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. 1999 Nov 15;104(10):1421–1429. doi: 10.1172/JCI6590

Figure 3.

Figure 3

Change in fractional blood flow to the left lung (QLPA/QPA) 5 minutes after LMBO in wild-type mice (+/+) and NOS2-deficient mice (–/–) treated with saline (control, open bars; n = 7 each), endotoxin (endotoxin, closed bars; n = 6 each), or endotoxin with 5 mg/kg L-NIL intraperitoneally (endotoxin with L-NIL, striped bar; n = 5) 3 hours after the endotoxin challenge. (*P < 0.05, endotoxin versus control; ‡P < 0.01, wild-type versus NOS2-deficient; #P < 0.01 endotoxin + L-NIL versus endotoxin alone). Measurements were obtained following 1 hour after discontinuation of breathing air or 40 ppm NO in air for 22 h (§P < 0.05 NO versus without NO). Endotoxin challenge caused a marked reduction of pulmonary blood flow redistribution after LMBO in wild-type, but not in NOS2-deficient mice. After prolonged inhalation of 40 ppm NO, endotoxin-treated NOS2-deficient mice, measured 1 hour after discontinuation of NO inhalation, showed the same loss of HPV as endotoxin-treated wild-type mice. Saline-treated NOS2-deficient mice and wild-type mice breathing 40 ppm NO for 22 hours retained their ability to redistribute pulmonary blood flow after LMBO, when measured 1 hour after discontinuing NO inhalation.