Microcirculatory norepinephrine constrictor response in hemorrhagic shock

Hemorrhagic shock is characterized by a phase of compensation that preserves central blood flow and intravascular pressure through an integrated vasoconstrictor response mediated by catecholamines, particularly norepinephrine (NE). The skeletal muscle microcirculation is important in this response. Decompensation occurs when arteriolar vasodilation occurs despite continued hypovolemia and high circulatory levels of NE. Using an isolated decerebrate rat cremaster muscle, we measured constrictor response to NE (10(-7)M tissue concentration) in compensated and decompensated shock. Our data indicate that larger arterioles (143 to 152 microns) show persistent constrictor response with lowered sensitivity to NE. Smaller arterioles (11 to 22 microns) and all venules dilate late in shock but retain constrictor responses to NE. Dilator responses contribute to decompensation in small arterioles and venules but not because of altered NE constrictor response.