EFFECTS OF AMYL NITRITE ON CIRCULATION, RESPIRATION AND BLOOD HOMOEOSTASIS IN CYANIDE POISONING
EFFECTS OF AMYL NITRITE ON CIRCULATION, RESPIRATION AND BLOOD HOMOEOSTASIS IN CYANIDE POISONING
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DOI：
10.1007/bf00570134
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发表时间：
1988-09-01
影响因子：
6.1
通讯作者：
KRETTEK, C
中科院分区：
文献类型：
--
作者：
KLIMMEK, R;KRETTEK, C
静脉内（i. v.）给药或吸入亚硝酸戊酯（AN）后，在氯醛糖麻醉下，在完整的和氰化物中毒，自主呼吸的比格犬。静脉注射AN的剂量为0.03和0.15 mmol/kg，静脉注射KCN的剂量为0.06 mmol/kg。AN吸入在一个封闭的系统中，在0.15 mmol/kg，没有以前的中毒，此外，在人工通气期间，在0.074 mmol/kg（两个安瓿在0.3 ml AN）中毒后，与0.045 mmol KCN/kg静脉注射。静脉注射AN后，平均动脉压分别下降15和40 mmHg，与心动过缓和外周血流量降低相关。随着剂量的增加，每分钟呼吸量增加了65%。动脉pO 2降低20 mmHg，而pCO 2升高6 mmHg。在注射后30分钟内，这些变化仅部分可逆。在封闭系统中吸入AN后获得了类似的结果。乳酸酸中毒和pH值降低是通过静脉途径产生的，而不是通过吸入产生的。总血红蛋白升高。KCN的致死性在产生10-30%铁血红蛋白的AN剂量下被消除。人工通气和同时吸入硝酸铵中毒后，致命剂量的KCN被证明是无效的治疗措施。并与氰化物中毒和AN的研究结果进行了比较。据指出，目前，没有实验证据的另一个解毒机制的行动AN比铁血红蛋白的形成。
The effects of intravenously (i.v.) administered or inhaled amyl nitrite (AN) were followed under chloralose anaesthesia in intact and cyanide-poisoned, spontaneously breathing beagles. The i.v. doses of AN were 0.03 and 0.15 mmol/kg and the i.v. dose of KCN was 0.06 mmol/kg. AN was inhaled in a closed system at 0.15 mmol/kg without previous poisoning and, in addition, at 0.074 mmol/kg (two ampoules at 0.3 ml AN) during artificial ventilation after poisoning with 0.045 mmol KCN/kg i.v.. Mean arterial pressure decreased by 15 and 40 mmHg, respectively, after i.v. injection of AN, associated with bradycardia and lowered peripheral blood flow. Respiratory minute volume rose by 65% with the higher dose. Arterial pO2 decreased by 20 mmHg while pCO2 rose by 6 mmHg. Within 30 min of injection, these changes were only partially reversible. Similar results were obtained following inhalation of AN in a closed system. Lactic acidosis and lowering of pH were produced by the i.v. route, but not by inhalation. Total haemoglobin increased. The lethality of KCN was abolished with AN doses that produced 10-30% ferrihaemoglobin. Artificial ventilation and simultaneous inhalation of AN after poisoning with lethal doses of KCN turned out to be ineffective therapeutic measures. The findings are compared with those of other papers dealing with cyanide poisoning and AN. It is pointed out that, for the present, there is no experimental proof for another antidotal mechanism of action of AN than ferrihaemoglobin formation.