SODIUM-NITROPRUSSIDE DOES NOT INFLUENCE TISSUE OXYGEN EXTRACTION CAPABILITIES DURING A CRITICAL REDUCTION IN OXYGEN DELIVERY

By its regulating effects on blood vessel tone, nitric oxide (NO) may play an important role in the coupling of oxygen delivery (DO2) to met abolic rate. We reasoned that if endogenous NO synthesis is an importa nt modulator of oxygen extraction ratio (O(2)ER), then administration of a NO donor will alter oxygen extraction capabilities during a fall in blood flow. We studied the effects of the NO donor, nitroprusside, on the relationship between DO2 and oxygen uptake (VO2) during an acut e reduction in DO2 induced by cardiac tamponade. Twenty-one healthy, a naesthetised, mechanically ventilated dogs were randomly divided into 3 groups. Group 1 (n = 7) served as control; Groups 2 and 3 were given sodium nitroprusside at 1.0 mu g/kg . min (n = 7), and 2.5 mu g/kg . min intravenously (n = 7), respectively. All animals were given normal saline i.v, at a rate of 20 ml/kg . h throughout the study. Cardiac t amponade was induced by bolus injections of normal saline into the per icardial space. In the control animals the critical DO2 (DO(2)crit) wa s found at 10.1 +/- 1,5 ml/kg . min and critical O(2)ER (O(2)ERcrit) a t 63.3 +/- 10.9%. Nitroprusside at the lower dose decreased systemic v ascular resistance but did not significantly influence arterial pressu re, cardiac output, DO2 or VO2; neither DO2 crit nor O(2)ERcrit was al tered (9.3 +/- 2.9 ml/kg . min and 70.4 +/- 20.9%). Nitroprusside at t he higher dose induced significant decreases in mean arterial pressure and systemic vascular resistance, but had no significant effect on ca rdiac output. DO(2)crit (9.2 +/- 2.0 ml/kg . min) and O(2)ERcrit (59.8 +/- 13.2%) were similar to the control group. We concluded that the N O donor, sodium nitroprusside, does not significantly influence tissue oxygen extraction capabilities during a fall in cardiac output.