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Titolo:
PARASYMPATHETIC MUSCARINIC STIMULATION LIMITS NORADRENALINE-INDUCED MYOCARDIAL CREATINE-KINASE RELEASE - A STUDY IN THE ISOLATED-PERFUSED WORKING RAT-HEART
Autore:
WALDENSTROM A; MARTINUSSEN HJ; KOCK J; RONQUIST G; HULTMAN J;
Indirizzi:
UNIV UPPSALA HOSP,DEPT CARDIOL S-75185 UPPSALA SWEDEN UNIV UPPSALA HOSP,DEPT ANAESTHESIOL S-75185 UPPSALA SWEDEN UNIV UPPSALA HOSP,DEPT CLIN CHEM S-75185 UPPSALA SWEDEN
Titolo Testata:
Scandinavian journal of clinical & laboratory investigation
fascicolo: 8, volume: 54, anno: 1994,
pagine: 615 - 621
SICI:
0036-5513(1994)54:8<615:PMSLNM>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
INFARCT SIZE; METOPROLOL; TRIAL;
Keywords:
RAT; MYOCARDIUM; NORADRENALINE; CARBACHOL; ALPHA-RECEPTOR; BETA-RECEPTOR; MUSCARINIC RECEPTOR; CYCLIC NUCLEOTIDES; ATTENUATION; MECHANICAL RESPONSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
25
Recensione:
Indirizzi per estratti:
Citazione:
A. Waldenstrom et al., "PARASYMPATHETIC MUSCARINIC STIMULATION LIMITS NORADRENALINE-INDUCED MYOCARDIAL CREATINE-KINASE RELEASE - A STUDY IN THE ISOLATED-PERFUSED WORKING RAT-HEART", Scandinavian journal of clinical & laboratory investigation, 54(8), 1994, pp. 615-621

Abstract

It has long been known that high concentrations of catecholamines mayinduce myocardial damage, and aggravate ischaemic injury. It has alsobeen shown that beta-blockade may protect the myocardium from ischaemic damage. Stimulation of muscarinic receptors modulates beta-adrenergic receptor affinity for isoproterenol and attenuates isoproterenol induced adenylyl cyclase activation. Effects of muscarinic receptor stimulation were therefore investigated in isolated anterogradely perfusedrat hearts under different experimental conditions. One group of hearts was perfused with noradrenaline, 10(-6) moll(-1) for 45 min, and another group was perfused with different carbachol concentrations (3 x 10(-7) -10(-5) moll(-1)) with or without noradrenaline 10(-6) moll(-1), for 45 min. Release of creatine kinase to the perfusion buffer was taken as a sign of cell damage. Heart rate, left ventricular (max)dP/dtand left ventricular pressure were measured throughout the perfusion time by insertion of a 20 gauge cannula through the left ventricular wall near the base. Carbachol (3 x 10(-7) moll(-1)) alone induced a decrease of heart rate by 25% and (max)dP/dt by 13%. Noradrenaline produced a 20% increase in heart rate, whereas the combination of noradrenaline plus carbachol induced a minor decrease in heart rate. Muscarinic receptor stimulation alone decreased myocardial contractility. However, when combined with noradrenaline no decrease in contractility was seen. Also, the release of creatine kinase to the perfusion buffer containing the combination of carbachol plus noradrenaline was reduced. Thus, muscarinic receptor stimulation protected the myocardium from catecholamine induced damage at concentrations where no change in contractility was seen. This sheds new light on vagal tone and atropine treatment of the bradycardic acute myocardial infarction patients.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 10:34:57