Animal models in cardiovascular research by David R. Gross DVM, PhD (auth.)

By David R. Gross DVM, PhD (auth.)

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1 g/kg/min 4 mg/kg, IV Under these conditions, with the isoproterenol infusion, the heart rate, left ventricular dP/dt, cardiac index, stroke volume and aortic pressure all decreased. There was no change in systemic resistance or pulmonary arterial wedge pressure 13 Same as above with addition of 10 glkg, IV propranolol 15 mg/kg, IV Heart rate decreased but all other Reart parameters did not change. 1:1 Dogs Induction with thiopentone (10 mglkg, IV), 70% nitrous oxide, 30% oxygen 4 mglkg, mg/kg, IV Severe and rapid fall in peripheral perfusion as measured by skeletal muscle musc1e surface pH.

The initial decrease in resistance could be blocked by antihistamine or high doses of atropine, not blocked by propranolol or low doses of atropine. 123 Anesthetized with chloralose (90 mg/kg IV) S 5 Ilg/kg, IV Augmented bradycardia produced by electrical stimulation of carotid sinus nerves but no response to stimulation of the nucleus of the solitary tract (NTS) 124 Same 20 Ilg/kg, IV After bilateral destruction of NTS and cutting of afferent baroreceptor fibers caused marked decrease in heart rate and blood pressure.

In general, the opiods are reported to decrease preload, contractility, afterload and heart rate. 1 As a result cardiac output must also decrease. Actual reported cardiovascular responses to the various opiods do not always follow this scheme, especially in cats and horses, where the narcotic analgesics have repeatedly been reported to cause a paradoxical excitement and stimulation, usually as a result of central stimulation arising from ataxia. 1:1 Dogs Used as a preanesthetic. Onset of action within a few minutes following injection.

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