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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pentobarbital-anesthetized greyhounds were passively hyperventilated using intermittent positive-pressure breathing (IPPV) and the effects of raised airway pressure, accompanied by hypocapnia and then by normocapnia, on liver blood flow and oxygen consumption were studied. Electromagnetic flowmeters were used to measure hepatic arterial, portal venous, and splenic venous blood flow. Studies were carried out at three levels of raised airway pressure, both at normocapnia and hypocapnia. It was found that hypocapnic hyperventilation produced a decrease in portal venous and hepatic arterial blood flow. Normocapnic hyperventilation resulted in a restoration of portal venous blood flow but with a further decrease in hepatic arterial blood flow. A decrease in oxygen consumption with hypocapnia, returning to control values with normocapnia, was seen. It is suggested that the reduction in liver blood flow and oxygen consumption seen with passive hyperventilation is chiefly an effect of hypocapnia and is largely reversed by restoration of normocapnia.
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PMID:Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound. 38 Dec 63

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
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PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

In a prospective study of 225 consecutive pediatric patients who required sedation for CT imaging, we monitored oral and nasal air flow, transcutaneous oxygen saturation, and cardiac rate and rhythm before and after the administration of IV Nembutal. In addition, the first 50 patients in this series had blood pressures mechanically monitored at 1-min intervals. There was no significant change in the cardiac rate, rhythm, or blood pressure in any patient. Seventeen episodes (7.5%) of transient oxygen desaturation to 80% of baseline or less occurred after sedation. The patterns of oxygen desaturation in this series can be explained by the following mechanisms: (1) hyperventilation leading to hypocapnia with resultant loss of the CO2 stimulus of respiration (12 patients); (2) upper airway obstruction from pharyngeal muscle relaxation (three patients); (3) a shift in sensitivity of CNS CO2 receptors (one patient); and (4) central apnea (one patient). Oxygen desaturation normalized spontaneously in 14 patients. In two patients, oxygen saturations returned to normal after modification of head position to optimize airway patency. In one patient, mild stimulation was required to interrupt transient apnea. All but one patient in whom desaturation occurred showed oxygen desaturation within the first 5 min after IV sedation. At The Children's Hospital of Denver, IV Nembutal has been used in over 870 pediatric patients. No patient required resuscitation, intubation, or assisted ventilation. Only one patient required prolonged observation, and one patient demonstrated an idiosyncratic hyperactive response. The sedation failure rate was less than 1%. The average dose of sedation was reduced when compared with IM Nembutal because the rapid onset of activity after IV administration allowed titration of dose to patient response.
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PMID:IV Nembutal: safe sedation for children undergoing CT. 326 31

A technique is described for the chronic measurement of cerebral blood flow in conscious, unrestrained rodents, utilizing laser doppler flowmetry (LDF) removably coupled to an optical fiber permanently implanted into brain tissue by established stereotaxic procedures. Changes in relative blood flow in response to a range of pharmacological and behavioral challenges were measured in the hippocampus (HBF) and striatum (StBF) 24-72 h and up to 28-32 days after surgical implantation of the optical fiber. Intraseptal microinfusion of L-glutamate in artificial cerebrospinal fluid 48-96 h and 28-32 days after surgery increased HBF. Pentobarbital (Nembutal) and urethane anesthesia decreased HBF. On the day of euthanasia under urethane anesthesia, HBF was demonstrated to be responsive to alteration of blood CO2 via hyper/hypocapnia, and autoregulation was demonstrated in response to hypovolemic hypotension. In behavioral experiments, blood flow was found to increase with activity and locomotion, as well as during paradoxical (PS) and slow-wave sleep (SWS). The greatest increase in CBF was measured during PS. Although basal levels of blood flow were similar between regions, the increase in blood flow during PS was greater in the hippocampus. This simple procedure enables real-time measurement of qualitative changes in regional cerebral blood flow during behaviors in conscious, unrestrained animals. The observation that constancy of measurements was obtained for 1 month enables within-subject analysis in longitudinal studies and reduces the number of animals required for investigations.
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PMID:Hippocampal and striatal blood flow during behavior in rats: chronic laser Doppler flowmetry study. 910 65