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However, other studies reported that indomethacin does not reduce hypercapnia-induced cerebral vasodilation. In adult humans and animals, some studies reported that indomethacin, a cyclooxygenase inhibitor, reduces hypercapnia-induced cerebral vasodilation. The principle vasoactive prostanoids in the brain are prostaglandin E 2(PGE 2) and prostacyclin (PGI 2), both dilator prostanoids, and the constrictor prostanoid prostaglandin F 2alpha (PGF 2alpha). Cyclo-oxygenase converts arachidonic acid to prostaglandin H2, which is subsequently modified by other enzymes to yield both vasoconstrictor and vasodilator prostanoids. Production of prostaglandins is controlled by the availability of arachidonic acid, which is cleaved from membrane lipids by phospholipase. However, changes in extracellular pH do affect intracellular pH in cerebral vascular smooth muscle, and due to complex interactions between extracellular and intracellular pH, it is not known whether extracellular or intracellular pH controls cerebral vascular tone. Data in isolated cerebral arteries also indicate that extracellular pH is more important than intracellular pH in hypercapnic-induced dilation of cerebral arteries. Because CO 2diffuses freely through cell membranes and bicarbonate does not, these data suggest that extracellular pH is more important than intracellular pH in altering cerebral vascular tone. During alterations of fluid P CO 2, the pH of the artificial CSF was held constant by altering its bicarbonate concentration. Applying artificial cerebrospinal fluid (CSF) topically to the cerebral cortex of anesthetized cats, they showed that the diameter of cerebral arterioles responded only to changes in pH, regardless of fluid P CO 2. offered the best evidence that pH rather than CO 2is the controlling messenger for CO 2-mediated alterations of cerebral vascular tone. showed that cerebral blood flow (CBF) was normal during chronic hypocapnia, which suggests that CO 2itself does not alter cerebral vascular tone.
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Applying acidotic or alkalotic solutions to the brain dilates or constricts cerebral arteries in vivo, which indicates that pH can affect cerebral vascular tone. When cerebral vascular tone is altered by a change in P CO 2, it is possible that CO 2itself, a CO 2-mediated change in pH, or both are signals leading to a change in vascular tone. No data exist regarding a potential role for glia in the CO 2response of the cerebral circulation. Although these data in adults suggest that the endothelium, parenchymal neurons, and perivascular nerves are not important during hypercapnia-induced cerebral vasodilation, it is also possible that these cells produce overlapping vasodilator messengers, and removal of an individual messenger is not sufficient to alter the response. Selective destruction of cortical neurons also does not alter the cerebral vascular response to hypercapnia. Tetrodotoxin, which blocks sodium channels and prevents neuronal depolarization, does not reduce CO 2-mediated cerebral vasodilation, indicating that depolarization of perivascular nerves or parenchymal neurons is not important. In neonates, however, the endothelium does contribute to cerebral vasodilatation during hypercapnia. This suggests that in adults the endothelium is not involved in the response to CO 2. In adult animals, removal of the endothelium in vitro or endothelial damage in vivo does not alter the response of cerebral arteries to hypercapnia. Cellular elements that could contribute to the cerebral vascular response to CO 2include vascular cells (endothelium and smooth muscle) and extravascular cells (perivascular nerves, parenchymal neurons, and glia). In vivo, cerebral arteries respond to highly localized perivascular alteration of P CO 2and pH, which indicates that the mechanisms that affect cerebral vascular tone are localized to the area of the blood vessel wall. Increased carbon dioxide tension (P CO 2) relaxes cerebral arteries in vitro, which indicates that CO 2can cause cerebral vascular relaxation independent of extravascular cells.