Role of no synthase in the development of Trypanosoma craz/-induced cardiomyopathy in mice

Trypanosoma cruzi infection results in an increase in myocardial NO and intense inflammation. NO modu-lates the T. craz/-induced myocardial inflammatory reaction. NO synthase (NOS)l-, NOS2-, and NOS3-null mice were infected with T. cruzi (Brazil strain). Infected NOSl-null mice had increased parasitemia, mortality, and left ventricular inner diameter (LVID). Chronically infected NOS1-and NOS2-null and wild-type mice (WT) exhibited increased right ventricular internal diameter (RVID), although the fold increase in the NOS2-null mice was smaller. Infected NOS3-null mice exhibited a significant reduction both in LVID and RVID. Reverse transcriptase-polymerase chain reaction showed expression of NOS2 and NOS3 in hearts of infected NOS1-null and WT mice, whereas infected NOS2-null hearts showed little change in expression of other NOS isoforms. Infected NOS3-null hearts showed an increase only in NOS1 expres-sion. These results may indicate different roles for NOS isoforms in T. cruzi-induced cardiomyopathy.