| REVIEW ARTICLE |
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| Year : 1993 | Volume
: 25
| Issue : 1 | Page : 5-13 |
Systemic toxicity of methyl isocyanate in mammals
K Jeevaratnam
Correspondence Address:
K Jeevaratnam
 Source of Support: None, Conflict of Interest: None  | Check |
Between that tragic incident at Bhopal and now, much progress has been made to understand the systemic effects of methyl isocyanate (MIC). Being a potent pulmonary irritant, inhaled MIC causes respiratory depression and extensive alveolar damage. In spite of its high reactivity, MIC either inhaled or administered through systemic route reaches various organs in its active form and produces a dose dependent hypotension, haemoconcentration, hyperglycemia, clinical lactic acidosis and uraemia in rats. The sequence of events after MIC intoxication subcutaneously clearly indicates the primary event to be hypotension, persisting for a longer duration with increasing severity possibly due to fluid loss (hypovolemia). However, the predominant biological effect of MIC intoxication in mammals is severe tissue hypoxia leading to acute metabolic acidosis, The raison d'etre for the induction of tissue hypoxia by MIC are many fold. Besides, the respiratory depression, MIC causes stagnant hypoxia affecting cardiovascular system and histotoxic hypoxia through its effects on the mitochondrial respiration Apart from the acute necrotizing bronchiolitis due to corrosive action of MIC, the histological changes such as the severe intraseptal edema, collection of fluid and exuded plasma proteins within the interstitial and alveolar spaces and those observed in the other vital organs provides clear evidence for the occurrence of fluid loss from the vascular compartment leading to hypovolemic shock.
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