[Effect of hypoxia and carbon monoxide on rat pulmonary arterial smooth muscle cell]

To investigate the effect of carbon monoxide on rat pulmonary arterial smooth muscle cell (VSMC).

Three groups were randomly divided, (1) Normoxia group(N), (2) Hypoxia group(H), (3) 3% CO + 1% O2 group (CO + H), then tested by immunocytochemical analysis 3H-TdR in incorporation.

(1) Hypoxia initiated the chang of VSMC from contractile phenotype to synthetic phenotype, the endoplasmic reticulum became dilated, the mitochondria became swollen and myelin figure appeared. alpha-actin and muscle fiber decreased. The form of VSMC in CO + H was similar to that in N. (2) Intracellular Ca2+ level of VSMC in H [4 h, 8 h, 12 h, 24 h, 36 h were (382.00 +/- 37.92) mmol/L, (456.00 +/- 53.76) mmol/L, (517.00 +/- 47.34) mmol/L, (608.00 +/- 35.92) mmol/L, (567.00 +/- 46.72) mmol/L, respectively] increased significantly(P < 0.01) than in N[4 h was(319.00 +/- 47.45) mmol/L], but that in CO + H increased slightly. (3) cAMP and cGMP level of VSMC in H increased significantly, cAMP of VSMC in CO + H increased significantly [2 h, 8 h, 12 h, 24 h were (1.87 +/- 0.36) pmol/mg protein, (2.16 +/- 0.36) pmol/mg protein, (2.36 +/- 0.41) pmol/mg protein, (2.12 +/- 0.39) pmol/mg protein, respectively] but cGMP of VSMC in CO + H increased slightly[2 h, 8 h, 12 h, 24 h were (0.52 +/- 0.21) pmol/mg protein, (0.58 +/- 0.21) pmol/mg protein, (0.60 +/- 0.24) pmol/mg protein, (0.68 +/- 0.29) pmol/mg protein, respectively].

Hypoxia may promote the proliferation of VSMC by second messenger system and CO in low desities can depress the action of hypoxia partly by Ca(2+)-cGMP system or by the expression of E2F-1 gene.