Protective effect of coexistent thiamine deficiency upon the experimental cardiomyopathy associated with acute magnesium deficiency in the Syrian golden hamster.

Repeated efforts to induce beriberi heart disease by experimental thiamine deficiency (B1d) have failed in many species. To test the hypothesis that magnesium deficiency (Mgd) might be the cofactor necessary for heart failure, 10-week-old Syrian golden hamsters were divided into four groups-control (C), B1d, Mgd, and combined MgB1d-and were fed the diets ad libitum for 3 weeks. On day 21, animals were studied under intraperitoneal pentobarbital anesthesia (50 mg/kg). Electrocardiograms were taken and right and left ventricular pressures were measured by transthoracic needle puncture. Cardiac output was measured by the direct Fick method. The complete study was performed in 9 C, 13 B1d, 9 Mgd, and 14 MgB1d animals. B1d was proven by low red blood cell transketolate high B1 pyrophosphate effect, and was accompanied by tachycardia and hypercalcemia. B1 did not differ from C in any other parameter. Mgd was characterized by hypomagnesemia, hypercalcemia, prolongation of the PR interval, widening of the QRS interval, low O2 consumption, low cardiac output, and increased heart weight to body weight ratio (HW/BW) as compared to control. No differences were observed in right and left ventricular pressures or peak /dt. MgB1d was characterized by hypomagnesium, hypercalcemia, low red blood cell transkeotlase, and high B1 pyrophosphate effect. MgB1d minimized the deleterious effects of Mgd: animals were more active and the mortality was low, the PR interval remained normal, the QRS interval widened significantly less, cardiac output remained normal, and HW/BW increased significantly less. Although, once again, beriberi heart disease was not produced, B1d appeared to exert a protective effect upon the Mg-deficient myocardium.