Skeletal microcirculatory responses to hyperdynamic Escherichia coli sepsis in unanesthetized rats.
To determine the microvascular site of vasodilation during hyperdynamic sepsis, we measured arteriolar and venular responses to live Escherichia coli bacteremia in the rat cremaster muscle by direct in vivo videomicroscopy. Our data indicate that cardiac output (by thermodilution) increased, systemic vascular resistance decreased, and a differential arteriolar response occurred, with constriction of large arterioles and dilation of small terminal arterioles. We conclude that dilation of small terminal arterioles in skeletal muscle could contribute to decreased systemic vascular resistance during hyperdynamic sepsis. This may be an appropriate response to increased oxygen demand or decreased tissue utilization of oxygen. Alternatively, small-arteriole dilation may be an inappropriate response and secondary to release of vasoactive inflammatory mediators. If the latter is true, there is a potential therapeutic role for selective manipulation of the tone of small terminal arterioles in hyperdynamic sepsis.
D000818:Animals; D001160:Arterioles / Q000503:physiopathology; D002302:Cardiac Output; D004927:Escherichia coli Infections / Q000503:physiopathology*; D006439:Hemodynamics; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D009132:Muscles / Q000098:blood supply*; D051381:Rats; D011919:Rats, Inbred Strains; D018805:Sepsis / Q000503:physiopathology*; D013815:Thermodilution; D014699:Venules / Q000503:physiopathology