ABSTRACT
<p><b>AIM AND METHODS</b>To study the roles of carbon monoxide on hypoxic pulmonary vasoconstriction (HPV) by investigating the effects of exogenous carbon monoxide and heme oxygenase inhibitor ZnPPIX on hypoxic vasoconstriction reaction of isolated rat pulmonary arterial rings (PAR).</p><p><b>RESULTS</b>Hypoxia caused constriction in PAR preconstricted by PE. Both ZnPPIX and carbon monoxide inhibited hypoxic pulmonary constriction significantly by increasing the cGMP level after hypoxia.</p><p><b>CONCLUSION</b>ZnPPIX and exogenous carbon monoxide can inhibit HPV. The reduction of cGMP induced by the decreased of CO may be one of reasons of HPV.</p>
Subject(s)
Animals , Male , Rats , Carbon Monoxide , Physiology , Hypoxia , In Vitro Techniques , Pulmonary Artery , Physiology , Rats, Wistar , Vasoconstriction , PhysiologyABSTRACT
The present study investigates the vasodilative action of carbon monoxide on rat pulmonary artery in vitro. After isolation of the pulmonary artery rings (PAR) from Wistar rats, an ACh concentration-response curve was generated; the PARs were incubated with the NOS inhibitor L-NAME (30 micromol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 micromol/L)+L-NAME (30 micromol/L, n=10) for 30 min. After that, a second ACh concentration-response curve was elicited. Other isolated PARs were randomly divided into two groups: endothelium-intact group (n=8) and endothelium-denuded group (n=8). The effect of exogenous carbon monoxide (CO) on pulmonary arterial vessel tone was observed. The results showed that ACh induced a concentration-dependent pulmonary vasorelaxation. This relaxation disappeared after endothelium was denuded. The ACh induced relaxation was attenuated after pretreatment with 30 micromol/L L-NAME, and attenuated further after pretreatment with 10 micromol/L ZnPPIX+30 micromol/L L-NAME. Exogenous carbon monoxide relaxed pulmonary artery in both the endothelium-intact group and the endothelium-denuded group. These data suggest that ZnPPIX inhibits ACh induced endothelium-dependent pulmonary artery relaxation and that CO is an endothelium-derived relaxation factor, and exogenous CO can relax pulmonary artery.