PubMed · 12501643
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T Yang, W X Yao, M X Jiang. 1998. [Ionic channel pathies].. https://pubmed.ncbi.nlm.nih.gov/12501643/
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Ventricular fibrillation (VF) and myocardial ischemia are inseparable. The first clinical manifestation of myocardial ischemia or infarction may be sudden cardiac death in 20-25% of patients. The occurrence of potentially lethal arrhythmia is the end result of a cascade of pathophysiological abnormalities that result from complex interactions between coronary vascular events, myocardial injury, and changes in autonomic tone, metabolic conditions and ionic state of the myocardium. It is also related to the time from the onset of ischemia. Within the first few minutes there is abundant ventricular arrhythmogenesis usually lasting for 30 min. Triggers for ischemic VF occur at the border zone or regionally ischemic heart. The border zone of ischemia is the predominant site of fragmentation. Acute ischemia opens K(ATP) channels and causes acidosis and hypoxia of myocardial cells leading to a large dispersion in repolarization across the border zone. Abnormalities of intracellular Ca2+ handling also occur in the first few minutes of acute myocardial ischemia and may be an important cause of arrhythmias in human coronary artery disease. Substrate on the other hand transforms triggers into VF and serves to maintain it through fragmentation of waves in the ischemic zone. Thrombin levels, stretch, catecholamine, genetic predisposition, etc. are some of these factors. Reentry models described are spiral wave reentry, 3 dimensional rotors, reentry around 'M' cells and figure-of-eight reentry. Continuing efforts to better understand these arrhythmias will help identify patients of myocardial ischemia prone to arrhythmias.
Allyl isothiocyanate, the pungent principle of wasabi and other mustard oils, produces pain by activating TRPA1, an excitatory ion channel on sensory nerve endings. Isothiocyanates are membrane-permeable electrophiles that form adducts with thiols and primary amines, suggesting that covalent modification, rather than classical lock-and-key binding, accounts for their agonist properties. Indeed, we show that thiol reactive compounds of diverse structure activate TRPA1 in a manner that relies on covalent modification of cysteine residues within the cytoplasmic N terminus of the channel. These findings suggest an unusual paradigm whereby natural products activate a receptor through direct, reversible, and covalent protein modification.
Cerebral palsy (CP) is a motor disorder due to cerebral damage. It is commonly associated with neuro-psychological retardation and also with epilepsy; hence, its management warrants a multi-dimensional approach. In a significant number of CP patients, interictal epileptiform discharges (IEDs) are obtained in their EEG even in absence of clinical epilepsy. Epileptiform discharge-firing cortical neurons are found to be associated with elevated intracellular Ca(2+) levels and exhibition of abnormal response on exposure to excitotoxic glutamate; both these features have been found to lead to subsequent death of these neurons. This further damage is likely to aggravate the already existing cortical damage in CP patients thereby worsening their prognosis. IEDs are also known to be associated with other neuro-psychological disorders like cognitive impairment and behavioral problems even in absence of clinical epilepsy. Thus, the IEDs cannot be viewed as benign events and their occurrence even in absence of clinical epilepsy cannot be ignored. A few trials aimed at treating IEDs in autistic patients without epilepsy and in children with behavior problems have yielded favorable results. Based on these studies, the author proposes inclusion of EEG investigation in the management protocol of CP patients and treatment of IEDs (when detected even in absence of clinical epilepsy) for a better outcome in their prognosis.