Literature DB >> 8967389

Oxygen saturation and pH changes in cremaster microvessels of the rat.

H Kobayashi1, N Takizawa.   

Abstract

Recent studies have shown a considerable extent of diffusive O2 transfer from precapillary vessels, but the occurrence of O2 influx into postcapillary vessels (diffusive shunting) is still controversial. In this study, we investigated diffusive shunting between pre- and postcapillary vessels in muscle tissue and pH changes in the microvessels in an attempt to determine the physiological significance of the parallel arrangement of arterial and venous vessels in tissue oxygenation. We used rat cremaster muscles and controlled the breathing of anesthetized rats using urethane with FIO2 set at 0.3 and 0.12. We employed a noninvasive spectrophotometric method of measuring pH, using a pH-sensitive dye (1-hydroxypyrene-3,6,8-trisulfonic acid) and the O2 saturation level of hemoglobin (SO2) in microvessels from small arteries down to arterioles and from venules up to small veins. At FIO2 0.30, pH significantly decreased from 7.39 +/- 0.02 to 7.26 +/- 0.05 (SD) in precapillary vessels and remained close to constant during passage through postcapillary vessels. At FIO2 0.12, pH decreased from 7.36 +/- 0.03 to 7.01 +/- 0.06 in precapillary vessels and then increased in postcapillary vessels from 6.75 +/- 0.19 to 7.27 +/- 0.08. At FIO2 0.30, SO2 decreased from 98.6 +/- 5.4 to 64.2 +/- 4.5% in precapillary vessels and increased from 62.5 +/- 6.5 to 89.4 +/- 4.1% in postcapillary vessels. At FIO2 0.12, SO2 decreased from 47.0 +/- 5.5 to 25.1 +/- 3.8% in precapillary vessels and remained close to constant in postcapillary vessels. In conclusion, during hyperoxia, diffusive shunting of O2 was enhanced, and during hypoxia, acid was accumulated in peripheral vessels. It is speculated that acid accumulated due to back-diffusion of CO2 from venous to arterial microvessels, liberating O2 bound to hemoglobin via the Bohr effect. The diffusive shunting of O2 and counterdiffusion and accumulation of CO2 may contribute to the homeostasis of tissue oxygenation levels.

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Year:  1996        PMID: 8967389     DOI: 10.1152/ajpheart.1996.270.4.H1453

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


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