The relationship of muscle perfusion and metabolism with cardiovascular variables before and after detomidine injection during propofol-ketamine anaesthesia in horses.

OBJECTIVES

To study in horses (1) the relationship between cardiovascular variables and muscle perfusion during propofol-ketamine anaesthesia, (2) the physiological effects of a single intravenous (IV) detomidine injection, (3) the metabolic response of muscle to anaesthesia, and (4) the effects of propofol-ketamine infusion on respiratory function.

STUDY DESIGN

Prospective experimental study.

ANIMALS

Seven standardbred trotters, 5-12 years old, 416-581 kg.

METHODS

Anaesthesia was induced with intravenous (IV) guaifenesin and propofol (2 mg kg) and maintained with a continuous IV infusion of propofol (0.15 mg kg minute) and ketamine (0.05 mg kg minute) with horses positioned in left lateral recumbency. After 1 hour, detomidine (0.01 mg kg) was administered IV and 40-50 minutes later anaesthesia was discontinued. Cardiovascular and respiratory variables (heart rate, cardiac output, systemic and pulmonary artery blood pressures, respiratory rate, tidal volume, and inspiratory and expiratory O and CO) and muscle temperature were measured at pre-determined times. Peripheral perfusion was measured continuously in the gluteal muscles and skin using laser Doppler flowmetry (LDF). Muscle biopsy samples from the left and right gluteal muscles were analysed for glycogen, creatine phosphate, creatine, adenine nucleotides, inosine monophosphate and lactate. Arterial blood was analysed for PO, PCO, pH, oxygen saturation and HCO. Mixed venous blood was analysed for PO, PCO, pH, oxygen saturation, HCO, cortisol, lactate, uric acid, hypoxanthine, xanthine, creatine kinase, creatinine, aspartate aminotransferase, electrolytes, total protein, haemoglobin, haematocrit and white blood cell count.

RESULTS

Circulatory function was preserved during propofol-ketamine anaesthesia. Detomidine caused profound hypertension and bradycardia and decreased cardiac output and muscle perfusion. Ten minutes after detomidine injection muscle perfusion had recovered to pre-injection levels, although heart rate and cardiac output had not. No difference in indices of muscle metabolism was found between dependent and independent muscles. Anaerobic muscle metabolism, indicated by decreased muscle and creatine phosphate levels was evident after anaesthesia.

CONCLUSION

Muscle perfusion was closely related to cardiac output but not arterial blood pressure. Total intravenous anaesthesia with propofol-ketamine deserves further study despite its respiratory depression effects, as the combination preserves cardiovascular function. Decreases in high-energy phosphate stores during recovery show that muscle is vulnerable after anaesthesia. Continued research is required to clarify the course of muscle metabolic events during recovery.