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

Arteriovenous malformations (AVM's) are congenital tangles of vessels that have a high blood flow through a low-resistance nidus. The vessels in the nidus may lack normal vasoreactivity in response to changes in PaCO2 or perfusion pressure (autoregulation). Arteriovenous malformation hemodynamics have been assessed based on the response of AVM feeding arteries to hypocapnia. Twenty-five AVM patients, aged 34 +/- 11 years (mean +/- standard deviation), were admitted to the Massachusetts General Hospital for proton-beam radiation therapy. Fourteen healthy volunteers aged 30 +/- 7 years served as control subjects. Angiograms with calibrated markers permitting magnification correction were available for all patients. The limits of the middle cerebral artery, as determined by transcranial Doppler ultrasonography, were compared to measurements made on the angiograms. Hyperventilation was induced at a rate set by a metronome. Fixed bilateral Doppler probes allowed almost simultaneous sampling of two vessels. Volunteer control subjects were hyperventilated in two steps. The two PaCO2 step decreases were significant (mean resting PaCO2 40.6 +/- 3.5 mm Hg, Step 1 level 29.4 +/- 3.5 mm Hg and Step 2 level 23.8 +/- 3.5 mm Hg; p < 0.01). These decreases induced a significant decrease in mean flow velocity (Vm) and an increase in the pulsatility index (p < 0.001). Mean carbon dioxide reactivity (% delta Vm/delta PaCO2) was 2.74 +/- 1.0 for Step 1 and 1.44 +/- 1.8 for Step 2 (p < 0.003). The mean PaCO2 decrease in patients was from 39.5 +/- 4.0 mm Hg to 27.0 +/- 3.5 mm Hg. Carbon dioxide reactivity was 0.92 +/- 1.12 for feeding vessels and 2.59 +/- 1.78 for nonfeeding vessels (p < 0.001). Transcranial Doppler ultrasound and angiographic depth measurements correlated well. Hyperventilation induced significantly more hemodynamic changes in control and nonfeeding middle cerebral arteries than in feeding vessels. Impaired CO2 reactivity may help to identify AVM feeding vessels as well as the relative magnitude of the flow provided to the malformation.
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PMID:CO2 reactivity in arteriovenous malformations of the brain: a transcranial Doppler ultrasound study. 793 37

To study the pathophysiology of idiopathic postoperative brain swelling or hemorrhage after arteriovenous malformation resection, termed normal perfusion pressure breakthrough (NPPB), we performed cerebral blood flow (CBF) studies during 152 operations in 143 patients, using the xenon-133 intravenous injection method. In the first part of the study, CBF was intraoperatively measured (isoflurane/N2O anesthesia) during relative hypocapnia in 95 patients before and after resection. The NPPB group had a greater increase (P < 0.0001) in mean +/- standard deviation global CBF (28 +/- 6 to 47 +/- 16 ml/100 g/min, n = 5) than did the non-NPPB group (25 +/- 7 to 29 +/- 10 ml/100 g/min, n = 90); both arteriovenous malformation groups showed greater increase (P < 0.05) than did controls undergoing craniotomy for tumor (23 +/- 6 to 23 +/- 6 ml/100 g/min, n = 22). Ipsilateral and contralateral CBF changes were similar. In a second cohort of patients with arteriovenous malformations, CBF was measured at relative normocapnia and it increased (P < 0.002) from pre- to postresection (40 +/- 13 to 49 +/- 15 ml/100 g/min, n = 57). There were no NPPB patients in this latter cohort. The feeding mean arterial pressure was measured intraoperatively before resection or at the last embolization before surgery (n = 64). The feeding mean arterial pressure (44 +/- 16 mm Hg) was 56% of the systemic arterial pressure (78 +/- 12 mm Hg, P < 0.0001) and was not related to changes in CBF from pre- to postresection. There was an association between increases in global CBF from pre- to postresection and NPPB-type complications, but there was no relationship of these CBF changes to preoperative regional arterial hypotension. These data do not support a uniquely hemodynamic mechanism that explains cerebral hyperemia as a consequence of repressurization in hypotensive vascular beds.
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PMID:Cerebral hyperemia after arteriovenous malformation resection is related to "breakthrough" complications but not to feeding artery pressure. The Columbia University Arteriovenous Malformation Study Project. 872 37

The purpose of this study was to determine if baseline oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in brain tissue adjacent to an arteriovenous malformation (AVM) is different from measures in control patients. In addition, PO2, PCO2, and pH changes were measured during the course of AVM resection. Two groups were studied. Group 1 (n = 8) were non-ischemic patients scheduled for cerebral aneurysm clipping. Group 2 (n = 13) were patients undergoing neurosurgery for AVM resection. Following craniotomy, the dura was retracted and a PO2, PCO2, pH sensor inserted into non-ischemic brain tissue in Group 1. In Group 2, the sensor was inserted into tissue adjacent to the AVM. Following equilibration, tissue gases and pH were measured during steady state anesthetic conditions in Group 1 and during AVM resection in Group 2. The results show that under baseline conditions before the start of surgery, tissue PO2 was decreased in AVM compared to control patients but PCO2 and pH were not changed. During AVM resection, PO2 increased, PCO2 decreased, and pH increased compared to baseline measures. These parameters did not change in control patients over a similar time period. The results suggest that chronic cerebrovascular adaptation occur in AVM patients with decreased tissue perfusion pressure as an adjustment for decreased oxygen delivery. During AVM resection, this adaptation produces a hyperemic environment with relative tissue hyperoxia, hypocapnia, and alkalosis which is not corrected by the end of surgery.
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PMID:Increased brain tissue oxygenation during arteriovenous malformation resection. 1023 2