Ten dogs were studied to determine the effects of xylazine, ketamine, and xylazine combined with ketamine on the dosage of epinephrine required to produce ventricular arrhythmia. Untreated dogs required an arrhythmogenic dose (AD) of 5.88 +/- 2.85 micrograms/kg/min. The AD was 4.28 +/- 3.25 micrograms/kg/min in xylazine-treated dogs, 3.05 +/- 2.3 micrograms/kg/min in ketamine-treated dogs, and 2.96 +/- 1.95 micrograms/kg/min in xylazine/ketamine-treated dogs. The latter two dosages were significantly less than that of the controls (p less than 0.025). The duration of increased arrhythmogenicity was also examined. Four hours after drug administration, the AD for xylazine-treated dogs was decreased further to 3.87 +/- 2.52 micrograms/kg/min (p less than 0.05). Ketamine-treated dogs had returned partially to normal with an AD of 4.09 +/- 3.09 micrograms/kg/min, as had xylazine/ketamine-treated dogs, at 4.22 +/- 2.71 micrograms/kg/min.

Analysis of Variance↗

PubMedDate not supplied

Hemodynamic function during neurectomy in halothane-anesthetized horses with or without constant dose detomidine infusion.

Nine horses were premediated with acepromazine, and anesthesia was induced with guaifenesin and thiamylal. Anesthesia was maintained in four horses with halothane in oxygen, and in five horses with halothane in oxygen plus a constant dose infusion of detomidine. Both maintenance regimens produced a MAC equivalent of 1.4 at the ambient barometric pressure. Hemodynamic and respiratory measurements were made after the horses were anesthetized, during surgical manipulations involving skin or tissues other than nerves, during manipulation and transection of digital nerves, and after surgery while the limbs were being bandaged. Heart rate was significantly higher in horses anesthetized with halothane only than in horses that also received detomidine; there were no other differences in hemodynamic function or recovery characteristics. Respiratory rate was significantly higher than baseline during soft tissue and nerve manipulations; arterial blood pressure was significantly higher after surgery began and highest during neurectomy; cardiac output and cardiac index were significantly decreased during surgery; systemic vascular resistance was significantly increased during neurectomy and bandaging and highest during neurectomy. The data suggest that the increase in blood pressure often associated with surgical stimulation is caused by increased vascular resistance and may be accompanied by a decrease in cardiac output.

Analgesics↗

PubMedDate not supplied

Cell mediated immunity in experimental influenza and parainfluenza infection.

Cell mediated immunity (CMI) to Sendai and Kunz viruses, determined by a 51Cr release assay of cytotoxicity, has been shown to develop during the course of these infections. This virus specific response is mediated by sensitised T cells, and takes place against a background of innate cell mediated immunity. The mediator of this innate cytotoxicity exhibits none of the characteristics of T, B or K cells, but bears close resemblance to the NK cell which is spontaneously cytotoxic for certain tumour cells. Removal of the virus specific CMI by T cell depletion produces a moderate immunosuppressive effect. The nature of this effect and the role of CMI in these infections are discussed.

Animals↗