The cardiovascular effects of hypertonic sodium bicarbonate in conscious dogs: underlying mechanisms of action

Abstract

Mechanisms underlying the transient hypotensive effect (central or peripheral) of rapid bolus administration of hypertonic sodium bicarbonate (NaHCO3) were studied in conscious dogs. Thirteen animals equipped with an electromagnetic flow probe positioned around the ascending aorta were utilized. NaHCO3 (18.5 mequiv. of 1786 mosmol/L), hypertonic saline solution having the same sodium concentration as NaHCO3, and mannitol solution with the same osmolarity as NaHCO3, were injected in the right and in the left atrium. Intra-arterial NaHCO3 was tested to assess its direct peripheral vascular effects. Blood ionic as well as acid–base modifications following NaHCO3 were also studied. Our results indicate that right atrial injection of NaHCO3 elicited transient hypotension (−10 to −15 mmHg (1 mmHg = 133.322 Pa)) and myocardial depression as revealed by a significant decrease of stroke volume (−8%), stroke power (−18%), stroke work (−12%), maximum systolic flow (−13%), peak velocity (−13%), and maximum acceleration (−24%). When the solution is injected in the left atrium, myocardial depression is more pronounced suggesting that the coronary bed is the site of action. Hypertonic saline injections indicate that the sodium load plays a role in this decrement of myocardial function while hyperosmolarity per se, as exemplified with mannitol injections, elicits no negative effect. Transient ionic as well as acid–base disturbances are other mechanisms that have to be considered along with coronary vasoconstriction. Decrement in peripheral resistance appears only with right intra-atrial NaHCO3 suggesting that the pulmonary vascular bed is the origin of this reflex.