IN VIVO CHANGES IN SYSTEMIC PCO2 AND PO2 INFLUENCE THE THROMBOEMBOLIC REACTION FOLLOWING WALL PUNCTURE IN VENULES BUT NOT IN ARTERIOLES
Changes in pH and PCO2 influence the aggregation of blood platelets in response to various agents in vitro. In the present study intravital video-microscopy was used to investigate whether changes in systemic blood gas values influence the thromboembolic reaction in vivo as induced by vessel wall injury.The microtrauma was induced by puncturing the walls of microvessels in the rabbit mesentery (diameter range: 20-40 μm) with glass micropipets (tip diameters: 6-8 μm). The thromboembolic reactions were compared in two groups of anesthetized rabbits. The control group was ventilated to keep the blood gas values within normal ranges (means: pH=7.40, pCO2=32.9 mmHg, pO2=104.7 mmHg). The experimental group breathed spontaneously (mean blood gas values: pH=7.34, pCO2=50.5 mmHg, pO2=48.1 mmHg). The pCO2 and pO2 values were significantly different between both groups.In arterioles and venules of both groups bleeding and thrombus formation started immediately following wall puncture. Bleeding times were short (medians between 1.0 and 2.6 s). Parts of the thrombi started to embolize between 11.4 and 18.2 s following wall puncture (medians). In the control group embolization continued for 101 s in the arterioles and 17 s in the venules; during these periods 6 and 1 emboli were produced, respectively (all median values). In the experimental group the duration of embolization in the arterioles was 143 s in which period 7.5 emboli were produced, values not significantly different from control. In the venules of the experimental group embolization and hence platelet reaction went on uninhibited during the whole observation period of 600 s and 30 emboli were produced. Fluid dynamic factors cannot explain the differences in thromboembolic reaction between the control and experimental venules; vessel diameters and red blood cell velocities were not significantly different between both groups. Therefore, it is likely that the change in thromboembolic reaction in the venules results from the changes in systemic PCO2 and/or pO2. The different reactions in arterioles and venules in response to the altered systemic blood gas values might arise from different reactions in the vessel walls.