhabic hypotension and shock. During hemorrhagic hypotension, with the infusion of the angiotensin antagonist, [1-sarcosine, 8-alanine]angiotensin II, angiotensinogen concentration fell progressively from 693 to 208 ng/ml at 50 mmHg. Intravenous angiotensin II infused continuously after the mean blood pressure reached 50 mmHg significantly elevated plasma angiotensinogen concentration. In conclusion, during hemorrhagic hypotension and shock, the kidney and the liver appeared capable of maintaining elevated plasma renin activity and adequate plasma renin substrate, angiotensinogen, respectively. The mechanism responsible for the maintenance of plasma angiotensinogen is suggested to involve a positive-feedback effect of angiotensin II on the liver.

Angiotensin II↗
PubMedDate not supplied

Lipoprotein lipase and hepatic triacylglycerol lipase activities in peripheral and skeletal muscle lymph.

We studied the interstitial fluid concentration of two lipid-metabolizing enzymes (lipoprotein lipase and hepatic triacylglycerol lipase) to determine their importance in interstitial modification of filtered lipoproteins. Despite the use of a very sensitive lipase assay (1 nmol of fatty acid release/ml/hr), lipase activities in plasma and in peripheral and skeletal muscle lymph from control dogs were below the sensitivity of our assay. After heparin injection, hepatic triacylglycerol lipase and lipoprotein lipase activities in plasma were similar. However, the postheparin hepatic triacylglycerol lipase activities in peripheral and skeletal muscle lymph were only 1.4% and 1.1%, respectively, those of plasma. This concentration is considerably less than the lymph concentration of albumin, which has a similar size to the lipases but has a lymph concentration of 30% to 40% of plasma. Lipoprotein lipase activity in peripheral lymph and skeletal muscle lymph was 2.7% and 4.8%, respectively, of plasma activity. Since lipoprotein lipase has a similar size as hepatic triacylglycerol lipase, the disproportionate amount of lipoprotein lipase in lymph as compared to hepatic triacylglycerol lipase could be due to heparin crossing the capillary endothelium and displacing lipoprotein lipase from peripheral cells. Injection of radioactive heparin confirmed that it does cross into the interstitial space in sufficient concentrations to displace lipase from peripheral cells. We conclude that most of the lipase found in lymph after heparin injection is derived from peripheral cells and not from plasma. Furthermore, hepatic triacylglycerol lipase does not play a role in high density lipoprotein remodeling in interstitial fluid. Therefore, it seems likely that the considerable remodeling of high density lipoprotein that we found previously results from its interaction with peripheral cells.

Animals↗