Drugs online research references
Can J Cardiol. 1986 Jul;Suppl A:9A-18A.
Regional myocardial blood flow and function in experimental myocardial ischemia.
Ross J Jr, Gallagher KP, Matzusaki M, Lee JD, Guth B, Goldfarb R.
Experiments are reviewed in conscious dogs instrumented with ultrasonic crystals for measuring systolic wall thickening and myocardial blood flow (microsphere technique), and studied under a variety of conditions during acute or chronic circumflex coronary stenosis. With acute progressive stenosis, a nearly linear relation was found between normalized subendocardial flow and function. There were no consistent ST segment changes in the body surface electrocardiogram if wall thickening was less than 25%, although changes occurred in the subendocardial electrogram. The regional flow-function relation was then examined during exercise with various degrees of coronary stenosis; the mean flow-function relation was shifted to the right of the resting relation, but when subendocardial flow was expressed per beat and function normalized as a fraction of that in normal wall the relationship was superimposable upon the resting relation, suggesting that ischemia is absolute (not relative) in the subendocardium during steady state conditions. When the normal increase of wall thickening during exercise was prevented by mild coronary stenosis ischemia could not be clearly detected, but when function during exercise averaged 20% below the resting value, subendocardial blood flow changes and other evidence of ischemia were readily apparent, indicating the sensitivity of wall motion for detecting subcritical coronary stenosis. The regional flow-function relation was also studied in chronic single vessel coronary artery stenosis (ameroid constrictor), in which function was normal at rest (collateral development) but exercise produced large decreases in both regional flow and function. At matched levels of treadmill exercise, a calcium channel blocker (diltiazem) together with beta blockade (atenolol) produced an additive effect that was greater than with either drug alone, with substantial increases in both subendocardial flow and regional function. Finally, studies showing reversible post-reperfusion dysfunction after 15 minutes or two hours of coronary occlusion are reviewed. Partial ischemia for 5-hours, followed by reperfusion also produced regional dysfunction which persisted for at least 3 days but reverted to normal by one week, with little or no histologic damage of the free wall. These studies on regional flow and function during ischemia may carry implications for a number of important clinical phenomena.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3756604&dopt=Abstract
J Pharmacol Exp Ther. 1982 Oct;223(1):219-23.
Indications for vascular alpha- and beta-2 adrenoceptors in synapses of the muscarinic pathway in the pithed normotensive rat.
Wilffert B, Gouw MA, De Jonge A, Timmermans PB, van Zwieten PA.
In the pithed normotensive rat the adrenoceptors involved in the hypertensive and tachycardic effects of the indirectly acting sympathomimetic agent tyramine and of electrical stimulation of the spinal cord (TH5-L4 or C7-Th1) were analyzed. The tools used for the identification of the adrenoceptors were the selective alpha-1 adrenoceptor blocking drug prazosin, the selective alpha-2 adrenoceptor antagonist rauwolscine, the beta-1 blocker atenolol and the selective beta-2 adrenoceptor blocking agent ICI 118,551. The participation of vascular alpha-2 adrenoceptors in the pressor response of tyramine was shown. The increase in blood pressure induced by electrical stimulation of the spinal cord (TH5-L4) was used to demonstrate that alpha-2 adrenoceptors were activated via ganglionic muscarinic receptors. The tachycardia evoked by electrical stimulation of the spinal cord (C7-Th1) was not influenced by beta-2 adrenoceptor blockade. It was enhanced, however, by the alpha-2 adrenoceptor antagonist rauwolscine. It is hypothesized that activation of ganglionic nicotinic receptors leads to stimulation of the nearest varicosities interfering with alpha-1 adrenoceptors. However, activation of ganglionic muscarinic receptors may lead to an additional release of neurotransmitter in the more distant varicosities endowed with alpha-2 or beta-2 adrenoceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6288920&dopt=Abstract
Eur J Pharmacol. 1976 Jul;38(1):55-61.
Hypotensive responses following oral adminstration of beta-adrenoceptor blocking drugs to the conscious cat.
Burden DT, Hamilton TC.
On oral administration, the non-selective beta-adrenoceptor blocking drugs (+/-)-bufuralol, (-)-bufuralol, propanolol, oxprenolol, pindolol and alprenolol produced hypotensive responses in the conscious cat; (+)-bufuralol was without effect. The selective beta-adrenoceptor blocking drugs practolol and atenolol had no effect on blood pressure but tolamolol elicited a hypotensive response. All the drugs tested reduced the tachycardia due to intravenous isoprenaline in the conscious cat; however, not all doses of these drugs reduced blood pressure. (+)-Bufuralol was devoid to beta-adrenoceptive blocking activity. Only tolamolol reduced the pressor response to i.v. phenylephrine in the conscious cat, indicating that alpha-adrenoceptive blocking activity may contribute to its hypotensive action. The results suggest that beta-adrenoceptive blocking activity is necessary for the hypotensive responses of these drugs. However, for the different drugs, there was no correlation between peripheral beta-adrenoceptive blocking activity and hypotensive response.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8319&dopt=Abstract
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