Hypertonic saline resuscitation is prevented by intracerebroventricular saralasin but not by captopril

ABSTRACT

Hypertonic saline resuscitation (HR, 7.5% NaCl, 4 ml/Kg) effectively reverts severe hemorrhage, but a central neural component is probvably involved in the survival response. This experiment examines the role of central angiotensinergic pathways in the hemorrhage-hypertonic resuscitation interaction. Severely bled (43ñ 2 ml/Kg) pentobarbital-anesthetized dogs with chromically imnplanted cerebral ventricular cannulae were resusucitated with 4 ml/Kg 7.5% NaCl, iv 10 min after intracerebroventricular injection of 0.5 ml normal saline (CT), 159 µg saralasin (in 0.5 ml saline, SR), or 10 mg captopril (in 0.5 ml salaine, CP). ALL 10 SR-treated dogs died 2-6 h after HR. Their arterial pressure and cardiac index initially recovered to near pre-hemorrhage levels, but bradually decreased thereafter, base excess remaining ar severe metabolic acidosis levels throughout, al CT-and 8/10CP-treated dogs survived indefinitely,, with near normal arterial pressure, cardiac, index and base excess levels. It is there fore concluded that the inhibition of central angiotensinergic sites with the competitive antagonist saralasin effectively prevents survival after HR, whereas inhibition of angiotensin converting enzyme by captopril in cerebrospinal fluid is virtuallly ineffective