Woodman O L, Vatner S F
J Pharmacol Exp Ther. 1986 Apr;237(1):86-91.
Hemodynamic responses to the selective stimulation of alpha-1 and alpha-2 adrenoceptors were examined in chronically instrumented, conscious dogs. Norepinephrine (0.02-0.1 micrograms/kg/min), a mixed alpha-1/alpha-2 adrenoceptor agonist, phenylephrine (0.2-1.0 micrograms/kg/min), a selective alpha-adrenoceptor agonist and B-HT 920 (0.5-2.0 micrograms/kg/min), a selective alpha-2 adrenoceptor agonist, were infused i.v. after ganglionic (hexamethonium, 30 mg/kg i.v.), beta adrenoceptor (propranolol, 1, mg/kg i.v.) and muscarinic receptor (atropine methylbromide, 0.1 mg/kg i.v.) antagonism. Each of the alpha adrenoceptor agonists increased mean arterial pressure and total peripheral resistance but had no significant effect on cardiac output, stroke volume or heart rate. Equipressor doses of the alpha adrenoceptor agonists caused similar increases in left ventricular systolic and end-diastolic pressure, but there were no significant changes in left ventricular dP/dt or heart rate with any of the alpha adrenoceptor agonists. Selective antagonism of alpha-1 adrenoceptors with prazosin (1 mg/kg i.v.) abolished the pressor and vasoconstrictor responses to phenylephrine but had a lesser effect on the response to B-HT 920. Antagonism of alpha-2 adrenoceptors with rauwolscine (0.1 mg/kg i.v.) caused a significantly greater attenuation of the pressor and vasoconstrictor responses to B-HT 920 than to phenylephrine. The responses to norepinephrine were significantly attenuated by antagonism of either alpha-1 or alpha-2 adrenoceptors. Thus, in the conscious dog with reflex pathways blocked, selective stimulation of either postsynaptic alpha-1 or alpha-2 adrenoceptors increases arterial pressure and total peripheral resistance but does not significantly change heart rate, left ventricular dP/dt, stroke volume or cardiac output.
在长期植入仪器的清醒犬中，研究了对α-1和α-2肾上腺素能受体选择性刺激的血流动力学反应。静脉注射去甲肾上腺素（0.02 - 0.1微克/千克/分钟），一种α-1/α-2肾上腺素能受体混合激动剂，苯肾上腺素（0.2 - 1.0微克/千克/分钟），一种选择性α-肾上腺素能受体激动剂，以及B-HT 920（0.5 - 2.0微克/千克/分钟），一种选择性α-2肾上腺素能受体激动剂，在进行神经节（六甲铵，静脉注射30毫克/千克）、β肾上腺素能受体（普萘洛尔，静脉注射1毫克/千克）和毒蕈碱受体（甲基溴化阿托品，静脉注射0.1毫克/千克）拮抗之后。每种α肾上腺素能受体激动剂均增加平均动脉压和总外周阻力，但对心输出量、每搏量或心率无显著影响。α肾上腺素能受体激动剂的等压剂量导致左心室收缩压和舒张末期压力有相似的升高，但任何一种α肾上腺素能受体激动剂对左心室dp/dt或心率均无显著变化。用哌唑嗪（静脉注射1毫克/千克）选择性拮抗α-1肾上腺素能受体消除了对苯肾上腺素的升压和血管收缩反应，但对B-HT 920的反应影响较小。用萝芙木碱（静脉注射0.1毫克/千克）拮抗α-2肾上腺素能受体导致对B-HT 920的升压和血管收缩反应的衰减比对苯肾上腺素的衰减显著更大。对去甲肾上腺素的反应在拮抗α-1或α-2肾上腺素能受体后均显著减弱。因此，在反射通路被阻断的清醒犬中，选择性刺激突触后α-1或α-2肾上腺素能受体可增加动脉压和总外周阻力，但不会显著改变心率、左心室dp/dt、每搏量或心输出量。
