An analysis of the coronary vascular responses to catecholamines, using a modified Langendorff heart preparation

Abstract

Summary1. A modified Langendorff heart preparation from the guinea-pig was used to analyse catecholamine responses. Contractile force, heart rate and coronary perfusion pressure were recorded. 2. Four components of the vascular response could be identified.(a) The initial phase was a vasoconstriction mediated by a-adrenoceptors which preceded any effects on heart rate and force. (b) A secondary constriction followed, which was due to the increased myocardial compression during positive inotropic and chronotropic responses.(c) The third, more predominant, effect was a prolonged dilatation probably associated with the increased metabolic activity of the heart. (d) A fourth component was a direct vasodilatation mediated by /3-adrenoceptors which was evident when small doses of catecholamines were used but was usually masked by the more pronounced metabolically linked dilatation. 3. The actions of salbutamol were examined and since it caused direct vasodilatation by stimulation of /8-adrenoceptors without other myocardial effects, these adrenoceptors were classified as the fl2-type. 4. I.C.I. 50,172 was employed to block selectively the myocardial effects due to stimulation of f31-adrenoceptors and leave the vasodilator /32-adrenoceptors unaffected.5. Adrenaline, noradrenaline and isoprenaline were compared at two dose levels, in the presence or absence of effects on heart rate and force. 6. Constrictor or dilator effects were found in the absence of other effects and were shown to depend to some extent on the rate of coronary perfusion. IntroductionThe overall effect of catecholamines on the coronary circulation is vasodilatation

Characterization of the coronary vascular β‐adrenoceptor in the pig

“…resembles the peripheral vascular ,/-adrenoceptor (82-type) (Parratt & Wadsworth, 1970;Broadley, 1970;Mark, Abboud, Schmid, Heistad & Mayer, 1972); 2. differs from the peripheral vascular f3-adrenoceptor (Bohr, 1967); 3. resembles the myocardial f3-adrenoceptor (,81-type) (Somani, Laddu & Hardman, 1970;Lucchesi & Hodgeman, 1971); 4. differs from the myocardial /3-adrenoceptor (Adam, Boyles & Scholfield, 1970;Bussmann, Rauh & Krayenbuehl, 1970); 5. differs from both the vascular and myocardial /8-adrenoceptors (Ross & Jorgensen, 1970).…”

The Release of a Coronary Vasodilator Metabolite From the Guinea‐pig Isolated Perfused Heart Stimulated by Catecholamines, Histamine and Electrical Pacing and by Exposure to Anoxia

“…The direct effects on the coronary vasculature yield both vasoconstriction mediated via a-adrenoceptors (Saito, 1959;Kaverina, 1965;Parratt, 1967;Broadley, 1970) and vasodilatation mediated via 0-adrenoceptors differing from those of the myocardium (Adam, Boyles & Scholfield, 1970;Ross & Jorgensen, 1970;Bayer, Mentz & F6rster, 1972) and therefore assigned to the p2-type (Broadley, 1970;Parratt & Wadsworth, 1970;Mark, Abboud, Schmid, Heistad & Mayer, 1972;Ross, 1974). Others however disagree and claim that these resemble the Pf-adrenoceptors of the myocardium (Lucchesi & Hodgeman, 1971;Drew & Levy, 1972).…”

Rodent Working Heart Model for the Study of Myocardial Performance and Oxygen Consumption

“…2 Such preparations have been instrumental in elucidating mechanisms of myocardial action, 3 myocardial metabolism, [4][5][6] and effects of cardiotonic medications. [7][8][9] The use of medications that enhance myocardial contractility is common in critically ill patients. However, few data are available comparing the relative effects of these medications on contractility and myocardial oxygen consumption, data which may be useful in the care of patients with clinical signs of heart failure of in the postoperative setting.…”