Bubien J K, Woods W T
Toxicon. 1987;25(3):325-31. doi: 10.1016/0041-0101(87)90261-3.
Intravenous injection of T-2 toxin or roridin-A (2 mg/kg) into pentobarbital-anesthetized (30 mg/kg) dogs produced, respectively, decreased systolic pressure within 30 min and atrio-ventricular block within 60 min. Within 45 +/- 15 min after injection of each toxin heart rate increased and remained elevated for at least 4 hr. The increase in sinus rate was reduced by 50% when dogs were pretreated with i.v. propranolol--HCl (5 mg/kg); pretreatment with atropine sulphate (5 mg/kg) did not alter the effect of the trichothecenes. Upon administration of T-2 toxin or roridin-A (30 mg/l) to isolated arterially perfused canine right atria, sinus rate decreased by 12% and 28%, respectively, and sinus node cell diastolic potentials became more negative by 7% and 10%, respectively. Sino-atrial block observed in 50% of the isolated atrial preparations perfused with roridin-A disappeared when toxin perfusion was discontinued. Perfusion with T-2 toxin or roridin-A produced no significant effects on atrial muscle cell action potentials. The cardiovascular response to systemic trichothecenes was hypotension followed by propranolol-sensitive tachycardia. The direct effects on conduction system cells may contribute to the overall deleterious action on the cardiovascular system.
给戊巴比妥麻醉（30毫克/千克）的犬静脉注射T-2毒素或罗里丹-A（2毫克/千克），分别在30分钟内导致收缩压下降，在60分钟内导致房室传导阻滞。在注射每种毒素后的45±15分钟内，心率增加并至少持续升高4小时。当犬静脉注射盐酸普萘洛尔（5毫克/千克）预处理时，窦性心率增加减少50%；硫酸阿托品（5毫克/千克）预处理并未改变单端孢霉烯族毒素的作用。给离体动脉灌注的犬右心房施用T-2毒素或罗里丹-A（30毫克/升）时，窦性心率分别降低12%和28%，窦房结细胞舒张电位分别变得更负7%和10%。在用罗里丹-A灌注的50%离体心房标本中观察到的窦房传导阻滞，在停止毒素灌注时消失。用T-2毒素或罗里丹-A灌注对心房肌细胞动作电位无显著影响。对全身性单端孢霉烯族毒素的心血管反应是低血压，随后是普萘洛尔敏感的心动过速。对传导系统细胞的直接作用可能导致对心血管系统的整体有害作用。
