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Effects of altered carbon dioxide tension on hemoglobin oxygenation in hamster cheek pouch microvessels

Roland N.Pittman, Brian R.Duling/Microvascular Research, Volume 13, Issue 2, March 1977, Pages 21


Department of Physiology, Virginia Commonwealth University, Medical College of Virginia, Richmond, Virginia 23298 USA


Simultaneous determinations of percentage HbO2 and PO2 were made at various sites moving progressively downstream from large to small arterioles in the suffused hamster cheek pouch microcirculation. A new video densitometric technique was employed to measure intravascular percentage oxyhemoglobin (% HbO2), and oxygen tension (PO2) was determined polarographically with oxygen microcathodes. Microvascular diameter and red cell velocity were also measured. The above measurements were made under conditions of sustained maximal vasodilation with with 10−4Madenosine in the suffusion solution. The pairs of values for % HbO2and PO2 at each of the measurement sites were used to construct apparent in vivo HbO2 saturation curves. Lateral shifts of the saturation curve were produced by altering the carbon dioxide tension (PCO2) of the suffusion solution from 32 to 10 mm Hg, and from 32 to 75 mm Hg. Hill's equation for the HbO2 saturation curves was used to analyze the % HbO2 and PO2 data pairs. For each value of suffusion solution PCO2P50 was determined and yielded values of 25 ± 3, 30 ± 3, and 41 ± 4 mm Hg for solution PCO2's of 10, 32, and 75 mm Hg, respectively. The in vivo values are qualitatively in agreement with predictions from published HbO2saturation curves, although the predicted P50 during suffusion with the hypocapnic solution (PCO2 = 10 mm Hg) was somewhat higher than expected. The sustained vasodilation produced by adenosine did not in itself lead to a statistically significant change in P50between normal and dilated arterioles. A pronounced longitudinal decrease in PO2 from large to small arterioles with an accompanying fall in % HbO2 was observed in all experiments. This longitudinal gradient in arteriolar oxygen content confirms and extends the previous reports of a progressive decline in precapillary PO2. In addition, evidence is presented which suggests the existence of a precapillary longitudinal gradient in PCO2.


This investigation was supported in part by American Heart Association grant 71993, USPHS grant HL 12792, USPHS grant HL 18292, and a grant from the A. D. Williams Foundation. A preliminary report of this work appeared as an abstract in The Physiologist18, 353, 1975.


Volume 13, Issue 2, March 1977, Pages 211-224


Web source: https://doi.org/10.1016/0026-2862(77)90086-3

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