Effects of lung recruitment maneuvers on splanchnic organ perfusion during endotoxin-induced pulmonary arterial hypertension.
Lung recruitment maneuvers (RMs), used to reopen atelectatic lung units and to improve oxygenation during mechanical ventilation, may result in hemodynamic impairment. We hypothesize that pulmonary arterial hypertension aggravates the consequences of RMs in the splanchnic circulation. Twelve anesthetized pigs underwent laparotomy and prolonged postoperative ventilation. Systemic, regional, and organ blood flows were monitored. After 6 h (= baseline), a recruitment maneuver was performed with sustained inflation of the lungs. Thereafter, the pigs were randomly assigned to group C (control, n = 6) or group E with endotoxin-induced pulmonary arterial hypertension (n = 6). Endotoxemia resulted in a normotensive and hyperdynamic state and a deterioration of the oxygenation index by 33%. The RM was then repeated in both groups. Pulmonary artery pressure increased during lipopolysaccharide infusion from 17 ± 2 mmHg (mean ± SD) to 31 ± 10 mmHg and remained unchanged in controls (P < 0.05). During endotoxemia, RM decreased aortic pulse pressure from 37 ± 14 mmHg to 27 ± 13 mmHg (mean ± SD, P = 0.024). The blood flows of the renal artery, hepatic artery, celiac trunk, superior mesenteric artery, and portal vein decreased to 71% ± 21%, 69% ± 20%, 76% ± 16%, 79% ± 18%, and 81% ± 12%, respectively, of baseline flows before RM (P < 0.05 all). Organ perfusion of kidney cortex, kidney medulla, liver, and jejunal mucosa in group E decreased to 65% ± 19%, 77% ± 13%, 66% ± 26%, and 71% ± 12%, respectively, of baseline flows (P < 0.05 all). The corresponding recovery to at least 90% of baseline regional blood flow and organ perfusion lasted 1 to 5 min. Importantly, the decreases in regional blood flows and organ perfusion and the time to recovery of these flows did not differ from the controls. In conclusion, lipopolysaccharide-induced pulmonary arterial hypertension does not aggravate the RM-induced significant but short-lasting decreases in systemic, regional, and organ blood flows.
Daudel
Fritz
F
Department of Intensive Care Medicine, Inselspital, Bern University Hospital, Bern, Switzerland. fritz.daudel@insel.ch
Gorrasi
José
J
Bracht
Hendrik
H
Brandt
Sebastian
S
Krejci
Vladimir
V
Jakob
Stephan M
SM
Takala
Jukka
J
Rothen
Hans Ulrich
HU
D000768:Anesthesia, General; D000818:Animals; D002302:Cardiac Output; D019446:Endotoxemia / Q000150:complications / Q000503:physiopathology*; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology*; D007327:Insufflation; D017078:Laser-Doppler Flowmetry; D008070:Lipopolysaccharides / Q000633:toxicity; D008102:Liver Circulation; D008833:Microcirculation; D011175:Positive-Pressure Respiration; D001261:Pulmonary Atelectasis / Q000503:physiopathology / Q000628:therapy*; D011897:Random Allocation; D012079:Renal Circulation; D012129:Respiratory Function Tests; D013152:Splanchnic Circulation / Q000502:physiology*; D034421:Sus scrofa; D013552:Swine
D008070:Lipopolysaccharides; C440499:lipopolysaccharide, Escherichia coli O111 B4