HEMODYNAMIC AND METABOLIC CHANGES INDUCED BY REPEATED EPISODES OF HYPOXIA IN PIGS

Citation
M. Licker et al., HEMODYNAMIC AND METABOLIC CHANGES INDUCED BY REPEATED EPISODES OF HYPOXIA IN PIGS, Acta anaesthesiologica Scandinavica, 42(8), 1998, pp. 957-965
Citations number
31
Categorie Soggetti
Anesthesiology
ISSN journal
00015172
Volume
42
Issue
8
Year of publication
1998
Pages
957 - 965
Database
ISI
SICI code
0001-5172(1998)42:8<957:HAMCIB>2.0.ZU;2-C
Abstract
Background: Repeated hypoxia and surgical trauma trigger a potent neur oendocrine response and their association is thought to play a pivotal role in the pathogenesis of multi-organ dysfunction. We investigated the cardiovascular and metabolic responses to repeated acute hypoxia i n anaesthetised and surgically instrumented pigs. Methods: Under ketam ine-midazolam anaesthesia, 15 pigs were surgically instrumented for me asurements of cardiac output, vascular pressures and organ blood flows . Lactate production and O-2 uptake were determined in the brain, live r, kidney and intestine. Ten animals were subjected to two 12-min peri ods of ventilatory hypoxia (FIO2=7%) followed by re-oxygenation and 5 animals underwent 120-min normoxic ventilation (Control group). Result s: Both hypoxic challenges produced a comparable release of catecholam ines that was associated with increased cardiac output and redistribut ion of blood flow away from the intestinal and renal areas towards the brain and the liver; O-2 up-take was markedly reduced in the intestin e (-56+/-10%, P<0.05) and least affected in the brain and the kidney ( -19+/-12% and -23+/-21%, respectively). During the second hypoxic test , lethal cardiovascular depression occurred in 5 animals; these non-su rvivors demonstrated impaired hyperdynamic response and incomplete rec overy of intestinal O-2 uptake during the first hypoxia/reoxygenation test. In the Control group, normoxic ventilation was not associated wi th significant haemodynamic and metabolic changes. Conclusion: Intraop erative hypoxia causes marked heterogeneity in organ blood flow and me tabolism. The inability to develop a hyperdynamic cardiovascular respo nse during a first hypoxic event, as well as a persistent intestinal O -2 debt following re-oxygenation, predict the occurrence of death duri ng the second hypoxic insult.