Effects of sodium nitroprusside after load reduction and/or atropine pre-treatment prior to dexmedetomidine administration on cardiovascular variables in dogs

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The purpose of this study was to determine the cardiovascular effects of sodium nitroprusside (SNP)-induced after load reduction in dogs administered dexmedetomidine (DEX). Using a randomized crossover design and allowing at least 2 weeks between treatments 12 adult hound dogs of either sex weighing 22 ± 1.7 SD kg were anesthetized by face mask administration of 2.9% ET sevoflurane to facilitate instrumentation prior to administration of treatment drugs. Dogs were intubated and instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP) and diastolic (DAP) arterial pressures, mean pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), and cardiac output (CO). Systemic (SVR) and pulmonary vascular resistances were calculated. Following completion of instrumentation dogs were allowed to recover for 40 minutes. After collection of baseline data, dogs were administered one of four treatments at T–10 minutes prior to injection of DEX (500? g M–2 IM): 1) saline (SAL); 2) atropine (ATR, 0.02 [n = 6] or 0.04 [n = 6] mg kg–1 IM); 3) SAL + SNP (infused at 1–10 ?g kg–1 minute–1, IV as needed to maintain MAP between 90–110 mm Hg; or 4) ATR + SNP. Cardiovascular data were collected at T-20 minutes prior to administration of DEX, T-5 and at 5, 10, 20, 30, 40, and 60 minutes following DEX. Data were analyzed using anovafor repeated measures with post hoc differences between means identified using Bonferroni's method (p < 0.05). Differences in ATR dose were not found to be significant and thus results for ATR dose groups were pooled. Administration of SAL (dexmedetomidine alone) was associated with decreases in HR and CO and increases in SAP, MAP, DAP, CVP, and SVR. Administration of ATR was associated with an increase in HR and CO compared with SAL. Administration of SNP was associated with an increase in HR and CO and a decrease in SVR, MAP and CVP compared with SAL. Administration of SNP + ATR was associated with effects similar to that of SNP or ATR alone and resulted in an additive increase in CO. We conclude that SNP-induced afterload reduction with or without atropine is effective in mitigating DEX-induced impairment of cardiovascular function.