In conscious pigs, arteriovenous anastomoses (AVAs) are in a constricted state so that < 5% of intra-atrially injected radioactive (15-microns-diam) microspheres are shunted to the lungs. Many of the anesthetic regimens frequently used in cardiovascular research dilate AVAs, thereby greatly increasing the percentage of microspheres reaching the lungs. This may seriously limit extrapolation of results obtained under anesthesia to the conscious state. We now describe that anesthesia with a combination of fentanyl and thiopental preserves the tone of AVAs, maintaining shunting under 4% of cardiac output. Furthermore, we studied in the carotid circulation of this model whether norepinephrine or 5-hydroxy-tryptamine (5-HT), both contained in perivascular nerves, is responsible for this tone. Consecutive antagonism of alpha 1-, alpha 2-, 5-HT1, and 5-HT2 receptors was obtained by sequential injection of prazosin, phentolamine, ketanserin, and methiothepin. Prazosin increased AVA blood flow, partly at the expense of extracerebral tissue blood flow, but preserved cerebral blood flow. None of the other antagonists had any additional significant effect. Therefore, in this model the tone in AVAs seems to be maintained by sympathetic norepinephrine-containing nerves via alpha 1-adrenoceptors.
No abstract
Previous studies have shown that lidocaine has a negative inotropic effect on the myocardium. This effect could be mediated by a decrease in O2 supply and/or utilization, or abnormalities in intracellular Ca2+ handling by the myocardium. To investigate which of these mechanisms are involved we studied nine open-chest anaesthetized pigs, which received an infusion of lidocaine (4-16 mg.min-1) in the left anterior descending coronary artery (LADCA), sufficient to induce a severe depression of the regional myocardial function. Biopsies for high energy phosphate levels were obtained from both the LADCA and control regions before and during the infusion. After measurements at peak lidocaine dose, the hearts were rapidly excised for harvesting of LADCA, and control region sarcoplasmic reticulum (SR) vesicles for in vitro measurements of Ca2+ uptake rate. During lidocaine infusion, coronary blood flow increased (23%), while ATP, Ca2+ uptake by the SR and percentage segment length shortening decreased by 20%, 19% and 30% respectively. However, O2 consumption in the LADCA region did not differ before or during lidocaine infusion (102 +/- 20 and 104 +/- 29 ml.min-1, respectively). Hence, lidocaine in doses sufficient to depress regional myocardial function does not decrease O2 supply, but decreases the efficiency of oxygen utilization. Although we cannot entirely rule out the possibility that blockade of fast sodium channels is a contributory factor, the observed decrease in the tissue level of ATP and the rate of Ca2+ uptake by the SR may be related to the negative inotropic action of lidocaine.(ABSTRACT TRUNCATED AT 250 WORDS)
In 35 pigs atherosclerosis was induced by balloon abrasion and a diet containing 2% (w/w) cholesterol and 7% (w/w) lard fat. After 4 months of induction nine animals were killed (I) for analysis of the extent of atherosclerosis, while the diet of the other 26 pigs was changed to a low cholesterol diet containing either 9% (w/w) lard fat (L), 9% (w/w) fish oil (F) or 4.5% (w/w) lard fat and 4.5% (w/w) fish oil (LF). This diet was continued for 3 months to induce regression of atherosclerosis. The cholesterol-rich diet increased plasma total cholesterol, but did not affect plasma triglycerides. Low-cholesterol feeding decreased plasma total cholesterol in all three groups, but triglycerides only in LF and F. Lipid infiltration of the aortic wall was similar in I, L, LF and F. In the denudated coronary arteries of I mean luminal encroachment was 11 +/- 2%. This was similar in L (13 +/- 4%) but significantly lower (P less than 0.05) in LF (6 +/- 2%) and in F (3 +/- 1%). In the non-abraded coronary arteries of I mean luminal encroachment was 1.3 +/- 0.3%. For F and LF similar values were found, but in L there was an increase to 11 +/- 3% during low-cholesterol feeding. ADP-induced platelet aggregation was lower in LF and F than in L. Thromboxane A2 production was only reduced in F, while the production of the weak thromboxane A3 agonist was larger in F than in LF. It is concluded that fish oil retards the progression of and causes regression of coronary atherosclerosis.
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