Role of muscle microvasculature during hyperdynamic and hypodynamic phases of endotoxin shock in decerebrate rats.

Microcirculatory derangements in skeletal muscle could act to change cardiac output during endotoxemia. To explore this idea, we measured arteriole and venule responses to low-dose and high-dose endotoxemia in the rat cremaster muscle by direct in vivo videomicroscopy. Our data indicate that cardiac output increased in the low-dose group and decreased in the high-dose group. In both animal groups, a differential arteriolar response occurred to give small arteriole dilation and large arteriole constriction while venous diameters did not change. We conclude that: 1) changes in cardiac output during endotoxemia are not related to microvascular responses in skeletal muscle, and 2) the microvascular responses in skeletal muscle could be responsible for the decreased systemic vascular resistance during high cardiac output endotoxemia, but not for the elevated systemic vascular resistance during low cardiac output endotoxemia.