PubMed · 10550968
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C A Trant. 1999. Palpitations.. https://pubmed.ncbi.nlm.nih.gov/10550968/
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Clinical features on the first unexpected nerve gas terrorism using sarin (isopropyl methylphosphonofluoridate) on citizens in the city of Matsumoto is described. The nerve gas terrorism occurred at midnight on 27 June, 1994. About 600 people including residents and rescue staff were exposed to sarin gas. Fifty-eight victims were admitted to hospitals and seven died. Theoretically, sarin inhibits systemic acetylcholinesterase and damages all the autonomic transmission at the muscarinic and nicotinic acetylcholine receptor. Miosis was the most common finding in the affected people. In cases with severe poisoning, organophosphate may affect the central nervous system and cause cardiomyopathy. A few of the victims complained of arrhythmia and showed a decreased cardiac contraction. Abnormal electroencephalograms were recorded in two patients. The clinical features and follow-up studies are discussed with reference to the Tokyo subway terrorism and related articles.
BACKGROUND: Lysophosphatidylcholine (LPC), a naturally occurring phospholipid metabolite, accumulates in the ischemic heart and causes extracellular K(+) accumulation and action potential shortening. LPC has been incriminated as a biochemical trigger of lethal cardiac arrhythmias, but the underlying mechanisms remain poorly understood. METHODS AND RESULTS: We studied the effect of 1-palmitoyl-LPC (Pal-LPC) on currents resulting from human ether-a-go-go-related gene (HERG) expression in human embryonic kidney (HEK) cells using whole-cell patch-clamp techniques. Bath application of Pal-LPC consistently and reversibly increased HERG current (I(HERG)). The effects of Pal-LPC were apparent as early as 3 minutes after application of the drug, reached maximum within 10 minutes, and were reversible on washout. Pal-LPC increased I(HERG) at voltages between -20 and +30 mV, with greater effects at stronger depolarization. However, Pal-LPC did not affect the voltage-dependence of I(HERG) activation. In contrast, Pal-LPC significantly shifted the inactivation curve toward more positive potentials, causing a mean 20.0+/-2.2 mV shift in half-inactivation voltage relative to control. CONCLUSIONS: Our results indicate that apart from being a well-recognized target for drug inhibition, I(HERG) can also be enhanced by natural substances. An increase in I(HERG) by Pal-LPC may contribute to K(+) loss, abnormal electrophysiology, and arrhythmia occurrence in the ischemic heart.