Physiology of the Coronary Circulation

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

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Broadley¹

1970

“…When the increases in activity of the donor heart were prevented by propranolol then the anticipated vasodilatation no longer occurred. In the case of adrenaline only a rise in pressure remained in both hearts which was attributed to residual direct vasoconstriction of the coronary vessels mediated via a-adrenoceptors (Saito, 1959;Kaverina, 1965;Parratt, 1967;Broadley, 1970). The experiments were repeated with isoprenaline whose direct vascular effects are solely vasodilator.…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

Section: Introductionmentioning

confidence: 99%

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

Broadley

1976

I A procedure involving two guinea-pig isolated hearts perfused in series is described for detecting in the recipient heart the release of a possible coronary vasodilator metabolite from the donor heart. 2 Adrenaline and isoprenaline stimulated the rate and force of contraction and produced a multiphasic coronary vascular response, the predominant phase of which was vasodilatation. When the /-adrenoceptors of the recipient heart were blocked, stimulation of the donor heart by the catecholamines was associated with a coronary vasodilatation ofthe recipient heart. 3 Histamine stimulated rate and force of contraction and was predominantly coronary vasodilator.After blockade of histamine Hl-and H2-receptors in the recipient heart, coronary vasodilatation followed increases in activity of the donor heart in response to histamine. 4 These vasodilator responses of the recipient heart were attributed to the release from the donor heart of a vasodilator metabolite by the increased activity. This is the proposed mechanism for the predominant coronary vasodilator response to catecholamines and histamine. 5 Periods of electrically-paced tachycardia and anoxia of the donor heart also led to the release of vasodilator activity. 6 The possible identity of the metabolite is discussed.

“…In the present study it has been shown that papaverine considerably increases total myocardial oxygen consumption following acute ischaemic injury induced by ligation of a coronary artery. There is evidence that coronary occlusion triggers reflex coronary vasoconstriction mediated through the sympathetic nervous system (Kaverina, 1965;Grayson, Irvine & Parratt, 1971). Thus, whereas overall hypoxia of the heart results in considerable dilatation of the coronary vessels (stronger than the effect of any vasodilator) ischaemia in a limited zone of (1) (1) Perfusion at 4 ml/min; (2) perfusion at 1.5 ml/min; (3) 2 min after drug administration, at a perfusion of 1.5 ml/mir,; (4) 10 min after injection, perfusion at 1.5 ml/min.…”

Section: Spasm Of Coronary Arterymentioning

confidence: 99%

Acute Myocardial Ischaemia in Anaesthetized Cats: Effects of Papaverine

Kisin

1978

1 The effects of papaverine on coronary blood flow, myocardial oxygen consumption, myocardial oxygen tension and the ischaemic ECG pattern were studied in anaesthetized open-chest cats representing three models of acute coronary insufficiency: ligation, spasm, and perfusion of the coronary artery at a stabilized insufficient level. 2 Despite the increase in myocardial oxygen consumption reflecting elevation of oxygen demand, papaverine improved the signs of myocardial ischaemia (the myocardial oxygen tension and ECG pattern), as long as there was a possibility of an increase in blood supply to the affected zone. Where this was excluded, the symptoms were actually aggravated. 3 The results suggest that there is no basis for dividing coronary dilators into 'benign' and 'malignant' according to their ability to increase myocardial oxygen requirements. A coronary dilator enhancing oxygen demand may prove beneficial even following complete coronary artery occlusion.