Chandler C J, Ong B Y, Sitar D S
Department of Anesthesia, University of Manitoba, Winnipeg, Canada.
Toxicol Appl Pharmacol. 1991 Apr;108(2):214-22. doi: 10.1016/0041-008x(91)90112-r.
Hemodynamic alterations after hemorrhage were investigated using the microsphere technique in nitrous oxide-anesthetized 2-day-old piglets after acute ethanol intoxication (1.4 g/kg). After hemorrhage (20 ml/kg), mean arterial blood pressure decreased by 34% (p less than 0.01), cardiac output decreased by 58% (p less than 0.01), and systemic vascular resistance increased by 87% (p less than 0.01). In nonintoxicated piglets subjected to hemorrhage, mean arterial blood pressure decreased 17% (p less than 0.01) while alterations in cardiac output and systemic vascular resistance were not significant. Intoxicated piglets had delayed heart rate increases of 11% (p less than 0.01) while heart rate in nonintoxicated piglets increased 27% (p less than 0.01) immediately after hemorrhage. After hemorrhage, arterial perfusion to the liver, kidneys, gastrointestinal organs, and carcass was decreased in intoxicated piglets but only gastrointestinal and carcass perfusion were reduced in nonintoxicated piglets. In summary, acute ethanol intoxication significantly impaired the newborn piglet's cardiovascular response to moderate hypovolemia and delayed the onset of a compensatory tachycardia response. Such cardiovascular impairments may be extremely detrimental to neonates.
