Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.
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PMID:The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain. 1 66

A thoracotomy was performed at the left 5th intercostal space in 24 dogs. Dogs were assigned to 4 groups of 6 dogs each. Postoperative analgesia was administered as follows: group 1--control, no analgesia; group II--morphine (0.5 mg/kg of body weight); group III--oxymorphone (0.1 mg/kg); group IV--selective intercostal nerve block with bupivacaine HC1. Respiratory rate, minute volume (VE), and arterial blood gases were measured during the recovery period. Ventilation-perfusion mismatch was estimated by calculation of the alveolar-arterial oxygen tension difference. Arterial carbon dioxide tension (Paco2) in the control and selective intercostal nerve block groups remained within the normal range and did not differ significantly (P less than 0.05) between groups. During the first 60 to 90 minutes after surgery, Paco2 tension was increased significantly (P less than 0.05) in the groups given morphine and oxymorphone. Hypoventilation in the groups given narcotics resulted from significant reductions (P less than 0.05) in the respiratory rate and VE and produced significant (P less than 0.05) respiratory acidosis and hypoxemia. Three dogs in the groups given narcotics had a panting response that resulted in increased respiratory rates and VE. This response did not improve alveolar ventilation in these dogs, which was evidenced by increased Paco2 values. Hypoventilation, respiratory acidosis, and hypoxemia in the groups given narcotics improved significantly with time, presumably because of drug clearance. Values for alveolar-arterial oxygen tension difference indicated moderate ventilation-perfusion mismatch secondary to anesthesia in all groups; however, significant differences (P less than 0.05) between the groups were not observed.
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PMID:Pulmonary function in dogs after intercostal thoracotomy: comparison of morphine, oxymorphone, and selective intercostal nerve block. 242 Feb 41