We investigated pulmonary microembolism (PME) produced in mongrel dogs (10-15kg) by barium sulfate (BaSO
4). These studies were attempted to clarify the regulatory mechanisms of vasoactive substances (histamine, serotonin and prostaglandins), and the effect of platelet aggregation on the PME-induced changes of pulmonary arterial pressure (P
PA) or pulmonary perfusion pressure (PPP).
The results obtained were as follows;
In rive:
1) Infusion of 30mg/kg of BaSO
4 suspension in saline (30%, 0.1ml/kg) into the right ventricle caused rapid increase of P
PA, which rose to a maximum (P
PA-max) after 10-20 seconds and returned gradually to the original level (baseline). The ratios of P
PA-max to the baseline obtained by repeated embolizations were almost linearly elevated (control study). The oxygen pressure of the femoral artery following embolization decreased to the minimum value after 30-40 seconds and rather promptly returned to the original value.
2) The embolism-induced changes of P
PA under minimal administration of heparin (no more than 500 units total dose) was significantly enhanced as compared with a control study under sufficient heparinization (800-1000units/kg).
In the excised lower lung lobe:
3) Barium sulfate suspension in saline (10%, 0.05ml/kg) was infused in the excised left lower lung lobe under constant perfusion (130-170ml/min) with autologous blood. After repeated injections of 5mg/kg (10%, 0.05ml/kg) of BaSO
4 into the circuit, the pulmonary perfusion pressure (PPP) rapidly rose to the peak value (PPP-max). The ratio of PPP-max to the haseline just prior to each embolization was almost constant (150%) (control study). The administration of anti-histamine (mepyramine maleate, 100μg/ml) and anti-sorotonin (methysergide: 100μg/ml, cyproheptadine: 30μg/ml) into the reservoir significantly inhibited the embolism- induced elevation of PPP.
4) By adding aspirin (1mg/ml) into the reservoir the PME-induced elevation of PPP increased significantly, as compared with control studies.
5) The same experimental procedures were done in thrombocytopenia by using anti-canine platelet rabbit antibody. Aspirin administration also enhanced the elevation of PPP induced by PME.
These results suggest that prostaglandins as well as histamine and/or serotonin may play important roles in acute changes of PPP, and that acute pulmonary hypertension may be attenuated by endogenous vasodilator prostaglandins in the lung or the pulmonary capillaries, since PME-induced elevation of PPP was enhanced by aspirin which is a biosynthesis inhibitor of prostaglandins.
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