Comparison between pial and intraparenchymal vascular responses to sympathetic stimulation under hypercapnic conditions. With special reference to the mechanism for escape phenomenon.
We have shown that secondary vasodilation ('escape' phenomenon) during sympathetic nerve stimulation occurs in the intraparenchymal vessels but not remarkable in the pial vessels. To test a possible role of CO2 accumulation in the brain tissue in this phenomenon, the responses of pial and intraparenchymal vessels to sympathetic nerve stimulation were investigated during hypercapnia in 9 cats by using a video camera photoelectric system. The ipsilateral superior cervical ganglion was electrically stimulated for 5 min during hypercapnia (PaCO2 = 50 +/- 2 mm Hg). The intraparenchymal vessels as well as pial vessels remained constricted throughout the stimulation. Secondary dilation of the intraparenchymal vessels as seen at the later stage of sympathetic stimulation during normocapnia was not observed under the hypercapnic conditions. We assume that the arterial CO2 tension was so high that the constriction of inflow vessels could not result in accumulation of CO2 in the brain parenchyma. The accumulation of chemical metabolites as represented by CO2 is therefore considered to be the most probable mechanism underlying the escape phenomenon of the intraparenchymal vessels.
D000818:Animals; D001794:Blood Pressure; D001808:Blood Vessels / Q000503:physiopathology; D001921:Brain / Q000098:blood supply*; D002245:Carbon Dioxide / Q000097:blood; D002415:Cats; D005728:Ganglia, Sympathetic / Q000503:physiopathology*; D006935:Hypercapnia / Q000097:blood / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D010841:Pia Mater / Q000098:blood supply*; D014664:Vasodilation
D002245:Carbon Dioxide; D010100:Oxygen