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)

To evaluate the role of certain plasma biosubstances on the development of pulmonary hypertension and shock during severe hypoxia, hypercapnia and acidosis, plasma renin activity (PRA), angiotensin II (ATII), angiotensin converting enzyme (ACE), TXB2 and 6-Keto-PGF1 alpha (the stable metabolites of TXA2 and PGI2) were assayed in blood from pulmonary artery and aorta in seven pigs. Pulmonary arterial pressure (PAP) was monitored via Swan-Ganz catheter. During hypoxic and hypercapnic ventilation, PaO2 dropped to 4.7 kPa, PaCO2 rose to 21.1 kPa, pH dropped to 6.82, PAP increased from 2.43 +/- 0.06 to 4.46 +/- 0.45 kPa when acidotic shock developed (all P less than 0.05). Meanwhile ATII levels rose (all P less than 0.05). PRA significantly increased during acidotic shock as compared with normal ventilation (P less than 0.02). ACE dropped significantly (P less than 0.05), TXB2 and 6-keto-PGF1 alpha showed no significant change before and after hypoxic and hypercapnic ventilation.
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PMID:[Plasma renin activity, angiotensin II, angiotensin converting enzyme, thromboxane A2 and prostacyclin I2 levels in pigs with severe hypoxia and hypercapnea and acidosis shock]. 132 48

Effects of topical application of hydrogen peroxide (H2O2) on pial arteriolar diameter and cerebral prostanoid synthesis were examined in newborn pigs. H2O2 (10 mM) caused initial constriction during the 1st min, followed by prolonged (20 min) dilation that was reversed on removal of the H2O2 in piglets treated with deferoxamine. H2O2 also caused an increase in cortical periarachnoid 6-ketoprostaglandin F1 alpha, thromboxane (TX) B2, and prostaglandin (PG) E2. Indomethacin pretreatment or coadministration of SQ 29548 (PGH2/TXA2 receptor antagonist) with H2O2 blocked the constriction due to H2O2 but did not alter the dilation. The constriction, the dilation, and the increased prostanoids caused by H2O2 were not affected by topical and systemic deferoxamine (an iron chelator) or simultaneous application of FeSO4 and FeCl3. Neither prior treatment with H2O2 nor with H2O2 plus FeSO4 and FeCl3 altered pial arteriolar dilation in response to hypercapnia. Therefore the initial constriction caused by H2O2 appears to result from stimulation of prostanoid synthesis and activation of PGH2/TXA2 receptors, whereas the dilation is not caused by prostanoids. H2O2 alone does not produce detectable residual alteration of pial arteriolar responsiveness or cerebral prostanoid synthesis.
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PMID:H2O2 effects on cerebral prostanoids and pial arteriolar diameter in piglets. 233 73

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.
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PMID:[Observation on TXB2 and 6-keto-PGF1 alpha in serum of patients with cor pulmonale]. 938 73