Alkalosis increased baseline vascular resistance by 56% (p<0.0001) and enhanced norepinephrine vasoconstriction by 66%, while acidosis attenuated norepinephrine and sympathetic nerve stimulation effects.
Does acidosis or alkalosis alter baseline vascular resistance and response to norepinephrine or sympathetic nerve stimulation in the canine tibia?
Perfusion pH influences the sensitivity of long bone resistance vessels to circulating norepinephrine and sympathetic nerve stimulation, suggesting a mechanism for local autoregulation of blood flow.
Effect estimate: 56% increase in BVR with alkalosis
p-value: p=<0.0001
This study used an ex vivo perfusion model to investigate the direct effects of acidosis and alkalosis on the vascular resistance of the canine tibia. Baseline vascular resistance (BVR) and the vascular smooth muscle response to bolus doses of norepinephrine (NE) (0.025-3.2 nmol) and periarterial sympathetic nerve stimulation (NS) (10-25 Hz: 9 V, 2 ms pulses, 10 s) were studied. In Group I, these parameters were measured at normal pH (duration 7.34-7.44) and then during acidosis (pH 7.2-7.33). In Group II, they were measured at normal pH and then during alkalosis (pH 7.47-7.58). In Group III (control), they were measured serially at a normal pH. Alkalosis increased BVR by 56% (p < 0.0001). Acidosis attenuated (18% reduction) and alkalosis enhanced (66% increase) the vasoconstrictor action of NE (p < 0.0001). Acidosis also attenuated (11% reduction) the effect of sympathetic NS (p = 0.012). It is concluded that perfusion pH influences the sensitivity of long bone resistance vessels to circulating NE and sympathetic NS. Thus, local concentration of hydrogen ions may provide bone with a mechanism to autoregulate blood flow.
Davis et al. (Mon,) reported a other. Acidosis and alkalosis vs. Normal pH (7.34-7.44) was evaluated on Baseline vascular resistance and vascular smooth muscle response to norepinephrine and sympathetic nerve stimulation (56% increase in BVR with alkalosis, p=<0.0001). Alkalosis increased baseline vascular resistance by 56% (p<0.0001) and enhanced norepinephrine vasoconstriction by 66%, while acidosis attenuated norepinephrine and sympathetic nerve stimulation effects.
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