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Divisions of Pulmonary and Critical Care Medicine, Royal Victoria Hospital and Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada H2X 2P2
The in vitro responses to ACh, flow, and
hypoxia were studied in arterioles isolated from the diaphragms of
rats. The endothelium was removed in some vessels by low-pressure air
perfusion. In endothelium-intact arterioles, pressurized to 70 mmHg in
the absence of luminal flow, ACh
(10
5 M) elicited dilation
(from 103 ± 10 to 156 ± 13 µm). The response to ACh was
eliminated by endothelial ablation and by the nitric oxide synthase
antagonists NG-nitro-L-arginine
(L-NNA;
105 M) and
NG-nitro-L-arginine methyl ester
(L-NAME,
105 M) but not by
indomethacin (105 M).
Increases in luminal flow (5-35 µl/min in 5 µl/min steps) at
constant distending pressure (70 mmHg) elicited dilation (from 98 ± 8 to 159 ± 12 µm) in endothelium-intact arterioles. The response to flow was partially inhibited by
L-NNA,
L-NAME, and indomethacin and
eliminated by endothelial ablation and by concurrent treatment with
L-NAME and indomethacin. The
response to hypoxia was determined by reducing the periarteriolar
PO2 from 100 to 25-30 Torr by
changing the composition of the gas used to bubble the superfusing
solution. Hypoxia elicited dilation (from 110 ± 9 to 165 ± 12 µm) in endothelium-intact arterioles but not in arterioles from which
the endothelium had been removed. Hypoxic vasodilation was eliminated
by treatment with indomethacin and was not affected by
L-NAME or
L-NNA. In rat diaphragmatic
arterioles, the response to ACh is dependent on endothelial nitric
oxide release, whereas the response to hypoxia is mediated by
endothelium-derived prostaglandins. Flow-dilation requires that both
nitric oxide and cyclooxygenase pathways be intact.
respiratory muscles; blood flow; autoregulation; vascular smooth muscle
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