Microvascular hemoglobin oxygen saturation (SO 2 ) during prolonged hemorrhagic hypotension (HH)

Abstract

Since skeletal muscle represents up to 40% of body mass and suffers severe reductions in blood flow during HH, we examined the microcirculatory consequences of prolonged hypotension due to hemorrhage in the rat spinotrapezius muscle. An aortic transducer was implanted for continuous measurement of cardiac output. Systemic hemodynamic and respiratory variables were measured 7 days after the implantation. Functional capillary density, microvascular diameter, arteriolar SO2 and hemoglobin concentration ([Hb]) were measured using intravital microscopy. Measurements were made before and up to 4 h after HH. Additional bleeding or lactated Ringer's infusion were used to maintain mean arterial pressure at 40 mmHg. Controls were subjected to the same procedures except HH. Fifty-three percent of rats survived ≥ 3 h (S); others were considered nonsurvivors (NS). There was a positive correlation (r= 0.83, p ≤ 0.05) between microvascular SO2 and respiratory rate in S. Significant differences between S and NS were obtained for arteriolar SO2 (lower in S, p ≤ 0.05). Microvascular [Hb] was correlated with the systemic [Hb] (r= 0.93, p ≤ 0.001). Small arterioles constricted more in S than in NS, while large arterioles dilated in S. The diameter findings may explain why S showed higher total peripheral resistance levels for a longer period of time during HH. Our findings suggest that respiratory compensations and microvascular changes are essential for survival of prolonged HH. Support: DOD and NIH HL079087.