CIRCULATORY SEQUELAE OF ADMINISTERING CPAP IN HYPERDYNAMIC SEPSIS ARETIME-DEPENDENT

Citation
Ga. Fox et al., CIRCULATORY SEQUELAE OF ADMINISTERING CPAP IN HYPERDYNAMIC SEPSIS ARETIME-DEPENDENT, Journal of applied physiology, 81(2), 1996, pp. 976-984
Citations number
29
Categorie Soggetti
Physiology,"Sport Sciences
ISSN journal
87507587
Volume
81
Issue
2
Year of publication
1996
Pages
976 - 984
Database
ISI
SICI code
8750-7587(1996)81:2<976:CSOACI>2.0.ZU;2-A
Abstract
Evidence questions the circulation's ability to acutely compensate for abrupt changes in O-2 delivery (QO(2)). Because both sepsis and conti nuous positive airway pressure (CPAP) may alter the metabolic regulati on of tissue oxygenation, we designed an experiment to determine the i nteraction, if any, between sepsis and time on circulatory homeostasis after the application of CPAP. Twenty-four sheep were randomized to c ecal ligation and perforation (CLP) or sham procedure (Sham) and then rerandomized to receive either CPAP (10 mmHg) or no CPAP (No CPAP; CLP /CPAP, n=8; CLP/No CPAP, n=8; Sham/CPAP, n=4; Sham/No CPAP, n=4). Fort y-eight hours later, CLP animals demonstrated an elevated cardiac inde x (+63%), systemic QO(2) (+49%), and systemic O-2 uptake (+28%). Organ blood flow, measured with radiolabeled microspheres, was augmented to the heart and depressed in organs comprising the splanchnic circulati on. Compared with the CLP/No CPAP group and both Sham groups, myocardi al QO(2) in the CLP/CPAP group was significantly elevated when measure d both 2 and 8 h after CPAP. These changes were unrelated to differenc es in mean heart work between the study groups. Simultaneously, QO(2) to all of the small gut, large gut, pancreas, and kidney in the CLP/CP AP group was elevated during the 2-h study yet reverted to levels not different from baseline by the 8-h study. These data demonstrate 1) a unique sepsis X time interaction with the use of 10 mmHg of CPAP, part icularly in the ''nonvital'' circulations, and 2) CPAP effects on the septic coronary circulation, which were unexplained by changes in exte rnal determinants of myocardial O-2 need.