Sarifa Lakhdhir1, Nigel Caulkett2, Tanya Duke-Novakovski3, Murray Woodbury4, Søren Boysen1. 1. Department of Veterinary Clinical and Diagnostic Sciences, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada. 2. Department of Veterinary Clinical and Diagnostic Sciences, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada. Electronic address: nacaulke@ucalgary.ca. 3. Department of Small Animal Clinical Sciences, Western College of Veterinary Medicine, Saskatoon, SK, Canada. 4. Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, Saskatoon, SK, Canada.
Abstract
OBJECTIVE: In ungulates, α2-adrenergic agonists can decrease oxygenation possibly through alteration of pulmonary perfusion. Sodium nitroprusside can decrease pulmonary vascular resistance (PVR) and increase cardiac output (Q˙t) through vasodilation. The objective was to determine if sodium nitroprusside would improve pulmonary perfusion and attenuate the increased alveolar-arterial (a-a) gradient resulting from medetomidine-azaperone-alfaxalone (MAA) administration. STUDY DESIGN: Prospective, randomized, crossover study with a 2 week rest period. ANIMALS: A group of eight adult female captive white-tailed deer (Odocoileus virginianus). METHODS: Deer were administered MAA intramuscularly (IM), and auricular artery and pulmonary artery balloon catheters were placed. Deer spontaneously breathed air. Saline or sodium nitroprusside (0.07 mg kg-1) were administered IM 40 minutes after MAA injection. Heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), pulmonary artery occlusion pressure (PAOP), right atrial pressure (RAP), Q˙t, arterial pH, PaCO2 and PaO2 were obtained immediately before nitroprusside injection (baseline) and 5, 10 and 15 minutes afterwards. Mixed venous blood samples were obtained at baseline and at 5 minutes. Systemic vascular resistance (SVR), PVR, intrapulmonary shunt fraction (Qs˙Qt˙), a-a gradient, oxygen delivery (D˙O2) and oxygen extraction ratio (O2ER) were calculated. Statistical analysis was performed with repeated measures analysis of variance with correction factors. A p value < 0.05 was considered significant. RESULTS: With nitroprusside, MAP, MPAP, PAOP, RAP, SVR and O2ER significantly decreased and HR, Q˙t and D˙O2 increased compared with baseline and between treatments. There was a significant decrease in PVR and a-a gradient and increase in PaO2 compared with baseline and saline treatment. Changes were not sustained. CONCLUSIONS AND CLINICAL RELEVANCE: Nitroprusside temporarily changed hemodynamic variables, increased PaO2 and decreased a-a gradient. Nitroprusside possibly led to better pulmonary perfusion of ventilated alveoli. However, IM nitroprusside at this dose is not recommended because of severe systemic hypotension and short action.
OBJECTIVE: In ungulates, α2-adrenergic agonists can decrease oxygenation possibly through alteration of pulmonary perfusion. Sodium nitroprusside can decrease pulmonary vascular resistance (PVR) and increase cardiac output (Q˙t) through vasodilation. The objective was to determine if sodium nitroprusside would improve pulmonary perfusion and attenuate the increased alveolar-arterial (a-a) gradient resulting from medetomidine-azaperone-alfaxalone (MAA) administration. STUDY DESIGN: Prospective, randomized, crossover study with a 2 week rest period. ANIMALS: A group of eight adult female captive white-tailed deer (Odocoileus virginianus). METHODS: Deer were administered MAA intramuscularly (IM), and auricular artery and pulmonary artery balloon catheters were placed. Deer spontaneously breathed air. Saline or sodium nitroprusside (0.07 mg kg-1) were administered IM 40 minutes after MAA injection. Heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), pulmonary artery occlusion pressure (PAOP), right atrial pressure (RAP), Q˙t, arterial pH, PaCO2 and PaO2 were obtained immediately before nitroprusside injection (baseline) and 5, 10 and 15 minutes afterwards. Mixed venous blood samples were obtained at baseline and at 5 minutes. Systemic vascular resistance (SVR), PVR, intrapulmonary shunt fraction (Qs˙Qt˙), a-a gradient, oxygen delivery (D˙O2) and oxygen extraction ratio (O2ER) were calculated. Statistical analysis was performed with repeated measures analysis of variance with correction factors. A p value < 0.05 was considered significant. RESULTS: With nitroprusside, MAP, MPAP, PAOP, RAP, SVR and O2ER significantly decreased and HR, Q˙t and D˙O2 increased compared with baseline and between treatments. There was a significant decrease in PVR and a-a gradient and increase in PaO2 compared with baseline and saline treatment. Changes were not sustained. CONCLUSIONS AND CLINICAL RELEVANCE: Nitroprusside temporarily changed hemodynamic variables, increased PaO2 and decreased a-a gradient. Nitroprusside possibly led to better pulmonary perfusion of ventilated alveoli. However, IM nitroprusside at this dose is not recommended because of severe systemic hypotension and short action.