Itabisashi T
Natl Inst Anim Health Q (Tokyo). 1977 Winter;17(4):151-62.
Changes in electrocardiograms, blood pressure, pH, and partial pressure of gases (Po2 and Pco2) in arterial blood were studied in goats poisoned by urea or ammonium compounds under spontaneous and artificial respiration and in nonconvulsive state. Abnormal electrocardiogram patterns, such as ventricular flutter, ventricular premature beat, atrioventricular dissociation, depression of ST-segment and sinus tachycardia, were all observed after the occurrence of tetanic convulsion. The electrocardiogram pattern seen at the respiratory arrest showed sinus or supraventricular tachycardia; respiratory arrest preceded cardiac arrest in all the goats, but one. Blood pressure was markedly elevated, accompanied with tetanic convulsion. Po2 decreased gradually and the level was below 30 mm Hg (37.0 degrees C) at respiratory arrest and the final opisthotonus. Artificial respiration starting at the final opisthotonus could delay the cardiac arrest. Under nonconvulsive urea-poisoning with gallamine triethiodide and with artificial respiration of air or a mixture of air and oxygen to elevate the Po2 level, changes of electrocardiogram, blood pressure, and Po2 were similar to those seen under convulsive urea-poisoning. The main cause of death was discussed and presumed to be respiratory and cardiovascular failure.
对在自然呼吸和人工呼吸下处于非惊厥状态的尿素或铵化合物中毒山羊的心电图、血压、pH值以及动脉血气体分压（Po2和Pco2）变化进行了研究。在强直性惊厥发生后，均观察到异常心电图模式，如心室扑动、室性早搏、房室分离、ST段压低和窦性心动过速。呼吸停止时出现的心电图模式显示窦性或室上性心动过速；除一只山羊外，所有山羊的呼吸停止均先于心脏骤停。血压明显升高，并伴有强直性惊厥。Po2逐渐降低，在呼吸停止和最终角弓反张时水平低于30毫米汞柱（37.0摄氏度）。在最终角弓反张时开始人工呼吸可延迟心脏骤停。在使用三碘季铵酚的非惊厥性尿素中毒以及通过空气或空气与氧气的混合物进行人工呼吸以提高Po2水平的情况下，心电图、血压和Po2的变化与惊厥性尿素中毒时相似。对死亡的主要原因进行了讨论，并推测为呼吸和心血管衰竭。
