Research in veterinary science
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The effect of inhaling nitric oxide in the hypoxic pulmonary vascular response was measured in five calves anaesthetised with a combination of guaiacol, ketamine and xylazine. Alveolar hypoxia was induced by means of the inhalation of a gas mixture with an inspiratory oxygen fraction of 14-18 per cent. This alveolar hypoxia resulted in a pronounced pulmonary hypertension (mean pulmonary artery pressure in hypoxic animals: 30.2 mmHg). ⋯ A concentration of 40 ppm of nitric oxide fully abolished the hypoxia induced pulmonary hypertension (mean pulmonary artery pressure during inhalation of 40 ppm nitric oxide: 22.8 mmHg). Inhalation of nitric oxide had no effect on systemic arterial blood pressure nor on systemic vascular resistance. It was concluded that inhalation of 20 or 40 ppm of nitric oxide prevented a selective pulmonary vasoconstriction during alveolar hypoxia in calves, which may be helpful in the treatment of acute respiratory disorders in calves.
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Comparative Study
Cardiopulmonary effects of sevoflurane in cats: comparison with isoflurane, halothane, and enflurane.
The cardiopulmonary effects of sevoflurane (mean, 2.6, 3.8-3.9 and 5.2 per cent) were compared with those of halothane (1.2, 1.8 and 2.4 per cent), enflurane (2.4, 3.6 and 4.8 per cent) and isoflurane (1.6, 2.4 and 3.2-3.3 per cent) at end-tidal concentrations equivalent to 1, 1.5 and 2 minimal alveolar concentrations (MACs) during spontaneous or controlled ventilation (SV or CV) in 57 cats. Cats were assigned to four groups of nine animals each in SV trial and four groups of five or six animals each in CV trial. ⋯ During SV and CV, four anaesthetics decreased heart rate at 2 MAC when compared with control values, but there was no significant difference between anaesthetics. Sevoflurane, like halothane and isoflurane, induced hypotension at 2 MAC when compared with 1 MAC.
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Comparative Study
A pharmacodynamic study of propofol or propofol and ketamine infusions in ponies undergoing surgery.
The pharmacodynamics of infusions of propofol alone (group 1) were compared with the pharmacodynamics of infusions of propofol and ketamine together (group 2) in eight ponies undergoing castration. Anaesthesia was induced with detomidine, 20 micrograms kg-1, followed by ketamine, 2.2 mg kg-1. ⋯ Arterial hypotension and marked respiratory depression were evident in some of the ponies receiving propofol alone, whereas in the ponies anaesthetised with propofol and ketamine, respiratory and cardiovascular parameters were well maintained. All the ponies in both groups recovered quickly from anaesthesia, with mean times to sternal recumbency and standing of 19.8 (8.0) minutes and 27.2 (7.4) minutes respectively for group 1 and 8.4 (3.2) min and 14.9 (10.1) minutes for group 2.
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The pharmacokinetics of propofol and ketamine administered together by infusion were investigated in four ponies. Blood propofol and plasma ketamine and norketamine concentrations were measured by high performance liquid chromatography. After premedication with detomidine (20 micrograms kg-1) anaesthesia was induced with ketamine (2.2 mg kg-1 intravenously). ⋯ Norketamine, the main metabolite of ketamine, was detected throughout the sampling period. The mean residence time for norketamine was 144 (16) minutes. All the ponies recovered quickly from the anaesthesia; the mean times to sternal recumbency and standing were 11.1 (5.3) and 30.0 (20.8) minutes, respectively, from the end of the infusion.
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Observations were made on horses spontaneously breathing oxygen, with halothane at a constant end tidal concentration. The horses were positioned in dorsal recumbency for the first 45 minutes of each anaesthetic episode during which the arterial oxygen tension (PaO2) was found to peak and then decline. The remaining 60 minutes of each anaesthesia was used to test the effect of various manoeuvres on PaO2. ⋯ In contrast, placing the horses in sternal recumbency for these remaining 60 minutes caused the PaO2 to rise rapidly providing evidence for redistribution of ventilation. Replacing some inspired oxygen with less absorbable nitrogen did not improve PaO2 in dorsal recumbency. Thus there was no evidence that the low PaO2 of dorsal recumbency was associated with alveoli that had collapsed because of gas absorption.