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[Changes in several indices of gas exchange in dogs during the initial stage of Cannon's traumatic shock].

In experiments reproducing traumatic shock according to Cannon on 35 dogs it was shown that metabolic acidosis developed in shock against the background of sharply elevated oxgen consumption at the very beginning of injury, when the arterial pressure exceeds considerably the inital level. In traumatic shock the brain is under the most favourable conditions of gas exchange and the skeletal musculature of the extremities--under the worst ones. It was concluded that in severe trauma, despite the strain of respiratory and cardiovascular system function the tissues of the brain and the skeletal muscles failed to obtain an adequate O2 quantity because of their sharply increases needs in oxygen, as well as of hemodynamic disturbances.

Acid-Base Equilibrium

Protective actions of aprotinin in acute traumatic shock.

The effect of the protease inhibitor, aprotinin, was examined in rats during traumatic shock. In sham-operated control rats, intravenous administration of aprotinin (20,000 or 40,000 KIU/kg) showed no immediate changes in the mean arterial blood pressure and heart rate. In rats subjected to Noble-Collip drum trauma, aprotinin at a dose of 20,000 KIU/kg prolonged survival time to 2.1 +/- 0.3 hr (p less than 0.05) and 40,000 KIU/kg prolonged the survival time of rats to a greater extent (3.1 +/- 0.4 hr, p less than 0.001) compared to rats given only its vehicle (1.1 +/- 0.2 hr, mean +/- SE). The improved survival was accompanied by inhibition of the plasma accumulation of the cardiotoxic peptide, myocardial depressant factor (MDF). However, aprotinin showed no inhibitory effect on the plasma accumulation of the lysosomal enzyme, cathepsin D. Aprotinin has a beneficial effect on traumatic shock in rats possibly by its potent inhibitory action on MDF formation.

Animals