By David R. Gross D.V.M., Ph.D. (auth.)
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Extra resources for Animal Models in Cardiovascular Research
No change in pulmonary artery blood gases. 8 mg/kg,IV cumulative dose using the above dose No change in any of the above parameters No change in heart rate, stroke volume, cardiac output, mean aortic pressure, mean pulmonary artery pressure, pulmonary arterial wedge pressure, mean right atrial pressure, systemic or pulmonary arterial resistance o•3 mg/kg, IV Slight alterations in cardiovascular dynamics which can be blocked by prior administration of atropine. 8rng/kg, IV Same Decreased heart rate and cardiac output with increase in resistance.
This all results in abnormalities in cardiac muscle growth and differentiation 49 Delays in normal maturational design of the brain and heart ornithine decarboxylase activity from puppies of treated mothers 49 48 output, mean systemic and Decreased heart rate, cardiac aortic pressure and increases in pu~onary vascular resistance No hemodynamic data - led to retardation of heart growth in offspring. 33 Horses 1 X 10-5 to 1 X 1O-4M Isolated rat aortic strip preparations of sympa- The heart rate increased at 5 and 15 min.
Occas. 1 mg dose imuced an increased chronotropic response followed by a decrease. Did not prevent effects of vagal stimulation or of ACH injected into the SA nodal artery Measured evoked tension, dose-dependent depression of contractile response to transmural electrical stimulation. Contractile response to norepinephrine not affected. 0 . 2 mg/kg every 1-2 hrs. Paralyzed with gallamine triethiodide (3mg/kg, IV) positive pressure ventilation provided. 1 mg/kg,OC Same as above but not "debuffered" Recammemed analgesic dose - cats are not able to eliminate morphine by glyceronimation, this can result in increased sensitivity and toxicity 2 16 6 cats treated, 1 showed no changes, 5 had an initial increase in aortic blood pressure followed by a decrease.
Animal Models in Cardiovascular Research by David R. Gross D.V.M., Ph.D. (auth.)