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 metabolic rate. We reasoned that if endogenous NO synthesis is an important modulator of oxygen extraction ratio (O2ER), 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 acute reduction in DO2 induced by cardiac tamponade. Twenty-one healthy, anaesthetised, 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 μg/kg · min (n = 7), and 2.5 μg/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 tamponade was induced by bolus injections of normal saline into the pericardial space. In the control animals the critical DO2 (DO2crit) was found at 10.1 ± 1.5 ml/kg · min and critical O2ER (O2ERcrit) at 63.3 ± 10.9%. Nitroprusside at the lower dose decreased systemic vascular resistance but did not significantly influence arterial pressure, cardiac output, DO2 or VO2; neither DO2crit nor O2ERcrit was altered (9.3 ± 2.9 ml/kg · min and 70.4 ± 20.9%). Nitroprusside at the higher dose induced significant decreases in mean arterial pressure and systemic vascular resistance, but had no significant effect on cardiac output. DO2crit (9.2 ± 2.0 ml/kg · min) and O2ERcrit (59.8 ± 13.2%) were similar to the control group. We concluded that the NO donor, sodium nitroprusside, does not significantly influence tissue oxygen extraction capabilities during a fall in cardiac output.