作者: W. R Law , P. J Carney , M. P McLane
DOI: 10.1093/CVR/25.2.151
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摘要: Study objective – In vitro investigations have indicated that adenosine can inhibit β adrenergic stimulated increases in cardiac contractility. The present study was designed to determine the ability of isoprenaline induced contractility vivo. Adenosine has been reported exert its inhibitory effects on by inhibiting adenylate cyclase. Thus, should no effect positive inotropic agents act independently We therefore assessed this nucleoside insulin, a hormone exerts alterations cyclic AMP. Design Saline or (10 μmol·mT−1) infused into circumflex artery at 1 ml·min−1 as background. Isoprenaline (20 200 pmol·min−1) during saline infusion. response insulin determined hyperinsulinaemic euglycaemic clamp. Subjects 16 adult mongrel dogs were anaesthetised with pentobarbitone. Five used studies, and 11 studies. Measurements main results Dogs instrumented obtain measurements mean arterial blood pressure, heart rate, flow (Q), instantaneous left ventricular posterior wall thickness. slope end systolic pressure-dimension relationship (Ees) an index myocar-dal contractility, previously shown reflect changes myocardial state independent influence from afterload preload. Left dP/dtmax derived pressure respect time, Ees Neither adenosine, isoprenaline, nor alone caused any significant rate. increase Q. Both significantly increased either both doses isoprenaline. inhibited these indices but not those insulin. Conclusions is capable suggest does reponses stimulation