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)

We have previously shown that airway hypocapnia induced bronchoconstriction in the guinea pig lung by releasing tachykinins. To examine whether airway hypocapnia could also cause an increase in airway microvascular leakage, a tracheal segment was isolated in vivo in anesthetized guinea pigs and unidirectionally ventilated (200 ml/min) for 1 h with fully conditioned air (0% CO2) or isocapnic gas (5% CO2). The lungs were ventilated through a distally placed tracheal cannula. Microvascular leakage was quantitated by the injection of Evans blue (EB) and its extraction from the tracheal segment. EB extravasation was increased in tracheae exposed to 0% CO2 (52.3 +/- 2.0 micrograms/g wet tissue) compared with tracheae exposed to 5% CO2 (26.4 +/- 2.9 micrograms/g; p less than 0.05) and to tracheae from spontaneously breathing guinea pigs (25.2 +/- 2.3 micrograms/g; p less than 0.05). Groups of animals in which trachea were unidirectionally ventilated with 0% CO2 were then pretreated with a range of drugs in an attempt to determine the mediators responsible for the microvascular leakage with 0% CO2. Capsaicin and morphine pretreatment did not significantly alter 0% CO2-induced EB extravasation, and phosphoramidon prevented rather than increased extravasation, suggesting that tachykinins did not play a role. The hypocapnia-induced increase in microvascular leakage was, however, prevented by indomethacin pretreatment and significantly attenuated by dazmegrel, a thromboxane synthetase inhibitor. We conclude that airway hypocapnia causes microvascular leakage in the guinea pig trachea and that this effect is mediated by prostaglandins and/or thromboxane.
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PMID:Airway hypocapnia increases microvascular leakage in the guinea pig trachea. 173 4

Plasma perfusion patterns were investigated in brain capillaries during decreased cerebral blood flow induced by hyperventilation. Anesthetized rats were decapitated 3-4 s after being given an intravenous bolus injection of Evans blue dye. the measured steep increase of the arterial dye concentration at this moment ensures that different capillary plasma transit times are reflected in different intracapillary dye concentrations. The observed heterogeneity of capillary plasma transit time was expressed as the coefficient of variation (means +/- SD) of the intracapillary dye concentrations. For comparison, cerebral blood flow was determined at comparable PCO2 values in a second experimental group. At arterial PCO2 values between 40 and 25 mmHg, the cerebral blood flow and the coefficient of variation of the intracapillary dye concentration decreased with decreasing PCO2, whereas at PCO2 values <25 mmHg cerebral blood flow and coefficient of variation did not correlate with the arterial PCO2. However, it cannot be excluded that the coefficient of variation of the intracapillary dye concentration increases between 25 and 14 mmHg and decreases between 14 and 10 mmHg. It is concluded that the reduction of cerebral blood flow measured during moderate hypocapnia is paralleled by a decreased heterogeneity of the brain capillary perfusion. During severe hypocapnia this relationship is lost, indicating a potential disturbance of the cerebral microcirculation.
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PMID:Parallel changes of blood flow and heterogeneity of capillary plasma perfusion in rat brains during hypocapnia. 896 87