PULMONARY VENODILATION BY ISOFLURANE IMPROVES GAS-EXCHANGE DURING ESCHERICHIA-COLI BACTEREMIA

Citation
R. Fretschner et al., PULMONARY VENODILATION BY ISOFLURANE IMPROVES GAS-EXCHANGE DURING ESCHERICHIA-COLI BACTEREMIA, Critical care medicine, 21(5), 1993, pp. 747-752
Citations number
24
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
00903493
Volume
21
Issue
5
Year of publication
1993
Pages
747 - 752
Database
ISI
SICI code
0090-3493(1993)21:5<747:PVBIIG>2.0.ZU;2-D
Abstract
Objective: To determine how isoflurane affects the longitudinal distri bution of pulmonary vascular resistance and pulmonary gas exchange dur ing Escherichia coli bacteremia. Design: Prospective, controlled study with open-label assignment of animals to two groups. Setting. Laborat ory. Subjects. Goehingen minipigs. Interventions. Induction of acute r espiratory failure by a 4-hr infusion of live E. coli bacteria in 12 a nimals; six animals anesthetized with methohexital/piritramide; six an imals anesthetized with isoflurane. The control group consisted of fou r animals that received the same surgical procedure, but no E. coli in fusion. Two animals were anesthetized with methohexital/piritramide an d two with isoflurane, respectively. Measurements and Main Results: Ca rdiac output and pressures were measured by means of an arterial cathe ter, Swan-Ganz catheter, and a left atrial catheter. Effective pulmona ry capillary pressure was evaluated graphically from a pulmonary arter y occlusion pressure decay. Arterial-alveolar PO2 ratio was calculated to evaluate pulmonary function. Measurements were performed before an d after 1, 2, and 3.5 hrs of E. coli infusion. Statistical significanc e was tested with analysis of variance (ANOVA). E. coli infusion cause d hypodynamic shock, an increase in pre- and postcapillary pulmonary v ascular resistance and respiratory failure. Post-capillary pressure gr adient and effective pulmonary capillary pressure were lower in the is oflurane-group. Methohexital-anesthetized animals developed pulmonary dysfunction after 1 hr of bacteremia, whereas isoflurane-anesthetized animals developed pulmonary dysfunction after 3.5 hrs of E. coli infus ion (significantly different, ANOVA, p < .05). There were no significa nt changes in the sham group. Conculsions: Isoflurane is a pulmonary v enodilator. During lethal E. coli infusion, it ameliorates the increas e in pulmonary capillary pressure and preserves pulmonary function unt il vascular permeability increases.