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)

To assess the possibility that climbing to extremely high altitude may result in hypoxic injury to the brain, we performed neuropsychological and physiologic testing on 35 mountaineers before and 1 to 30 days after ascent to altitudes between 5488 and 8848 m, and on 6 subjects before and after simulation in an altitude chamber of a 40-day ascent to 8848 m. Neuropsychological testing revealed a decline in visual long-term memory after ascent as compared with before; of 14 visual items of information on the Wechsler Memory Scale, fewer were recalled after ascent by both the simulated-ascent group (a mean [+/- SD] of 10.14 +/- 1.68 items before, as compared with 7.00 +/- 3.35 items after; P less than 0.05) and the mountaineers (12.33 +/- 1.96 as compared with 11.36 +/- 1.88; P less than 0.05). Verbal long-term memory was also affected, but only in the simulated-ascent group; of a total of 10 words, an average of 8.14 +/- 1.86 were recalled before simulated ascent, but only 6.83 +/- 1.47 afterward (P less than 0.05). On the aphasia screening test, on which normal persons make an average of less than one error in verbal expression, the mountaineers made twice as many aphasic errors after ascent (1.03 +/- 1.10) as before (0.52 +/- 0.80; P less than 0.05). A higher ventilatory response to hypoxia correlated with a reduction in verbal learning (r = -0.88, P less than 0.05) and with poor long-term verbal memory (r = -0.99, P less than 0.01) after ascent. An increase in the number of aphasic errors on the aphasia screening test also correlated with a higher ventilatory response to hypoxia in both the simulated-ascent group (r = 0.94, P less than 0.01) and a subgroup of 11 mountaineers (r = 0.59, P less than 0.05). We conclude that persons with a more vigorous ventilatory response to hypoxia have more residual neurobehavioral impairment after returning to lower elevations. This finding may be explained by poorer oxygenation of the brain despite greater ventilation, perhaps because of a decrease in cerebral blood flow caused by hypocapnia that more than offsets the increase in arterial oxygen saturation.
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PMID:The cost to the central nervous system of climbing to extremely high altitude. 251 83

A 31-year old primigravida was admitted at 31 week gestation for subarachnoid haemorrhage. Cerebral angiography revealed an aneurysm on the left middle cerebral artery. Eleven days later, the aneurysm was clipped off. General anaesthesia was induced with thiopentone, pancuronium and fentanyl, and maintained with fentanyl (40 micrograms.kg-1) and isoflurane in air/O2 with a non-rebreathing circuit. The patient was mechanically ventilated to maintain mild hypocapnia. Arterial hypotension was induced by increasing the inspired isoflurane concentration from 1 to 3 vol%. The response was immediate and a mean arterial pressure of 60 mmHg was maintained for 80 min with an inspired isoflurane concentration of 2.5 vol%. Foetal heart rate was monitored before, during and after general anaesthesia. Loss of beat to beat variation was observed after induction, and foetal heart rate slowly decreased from 150 to 115 b.min-1 at the end of the operation. Postoperative state was good, except for transitory aphasia. At 35 week gestation, the patient went into premature labour, with hypothermia of 39.5 degrees C; an emergency caesarean section was performed. The 2,340 g female infant had a 10 min Apgar score of 8. One month later, clinical examination of the mother and daughter was quite normal. The precautions and anaesthetic management of patients suffering from ruptured cerebral aneurysm during the end of pregnancy are reviewed. Hypotensive agents are discussed.
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PMID:[Hypotension induced by isoflurane for the treatment of intracranial aneurysm in late pregnancy]. 343 89