Imad H. Abdul-Rasool

Ventilatory effects of dexmedetomidine, atipamezole, and isoflurane in dogs.

Dexmedetomidine (DMED) is a novel alpha 2 adrenergic agonist that has been shown to have potent analgesic and anesthetic sparing effects. This study was designed to investigate the effects of DMED, both alone and combined with isoflurane, on resting ventilation, the hypercapnic response, and the hypoxic response in dogs. When given alone, 1 microgram/kg decreased resting ventilation by 22% but at larger doses (10, 20, and 100 micrograms/kg) resting ventilation increased, doubling at 100 micrograms/kg. Doses of 10 micrograms/kg and greater caused a maximum depression of 60% in the slope of the hypercapnic response, but no dose had a significant effect on the hypoxic ventilatory response. A dose of 3 micrograms/kg of DMED reduced isoflurane MAC from 1.3% to 0.37%, and the ventilatory effects of this 1 MAC combination were intermediate between the awake values and those of isoflurane-anesthetized (1.3%) dogs. Atipamezole is a specific centrally acting alpha 2 receptor antagonist and when given with DMED in isoflurane-anesthetized dogs prevented the ventilatory depression. However, atipamezole alone also ventilatory stimulating effects, which may indicate tonic alpha 2 adrenergic activity. The ventilatory depression caused by DMED, either alone or combined with isoflurane, at doses that significantly reduce anesthetic requirements are relatively mild.

Cardiorespiratory and metabolic effects of dopamine and dobutamine infusions in dogs

The effects of iv dobutamine and dopamine infusions were studied at six incremental doses (range 5 to 160 micrograms/kg.min) in two groups of five dogs. Dobutamine decreased the systemic vascular resistance (SVR), without significant changes in mean arterial pressure (MAP), or pulmonary vascular resistance (PVR). Dopamine increased MAP, SVR, and PVR, except for a decrease at 10 micrograms/kg.min. Both drugs produced dose-related increases in cardiac output and venous admixture; however, with dopamine the dose-response curve reached a plateau at doses greater than 40 micrograms/kg.min. While the oxygen consumption (VO2) increased progressively in both groups, the oxygen availability ratio (DO2/VO2) and arteriovenous oxygen content difference (CaO2 - CvO2) were maintained mainly by increased cardiac output in the dobutamine group and hemoglobin concentration in the dopamine group. Thirty minutes after termination of drug infusions, the DO2/VO2 dropped, and CaO2 - CvO2 increased significantly in both groups. These changes were mainly due to sustained high VO2; however, in the dopamine group, a larger imbalance resulted from further decreases in cardiac output to levels below the control value.

Ventilatory and cardiovascular responses to sufentanil infusion in dogs anesthetized with isoflurane

The Ventilatory and hemodynamic responses to hypoxia, hyperoxia, and hypercapnia before and during sufentanil infusion were studied in 16 chronically tracheostornized dogs anesthetized with two concentrations, 1 and 0.5 minimal alveolar concentration (MAC) of isoflurane. Sufentanil was infused at a rate to obtain a constant end-tidal carbon dioxide (PETCO2) of ∼50 mm Hg for each isoflurane level. Before the sufentanil infusion, the PETCO2 was increased to 50 mm Hg by adding CO2 to the inspired gas, to allow comparisons at isocapnic conditions. Sufentanil caused only minor hemodynamic changes but significantly reduced ventilation during both levels of isoflurane. The Ventilatory response to hypercapnia decreased substantially, but there were no significant alterations in the ventilatory response to hypoxia. After sufentanil infusion, hyperoxia caused a larger decrease in minute ventilation and caused apnea in four dogs. These results suggest that administering sufentanil during isoflurane anesthesia causes a reduction in the contribution of the central chemoreflexes to ventilatory drive and, consequently, a relative increase in the contribution from the peripheral chemoreflexes.

Effects of Enflurane on the Ventilatory Response to Increased Carbon Dioxide and Metabolic Rate in Dogs

Inhaled anesthetic agents cause a dose related ventilatory depression as evidenced by an increase in arterial PCO2 (PaCO2) and blunting of the ventilatory response to hypercapnia and hypoxia (Hirschman et al., 1977). Ventilation is also closely coupled to metabolic rate, resulting in regulation of PaCO2 in spite of changes in metabolic rate (Wasserman et al., 1986). This study investigates the effects of inhalational anesthetics on this coupling.