[Hypoxic pulmonary vasoconstriction following lung damage by xanthine oxidase--studies in rats].

The main reason for an insufficient oxygenation of the arterial blood during acute lung injury should be an increased shunt fraction. The aim of this study was to check if in this connection the magnitude of hypoxic pulmonary vasoconstriction is reduced--a fact, which could be causal involved in the arising of increased shunt fraction. 21 male rats were anaesthetized (pentobarbitone) and ventilated artificially (F1O2 = 0.6). In 10-minute-intervals hypoxia (F1O2 = 0.06) was applied. After the first hypoxic exposure the animals were divided into 4 groups according to the application of 3 U xanthine oxidase (XO) or 0.5 ml physiological saline (NaCl) intratracheally (i.t.) or intravascularly (i.v.)--group A: XO i.t.; group B: XO i.v.; group C.: NaCl i.t.; group D: NaCl i.v. At the end of each hypoxic or hyperoxic period (steady state) mean blood pressure in the right ventricle (Prv) and in the A. carotis communis (Psa) were measured. Then blood samples (100 microliters each) were drawn from the artery and the right ventricle and pH, PO2, PCO2, SO2 and hemoglobin concentration were determined. During hyperoxic conditions from the latter values we calculated the shunt fraction. Additional the lung-thorax compliance before and after the application was measured body plethysmographically. As an indirect measure of the reagibility of the pulmonary vasculature the increase of Prv during hypoxic exposure was considered. In the groups B, C and D no significant changes between the measured parameters before and after the application procedure could be observed.(ABSTRACT TRUNCATED AT 250 WORDS)