Compromised microcirculation in acute murine Trypanosoma cruzi infection

Herbert B. Tanowitz, Dhananjaya K. Kaul, Bing Chen, Stephen A. Morris, Stephen M. Factor, Louis M. Weiss, Murray Wittner

Research output: Contribution to journalArticlepeer-review

71 Scopus citations


Microvascular compromise has been 1 of many factors implicated in the etiology of the cardiomyopathy associated with Chagas' disease. To further assess the effect of Trypanosoma cruzi infection on the microcirculation, we examined the cremaster microvascular model in CD-1 male mice infected with the Brazil strain at 20-25 days postinfection. There was a significant decrease in red cell velocity (Vrbc) in first and third-order arterioles and venules, which was reversed by verapamil treatment. Video recordings revealed a marked inflammatory response that was confirmed by transmission electron microscopy. A marked inflammatory response was not seen in verapamil-treated infected mice. Segmental vasospasm and dilatation was evident in the microvascular bed of infected mice. This was not seen in control or verapamil-treated mice. This model provides a readily accessible method to observe directly the effects of T. cruzi infection on the microcirculatory flow in vivo. In addition, it confirms and extends our previous observations regarding T. cruzi-associated microvascular spasm and underscores a role for verapamil, a calcium-channel blocker, in the amelioration of the Chagas' disease.

Original languageEnglish (US)
Pages (from-to)124-130
Number of pages7
JournalJournal of Parasitology
Issue number1
StatePublished - Feb 1996

ASJC Scopus subject areas

  • Parasitology
  • Ecology, Evolution, Behavior and Systematics


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