The objective of this study was to determine the influence of
chinonin on acute hypoxic pulmonary vasoconstriction (HPV) in Sprague-Dawley (SD) rats and investigate its mechanism. Sixty-five SD rats were divided into five groups at random: six in the control group; six in the
hypoxia group; 13 in the group of
hypoxia with
chinonin; 20 in the group of
endothelin-1 (ET-1) with
chinonin and 20 in the group of
platelet activating factor (PAF) with
chinonin. Their mean pulmonary arterial pressures (mPAP) were measured and the concentration of molondialdehyde (MDA) in plasma and the activity of
phospholipase A2 (PLA2) of the lung tissues were detected. The PAF and ET-1 levels of plasma and lung homogenates were detected in the control and
hypoxia groups. There was evidence of an increase in mPAP, MDA, PAF and ET-1 in the plasma, and activity of PLA2, PAF and ET-1 of the lung tissues when the rats inhaled
a 10% mixture of
oxygen in
nitrogen. It appeared that
chinonin may have been inhibiting the action of ET-1 and PAF.
Chinonin could have prevented an increase in MPAP caused by
hypoxia and inhibited the action of ET-1 and PAF. But
chinonin had no influence on the increase in MDA in the plasma and the PLA2 activity of the lungs when
hypoxia occurred.
Chinonin can reduce HPV, but does not influence normal mPAP. It may do this by blocking the action of ET-1 and/or PAF or others. The definite mechanism needs to be studied further.