Drugs online research references
J Cardiovasc Pharmacol. 1990 Jan;15(1):22-8.
Pronounced accumulation of metoprolol in ischemic myocardium after coronary venous retroinfusion.
Ryden L, Tadokoro H, Sjoquist PO, Kar S, Ervik M, Corday E.
Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
The myocardial availability of the beta 1-selective blocker metoprolol was compared following standard intravenous (i.v.) administration and after coronary venous retroinfusion. Thirteen open-chest farm pigs were subjected to 90-min occlusion of the left anterior descending coronary artery. In six of these pigs, metoprolol was administered as an i.v. injection while 7 pigs received the drug retrogradely into the coronary vein. The time of administration was 5 min. In both groups, metoprolol was administered after 30 min of coronary artery occlusion. Metoprolol did not influence heart rate (HR) or blood pressure (BP) whether administered i.v. or into the coronary vein. At the end of administration, plasma metoprolol was significantly higher when administered i.v. (2,955 +/- 543 nmol/L) than after coronary venous infusion (1,213 +/- 464 nmol/L; p less than 0.05). At 30 and 60 min after injection, plasma metoprolol did not differ significantly between the two groups. Myocardial tissue concentration of metoprolol in nonischemic myocardium was approximately 480 pmol/g for both groups and similar in the subendocardial, midmyocardial, and subepicardial layers of the myocardium. After i.v. administration, myocardial Metoprolol concentration in the ischemic zone was less than that in the nonischemic zone, averaging 150-300 pmol/g tissue. In contrast, coronary venous retroinfusion of metoprolol resulted in a substantial accumulation of the drug in the ischemic zone, as exemplified by a subendocardial concentration of 2,002 +/- 689; a midmyocardial concentration of 26,643 +/- 8,813 and a subepicardial concentration of 98,571 +/- 58,930 pmol/g, respectively (mean +/- SE). Coronary venous retroinfusion of metoprolol resulted in a pronounced accumulation of drug in the ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1688978&dopt=Abstract
Naunyn Schmiedebergs Arch Pharmacol. 1997 Jun;355(6):720-6.
Influence of blockade of alpha 1-adrenoceptors, beta 1-adrenoceptors and vasopressin V1A receptors on the cardiovascular effects of gamma 2-melanocyte-stimulating hormone (gamma 2-MSH).
Van Bergen P, De Winter TY, De Wildt DJ, Versteeg DH.
Department of Medical Pharmacology, Rudolf Magnus Institute for Neurosciences, Utrecht University, The Netherlands.
gamma 2-Melanocyte-stimulating hormone (gamma 2-MSH) and related melanotropins have been shown to have various cardiovascular effects, including acute, short-lasting increases in blood pressure (MAP) and heart rate (HR). gamma 2-MSH, administered intravenously, dose-dependently increased MAP and HR with an ED50 of approximately 30 nmol/kg and a maximal effect on MAP of approximately 55 mm Hg and on HR of around 70 beats per minute. Intravenous (i.v.) pretreatment with the alpha 1-adrenoceptor antagonist, prazosin, caused the dose-response curve for the effect of gamma 2-MSH on MAP to shift to the right with a decrease in slope, whereas it had no effect on the dose-response curve for the effect on HR. I.v. pretreatment with the beta 1-adrenoceptor antagonist, metoprolol, had no effect on the dose-response curve for the effect of gamma 2-MSH on MAP, but it caused the dose-response curve for the effect of the peptide on HR to shift to the right with a decrease in slope. Neither i.v. nor intracerebroventricular (i.c.v.) administration of the vasopressin V1A receptor antagonist, SR 49059 ((2S) 1-[(2R 3S)-5-chloro-3-(2-chlorophenyl)-1-(3,4-dimethoxy-benzene-sulfonyl)- 3-hydroxy-2,3-dihydro-1H-indole-2-carbonyl]-pyrrolidine-2-carboxamide), had significant effects on the dose-response curves for the effects of the peptide on either MAP or HR. The doses of prazosin, metoprolol and SR 49059 were found to be effective in counteracting the effects of agonists for these receptors (phenylephrine, isoprenaline and [Arg8]vasopressin, respectively). Taken together, these results support the postulate that the effects of gamma 2-MSH are, at least partially, due to an increase in sympathetic outflow to the periphery (Gruber and Callahan (1989), Am J Physiol 257: R681-R694), and that this increase leads to increased activation of vascular alpha 1-adrenoceptors and cardiac beta 1-adrenoceptors. If, as was suggested by these authors, gamma 2-MSH acts via activation of a central vasopressin system, it is via a vasopressin receptor subtype other than the vasopressin V1A receptor, since i.c.v. administration of a selective vasopressin V1A receptor antagonist failed to interfere with the pressor and cardioaccelerator effects of gamma 2-MSH.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9205956&dopt=Abstract
Arq Bras Cardiol. 1991 Dec;57(6):459-64.
[Effect of propranolol and metoprolol on cardiorespiratory and metabolic response to exercise]
[Article in Portuguese]
de Barros AL, Russo AK, de Barros Neto TL, Ferreira NM, Freire E.
Escola Paulista de Medicina, Sao Paulo.
PURPOSE--To study the effects of intravenous propranolol and metoprolol on cardiorespiratory and metabolic responses to exercise. METHODS--Two groups of anaesthetized dogs (sodium pentobarbital, 33 mg/kg) were studied at rest and moderate exercise (induced by electrical stimulation) before and after metoprolol (0.4 mg/kg, n = 7) or propranolol (0.2 mg/kg, n = 10). Haemodynamic, metabolic and respiratory variables were measured. RESULTS--There was a decrease in heart rate both at rest and during exercise after metoprolol and propranolol administration. The cardiac output, stroke volume and peripheral vascular resistance presented decreased responses to exercise after both drugs. O2 consumption and CO2 production were not altered significantly at rest but increased in a lesser degree during exercise. Propranolol administration reduced ventilation during rest and exercise, although the ventilatory response to exercise remained the same. Metoprolol administration did not affect ventilation at rest but reduced the ventilatory response to exercise leading to an increase of the PaCO2. CONCLUSION--Propranolol and metoprolol effects on cardiovascular and metabolic variables measured at rest and during exercise were the same. The ventilatory effect with metoprolol administration was different from the observed with propranolol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1824217&dopt=Abstract
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