Histamine and hypoxic pulmonary hypertension. A quantitative study

Hypoxia is the most effective and consistent stimulus to pulmonary hypertension in all species; however, the genesis of this phenomenon is still unclear. Histamine has been proposed as the possible mediator of this response and extensively studied. However, there remain doubts as to its behaviour in the different vascular districts during hypoxia. Accordingly, in seven dogs, histamine content was measured in the distal vena cava, hepatic vein, pulmonary artery and aorta; pulmonary artery pressure and systemic arterial pressure were also recorded. All measurements were repeated after 5 min of breathing a mixture containing 8% oxygen. Histamine content in the pulmonary artery blood was significantly increased during hypoxia (from 29±3 to 36±3 ng x cm -3 P<0.05) while it was unchanged in the aorta. Therefore, the difference between histamine content in the pulmonary artery and aorta increased. Moreover, the inferior vena cava content of this substance rose from 24±4 to 32±4 ng x cm -3(P<0.05) and it did not change in the hepatic vein. Simultaneously pulmonary artery pressure rose from 1.6±0.1 to 2.4±0.1 kPa (12±1 to 18± mmHg)(P<0.01) and systemic arterial pressure changed only slightly. These experiments seem to demonstrate that histamine is released by the muscle during hypoxia, since it is increased in the distal vena cava and uptake by the lungs, as shown by the increase in the pulmonary artery and aorta. The role, if there is any, of the muscle-released histamine in the hypoxic pulmonary hypertension is still to be elucidated.