PULMONARY SUBPLEURAL ARTERIOLAR DIAMETERS DURING INTESTINAL ISCHEMIA-REPERFUSION

Citation
Mb. Carter et al., PULMONARY SUBPLEURAL ARTERIOLAR DIAMETERS DURING INTESTINAL ISCHEMIA-REPERFUSION, The Journal of surgical research, 59(1), 1995, pp. 51-58
Citations number
41
Categorie Soggetti
Surgery
ISSN journal
00224804
Volume
59
Issue
1
Year of publication
1995
Pages
51 - 58
Database
ISI
SICI code
0022-4804(1995)59:1<51:PSADDI>2.0.ZU;2-S
Abstract
Adult respiratory distress syndrome (ARDS) often occurs in response to sepsis, shock, or ischemia/reperfusion (I/R) of a remote organ and is a frequent cause of mortality in the ICU patient. Pulmonary vascular resistance (PVR) increases during ARDS, yet direct observations of the pulmonary microcirculation are needed to characterize the vascular re sponse. The purpose of this study was to quantitate the changes in hem odynamic variables, subpleural arteriolar diameters (AD), and alveolar cross-sectional areas (ACSA) during intestinal I/R-induced lung injur y in rats, using a new method of in vivo videomicroscopy. Sprague-Dawl ey rats were anesthetized and cannulated, and superior mesenteric arte ries were looped. A thoracotomy was performed with animals ventilated with air with 1 cm PEEP. Hemodynamic and videomicroscopic data were ob tained before and during 45 min of SMA occlusion and after reperfusion , up to 120 min. Maximal vessel dilation was measured using topical 10 (-6) M nitroprusside. The ability of vessels to constrict was confirme d by applying topical 10(-6) M endothelin-1. Intestinal I/R produced d ecreases in arterial pH, mean arterial pressure, and cardiac output. D espite these alterations, subpleural AD remained maximally dilated. Ar terioles maintained the ability to constrict as demonstrated by the re sponse to topical endothelin-1. ACSA did not change, indicating a unif orm inflation of the lung. Using a unique method of in vivo pulmonary videomicroscopy, we have shown that AD do not change following 120 min of intestinal I/R, despite systemic hemodynamic instability. It appea rs that pulmonary arteriolar vasoconstriction does not contribute to i ncreased PVR during the early phase of lung injury. (C) 1995 Academic Press, Inc.