Effects of altered carbon dioxide tension on hemoglobin oxygenation in hamster cheek pouch microvessels.
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Biomedical subjects
Publications and source records attributed to B R Duling.
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A new method is presented for the spectrophotometric determination of percent oxyhemoglobin (percent saturation) in whole blood. The method is based on a theory of light absorption and scattering by particulate suspensions and requires the measurement of optical densities (D) of blood at three closely spaced wavelengths. The contribution of scattering to the optical density at each wavelength is determined from optical density values at two isosbestic wavelengths (546 and 520 nm) and the optical density at the third wavelength (555 nm) is related to the extent of oxygenation of the hemoglobin. The wavelength independence of the scattering contribution (B) induced by red cells was established from 510 and 575 nm. The optical density of red blood cell suspensions was measured with a spectrophotometer and a linear relationship was found between percent saturation and the corrected optical density ratio, (D555 B)/(D546 B). For a given saturation, this ratio was independent of optical path length (0.1-2 mm) and hematocrit (3-50%).
A new method is applied to the determination of percent oxyhemoglobin (percent saturation) in whole blood. The method is based on a theoretical treatment of light absorption and scattering by particulate suspensions and requires the measurement of optical densities (D) of blood at three closely spaced wavelengths. The optical density of red blood cell (RBC) suspensions was measured with a video microdensitometer and a linear relationship was found between percent saturation and the corrected optical density ratio, (D555 B)/(D546 B). For a given saturation, this ratio was independent of optical path length (12 mum-2 mm), hematocrit (3-50%), and RBC velocity (1.5-17 mm/s). The applicability to microvascular measurements has been assessed through the use of TV microdensitometry on micropipettes with flowing RBCs and on microvessels in the hamster cheek pouch.
The vasoactive properties of potassium were assessed in the microcirculation of the hamster cremaster muscle and the muscular and epithelial portions of the hamster cheek pouch. Tissues were transilluminated and suffused with a physiological salt solution whose potassium concentration varied from 0 to 20 mM. Vessel diameters were measured and normalized as a percent of the control diameter (+/- SE) observed during exposure to 4.7 mM K+. Altering the potassium concentration in the suffusion solution caused a transient vascular response. The peak changes in the vascular diameter of the arterioles supplying striated muscle varied directly with the suffusion solution potassium concentration from a minimum of 78 +/- 3% in 0 mM K+ to 155 +/- 15% in 15 mM K+. Vascular diameter increases were sustained for the full 5-minute test period only in 15 mM K+. In the epithelial portions of the cheek pouch, only the constrictor component of the potassium response was observed. The data indicate that potassium is sufficiently potent to participate in initiating functional hyperemia in striated muscle and might cause as much as a 6.3-fold increase in flow. Functional hyperemias exceeding approximately 3 minutes cannot be due to potassium ion, since the dilation induced by this agent is transient.
A radioisotope technique has been used to determine blood pressure changes in mice after lethal staphylococcal infection and after lethal endotoxin challenge. The method was verified by making simultaneous direct measurements in rats. Mice in both groups became hypotensive to a similar level (a fall 20-30 mm Hg). This tailcuff technique is simple and reliable but is dependent upon normal tail blood flow. Spurious low pressure readings are obtained in hypothermic or chilled mice because the tail is a major thermoregulator organ. These difficulties can be overcome by warming chilled or hypothermic mice.
We have looked at a fairly simple model of blood flow regulation at the microvascular level consisting of suffused microvascular preparations and isolated smooth muscles. When the O2 demand of the microvessel preparations was decreased by elevating suffusion solution PO2, changes in wall PO2 indicated that only the smallest microvessels could be controlled by a direct effect of oxygen. In vivo and in vitro studies of the oxygen sensitivity of smooth muscle indicated that even the smaller vessels were probably not directly controlled by oxygen availability during a free flow state, since measured perivascular PO2's did not fall to levels low enough to alter contractile performance of the vascular smooth muscle. Our data indicate that in any condition in which flow is interrupted for periods in excess of about 30 sec, one might anticipate vascular relaxation due to oxygen lack. It was judged resonable to extrapolate our findings to autoregulation of blood flow in resting skeletal muscle and to responses to modest exercise. Our data indicate that it is improbable that oxygen acts by a direct effect on the smooth muscle under these conditions. On the other hand, they suggest that a direct effect of oxygen might well be important in causing postocclusion hyperemia.
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