Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most abundant prostaglandin produced by brain tissue varies from species to species. The most abundant prostaglandin produced by brain microvessels is PGI2, PGG2, PGH2, PGI2, PGE2, PGD2, and arachidonic acid dilated cerebral arterioles. Cyclooxygenase inhibitors (indomethacin, AHR-5850), in doses that reduced prostaglandin synthesis substantially, did not affect resting vascular caliber and did not influence the responses of cerebral arterioles to arterial hypoxia, arterial hypercapnia, or arterial hypocapnia, suggesting that prostaglandins are not involved in the mediation of these responses. The vasodilator action of vasoactive intestinal peptide on cerebral arterioles was blocked by these cyclooxygenase inhibitors. The cerebral arteriolar damage induced by fluid-percussion brain injury was inhibited by pretreatment with cyclooxygenase inhibitors, or with free radical scavengers. Topical application of arachidonic acid or PGG2, reproduced the damage seen with brain injury. These findings show that prostaglandins are mediators of the cerebral arteriolar damage due to brain injury and that their mechanism of action is dependent on the generation of free oxygen radicals.
 ...
PMID:Prostaglandins in physiological and in certain pathological responses of the cerebral circulation. 723 14

To evaluate the effect of prostagrandin E1 (PGE1)-induced hypotension on cerebral blood flow (CBF) and carbon dioxide (CO2) reactivity of CBF, regional cerebral hemoglobin oxygen saturation (rSo2) was measured in non-neurosurgical patients (n = 10) under sevoflurane-anesthesia using near infrared spectroscopy. PGE1 was infused intravenously to maintain arterial pressure at a level of about 75% of the MAP (hypotensive group) under sevoflurane-anesthesia alone (normotensive group). Ventilation was controlled to adjust PaCO2 to hypocapnia (25-30 mmHg), normocapnia (35-40 mmHg) and hypercapnia (45-50 mmHg) in both normotensive and hypotensive groups. rSo2 during hypotension did not change by hypocapnia and normocapnia, but significantly increased by hypercapnia, compared with rSo2 during normotension. Significant correlations between rSo2 and PaCO2 during both normotensive and hypotensive groups were observed. Slope of the regression line of rSo2 and PaCO2 did not differ between the normotensive and hypotensive groups. When arterial oxygen content and cerebral metabolic rate of oxygen are constant, changes in rSo2 correlate with those of CBF. Therefore, CBF and CO2 reactivity of CBF that indicates autoregulation in response to changes in CO2 during hypotension were maintained as those during normotension. The results show that PGE2-induced hypotension maintains CBF and CO2 reactivity well in non-neurosurgical patients under sevoflurane anesthesia.
 ...
PMID:[Prostagrandin E1-induced hypotension well maintains cerebral circulation and carbon dioxide reactivity in non-neurosurgical patients under sevoflurane-anesthesia]. 907 Nov 2