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Interaction between hypoxia and hypercapnia in regulating canine diaphragm arteriolar diameter.

In alpha-chloralose-anesthetized mongrel dogs, the microvascular responses to hypoxia and hypercapnia were studied in the vascularly isolated ex vivo left hemidiaphragm. The diaphragm was perfused with arterial blood diverted from the femoral artery by a pump. A series of membrane oxygenators was used to adjust the blood gas composition of the blood perfusing the diaphragm. Arteriolar diameters were measured by intravital microscopy during an infusion of sodium nitroprusside, moderate hypoxia (phrenic venous PO2 25 Torr), severe hypoxia (phrenic venous PO2 13 Torr), hypercapnia (phrenic venous PCO2 100 Torr), and a simultaneous presentation of hypoxia and hypercapnia. Recordings were made after 15 min under each condition when a steady state had been established for vessel diameter and flow. Pump speed was adjusted manually under each condition to ensure that the steady-state perfusion pressure was the same as that under the control condition. Moderate hypoxia generally resulted in dilation; however, vasoconstriction was seen in some arterioles. Severe hypoxia caused vasodilation that was inversely related to baseline vessel diameter and paralleled the response to sodium nitroprusside. Hypercapnia resulted in vasodilation of the diaphragmatic circulation at values of phrenic venous PCO2 > 80 Torr. The arteriolar response to hypercapnia was also inversely related to baseline vessel diameter. Hypoxia and hypercapnia in combination exerted an additive effect on arteriolar diameter but produced a greater than additive effect on blood flow. Both PO2 and PCO2 may contribute to the local regulation of diaphragmatic blood flow. The vasodilator effects of both hypoxia and hypercapnia are greater in smaller than in larger arterioles. The interaction between PO2 and PCO2 on arteriolar diameter is additive. An apparent synergistic effect on blood flow results from the power function relating diameter to flow.