Hemodynamic and calorimetric changes induced by microcystin‐lr in the rat

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Abstract
Microcystin‐LR, a cyclic peptide from the cyanobacterium Microcystis aeruginosa, given at acutely toxic doses causes severe hepatic interstitial hemorrhage. Hemodynamic, calorimetric and acid–base balance changes after i.v. microcystin were measured. The effect of isoproterenol, dopamine, methylprednisolone and whole‐blood volume expansion on the immediate hemodynamic effects after toxin administration were also evaluated. A dose of 100 μg kg−1 was invariably lethal for rats in all studies. Pathophysiological changes included: a sustained, rapid decline in cardiac output and stroke volume; an acute hypotension responsive to volume expansion with whole blood; a decreased heart rate, responsive to both isoproterenol and dopamine; an early decline in oxygen consumption, carbon dioxide production and metabolic rate accompanied by progressive hypothermia; and acid–base balance changes indicating partially compensated metabolic acidosis. The lethal effects of microcystin‐LR were previously attributed to hypovolemic shock as a result of hepatic interstitial hemorrhage. These results indicate that, in addition, there may be a cardiogenic component that limits the physiological cardiac reserve, compromising a normal response to circulatory inadequacy.

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