RESUMO
Hypercapnia is not deliberately used nowadays even in the anesthetic management of carotid endarterectomy. Nevertheless, high PaCO2 level may occur during anesthetic procedures. Such altered carbon dioxide concentration trigger important changes in cardiovascular and renal function. This paper was designed to study some effects of hypercapnia upon the renal function in dogs. Twelve dogs fasted overnight were anesthetized with intravenous sodium pentobarbital (30 mg.kg elevado a menos um). The animals were intubated with a cuffed endotracheal tube, and ventilated with a takoaka respirator, using room air at the respiratory rate of 12 - 14 min elevado a menos um. Pancuronium bromide (0,08 mg.kg elevado a menos um) was injected to facilitate the ventilation. Cannulation of artery and vein was performed for blood sampling and fluid administration. In six dogs it was added CO2 to the room air at a concentration betwen 10 and 15 per cents. The following parameters were analized: mean arterial pressure (MAP), renal plasmatic flow (RPF), renal blood flow (RBF), glomerular filtration rate (GFR), urine output, carbon dioxide partial pressure (PaCO2), and oxygen partial pressure (PaO2). In the control group there was not any significant change in the analized parameters. In the group of dogs with high PaCO2 a MAP progressive decrease was observed from the begining of the experiment, that coned be explained by the direct action of CO2 on the peripheral vascular bed. The RBF values increased initially and decreased thereafter. This last result can be explained by the release of catecholamines due to hypercapnia, or by other factors such as interaction with the renin-angiotensin system, or acid-base imbalance. The decreased urinary output variedconversely to the PaCO2 remained unchanged throughout the experiment. This study shows that renal hemodynamic changes do not occur until PaCO2 level achieves 6,66 kPa (50 mm Hg). At the PaCO2 level of 9,33 kPa (70 mm Hg) slight elevation of the RPF and of the RBF is observed possibly due to the direct action of CO2 on the smooth muscles of the vessels. When 9,33 kPa is achieved, significant changes do occur in renal hemodynamics