Drugs online research references
Anesthesiology. 1983 Oct;59(4):322-6.
Identification of receptor mechanism mediating epinephrine-induced arrhythmias during halothane anesthesia in the dog.
Maze M, Smith CM.
The adrenergic receptor mechanism by which halothane sensitizes the myocardium to the ventricular arrhythmogenic properties of catecholamines is unknown. The new generation of selective adrenergic receptor antagonists have been used to determine which receptor blockade causes the greater increase in the dose of epinephrine needed to achieve a threshold for ventricular arrhythmias. Dogs anesthetized with 1.2 MAC halothane had an arrhythmogenic dose of epinephrine (ADE) of 2.2 micrograms X kg X min-1 that significantly increased (P less than 0.01) to 27 micrograms X kg-1 X min-1 after alpha 1 blockade with prazosin. beta 1 blockade with metoprolol also significantly increased the ADE to 12 micrograms X kg-1 X min-1 (P less than 0.05) but was less than the effect noted after prazosin treatment (P less than 0.05). The dramatic increase in the threshold for arrhythmias noted after prazosin could not be ascribed solely to its hemodynamic properties because treatment with sodium nitroprusside did not change the ADE (2.7 micrograms X kg-1 X min-1) significantly; yet nitroprusside treatment resulted in a similar drop in mean arterial pressure (59 mmHg) to that of prazosin treatment (51 mmHg) when compared with the control group. Thus postsynaptic myocardial alpha 1 adrenergic receptors mediate most of the sensitization by halothane to the ventricular arrhythmogenic effects of catecholamines, while a lesser contribution is conferred by the beta 1 adrenoceptors. These results have implications for the treatment and identification of patients particularly at risk from halothane-epinephrine interactions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6137172&dopt=Abstract
G Ital Cardiol. 1984 Jul;14(7):530-3.
[Effects of delayed-action metoprolol evaluated in hypertensive patients responsive to therapy subdivided in 2 different age groups]
[Article in Italian]
Carpentiere G, Marino S, Castello F, Castello A, Cellura M.
Thirty patients with essential hypertension, whose blood pressure was controlled by metoprolol, were divided according to age in two groups. All the patients were treated with long-acting metoprolol given as simple daily dose at 08.00 h. Blood pressure and heart rate were recorded before and at the 7th, 15th, 30th, 45th, 60th days of treatment. No significant difference in the antihypertensive effects of metoprolol was detected between the two groups of patients. A significantly higher reduction of the heart rate was observed in the older patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6489667&dopt=Abstract
Eur J Cardiol. 1978 Jun;7(4):317-25.
Effect of beta-blockade by metoprolol on global and regional left ventricular myocardial perfusion in coronary heart disease.
Frick MH, Korhola O, Valle M.
Utilizing semiselective 133Xenon injections and gamma camera recording, global and regional left ventricular myocardial perfusion were recorded under the influence of beta-blockade by metoprolol in 9 patients with angiographically proven coronary artery disease. Metoprolol reduced the rate--pressure variable in every patient, the mean reduction amounting to 24% (P less than 0.01). With one exception, the global left ventricular myocardial flow followed the change in the rate-pressure variable. No significant differences were detected in the flow responses of areas distal to only moderate coronary obstructions (less than 75%) and areas distal to significant (less than 75%) obstructions. The same was true when areas of asynergic contractions were compared with areas of normal contractions, or when areas supplied by collaterals were compared with areas devoid of collateral vessels. It is concluded that the reduction in myocardial flow after metoprolol is due to the reduction of the myocardial oxygen consumption, and no redistribution of flow occurs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=689064&dopt=Abstract
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