Acute Effects of Iron on Contractile Function in Isolated Rabbit Myocardium

Abstract

Changes in contractile function following exposure to iron (Fe) salts were evaluated in isolated isometrically contracting rabbit left atrial strips and right ventricular papillary muscles. Fe acutely depressed myocardial contractility as evidenced by dose-related declines in developed force and maximal rate of force development. There were no significant changes in duration of contraction or resting force. The tissue Fe content was increased nearly 3-fold after a 60 min exposure to Fe and subsequently was not decreased by repeated washing or by treatment with deferoxamine. Isoproterenol, but not deferoxamine, reversed the Fe-mediated impairment of myocardial contractility. These findings suggest that in cases of severe acute iron poisoning, depression of cardiac contractility might occur which may be improved by treatment with isoproterenol.

Myocardial Failure and Shock in Iron Poisoning

“…The changes were most marked in case 1 (Figure 1) and least obvious in case 3.DiscussionShock is a well-known complication of iron poisoning.3~ Its aetiology is multifactorial with hypovolaemia due to gastrointestinal blood loss, systemic acidosis due to the in vivo conversion of ferrous to ferric iron and primary cardiovascular dysfunction all contributing. Our understanding of the latter stems from the work of Whitten et alz They poisoned10 dogs with a lethal dose (225 mg kg-1) of elemental iron and obtained serial measurements of cardiac output, central venous pressure and arterial pressure. The animals received no supportive care and died at a mean time of 5.3 h (range: 3.0-9.5 h) post-poisoning.…”