Haemodynamic and cerebral effects of ATP-induced hypotension

Controlled decreases in mean arterial pressure to 20%, 40% and 60% of baseline were produced by the administration of increasing concentrations of adenosine triphosphate (ATP) i.v. in five anaesthetized baboons. Indices of the systemic circulation (arterial pressure, right atrial pressure, pulmonary artery pressures, cardiac output) and of the cerebral circulation (cerebral blood flow, cerebral metabolic rate for oxygen, cerebrovascular reactivity) were obtained as arterial pressure was decreased, and following discontinuation of the infusion of ATP. A neuropathological investigation was undertaken at the end of the experimental procedure. The infusion of ATP produced dose-dependent decreases in systemic vascular resistance and mean arterial pressure (MAP). Cardiac output and stroke volume were maintained close to baseline values, or increased slightly. Cerebral blood flow (CBF) increased initially (48 +/- 4 ml min-1/100 g to 68 +/- 9 ml min-1/100 g) and then decreased progressively as MAP was decreased to 40% and 60% of baseline. Cerebrovascular reactivity was shown to be impaired during, and for up to 90 min following, the administration of ATP. However, there was no morphological evidence of ischaemic cell damage in any animal. Tachyphylaxis was not observed during, and there were no instances of rebound hypertension following, the infusion of ATP. The concentration of uric acid had increased significantly by the 40% decrement in MAP, and remained so 60 min after the restoration of the arterial pressure.