Hemodynamic responses initiated by coronary stretch receptors with special reference to coronary arteriography

Abstract

Hyperosmotic solutions, of substances including polyvinylpyrrolidone, sodium or methylglucamine diatrizoate, sodium chloride, glucose, sucrose and mannitol, produced transient sinus bradycardia and a fall in arterial blood pressure when injected directly into the coronary arteries of the intact anesthetized dog. The same changes occurred with acute coronary venous hypertension induced by coronary sinus obstruction with a balloon catheter but not with injections of isosmotic saline solutions into the coronary artery or of the various substances into the aortic root, left ventricle or pulmonary artery. The bradycardia was prevented by atropine. Concomitant with the fall in blood pressure, femoral arterial blood flow increased and maximal rate of rise of left ventricular pressure ( dp dt ) decreased even when the bradycardia was prevented by pacing. In most experiments this reduction in maximal dp dt could be abolished by beta adrenergic blockade. All responses were abolished by bilateral vagotomy with the exception of the fall in pressure and maximal dp dt produced by the radiopaque media or 5 percent sodium chloride. These agents exert a direct myocardial depressant action. Simultaneously determined indicator-dilution curves using 125I-albumin and 131I-diatrizoate verified that the diatrizoate molecule leaves the circulation during its passage through the coronary vascular bed. Calculations derived from these curves demonstrated that injection of nonlabeled diatrizoate produces a large increase in coronary blood volume and flow. In 2 patients the bradycardia occurring with coronary injections of radiopaque media could be prevented by atropine. Sodium diatrizoate (50 percent Hypaque ®) usually produced more intense bradycardia than did methylglucamine diatrizoate (60 percent Renografin ®). The depressor effects of coronary injections of hyperosmotic solutions or coronary sinus obstruction result from activation of a reflex arc originating from stretch receptors in the coronary capillaries or small veins. The afferent limb of the reflex is bilaterally represented in the cervical vagosympathetic trunks of the dog. The efferent effects characterized in these experiments were increased vagal firing to the sinus node, decreased activity of adrenergic fibers to peripheral vascular alpha receptors and probably diminished adrenergic firing to beta receptors in the ventricular myocardium.