Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in six dogs each with a tracheostomy, awake and during anaesthesia with halothane, enflurane and isoflurane (1-2.5 MAC). Isocapnic hypoxic ventilatory response (HVR) was expressed as the parameter A, such that the greater the value of A, the greater the hypoxic response. In the anaesthetized dogs HVR (A) was reduced significantly from the awake value of 2010 +/- 172 (mean + SEM) to 630 +/- 173 by 1 MAC halothane, 495 +/- 105 by 1 MAC enflurane and 952 +/- 157 by 1 MAC isoflurane (PL0.05). All three anaesthetic agents produced significant depression of HUR at 1 MAC, but enflurane was more depressant than isoflurane. At 1.5 MAC all three anaesthetics produced equal and significant depression of HVR at equianalgesic concentrations. Further increases in anaesthetic concentration caused no increase in depression. Hypercapnic drive, as measured by the slope of the VE/PACO2 response curve, was reduced significantly from 9.75 litre min-1 kPa-1 +/- 2.4 in awake dogs to 0.83 +/- 0.56 after 1 MAC halothane, 0.68 +/- 0.53 after 1 MAC enflurane and 1.58 +/- 0.75 after 1 MAC isoflurane. In addition, hypercapnia-induced augmentation of the hypoxic drive was abolished by 1 MAC halothane or enflurane and diminished markedly by 1 MAC isoflurane. It may be clinically significant that hypoxia and hypercapnia during anaesthesia with these agents did not produce optimal stimulation of ventilation.
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PMID:Depression of hypoxic ventilatory response by halothane, enflurane and isoflurane in dogs. 92 74

With a sensitive enzyme-linked immunoadsorbent assay that can detect as little as 0.5ng/ml of myelin basic protein (MBP), we studied serum specimens from 34 patients with chronic cor pulmonale (CP) and 33 patients with chronic bronchitis (CB) during acute attack in hospital and 30 control subjects. The results showed that the serum mean MBP level of CP patients was markedly higher than those of CB patients and controls (P < 0.01), but no statistically significant differences were found between CB patients and controls (P > 0.05). There was a positive correlation between elevated levels of serum MBP and carbon dioxide partial pressure (PaCO2). This suggested that elevated serum MBP levels may be associated with brain destruction by hypercapnia and hypoxia of CP patients.
Hua Xi Yi Ke Da Xue Xue Bao 1995 Jun
PMID:[Myelin basic protein level in serum of patients with chronic cor pulmonale in acute phase]. 749 17

To know the changes of TXA2 and PGI2 in serum of patients with cor pulmonale, the levels of their stable metabolites TXB2 and 6-keto-PGF1 alpha in serum were examined in 28 patients with cor pulmonale during alleviation, 29 patients with cor pulmonale during exacerbation before and after treatment and 10 healthy subjects. TXB2 and 6-keto-PGF1 alpha were 109.74 +/- 56.14 ng/L and 54.76 +/- 35.62 ng/L respectively in healthy subjects; TXB2/6-keto-PGF1 alpha = 2.004. The TXB2 level of patients with cor pulmonale at every stage was higher than that of healthy subjects (P < 0.05-0.01). Patients with cor pulmonale during exacerbation had the highest TXB2 level of 709.22 +/- 354.49 ng/L, which decreased to 408.24 +/- 289.41 ng/L (P < 0.05) after treatment with traditional Chinese medicine combined with western medicine and the decreased level as such was not significantly different from that during alleviation (333.14 +/- 324.14 ng/L). The 6-keto-PGF1 alpha level in patients with cor pulmonale at every stage was not significantly different from that of healthy subjects. Since TXB2 increased, the value TXB2/6-keto-PGF1 alpha of patients with cor pulmonale was greater than that of healthy subjects. It is most likely that chronic hypoxia and hypercapnia lead to prostaglandin release in the lung of patients with cor pulmonale; hypoxia and hypercapnia become more severe during exacerbation resulting from infection; which lead to increased prostaglandin release, then high TXB2 level ensue as the result. TXB2 decreases after amelioration of hypoxia during treatment. But the change of 6-keto-PGF1 alpha is not obvious.
Hua Xi Yi Ke Da Xue Xue Bao 1996 Sep
PMID:[Observation on TXB2 and 6-keto-PGF1 alpha in serum of patients with cor pulmonale]. 938 73