Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Airway hypocapnia increases microvascular leakage in the guinea pig trachea. 173 4

The aim of this study was to determine whether hypocapnia causes bronchoconstriction by releasing tachykinins (TKs) from C-afferent nerves in airways. Hypocapnia-induced bronchoconstriction (HIBC) was induced in anesthetized vagotomized guina pigs by ventilating lungs with a heated humidified hypocapnic gas mixture for 15 min after sudden circulatory arrest. The intensity of bronchoconstriction was assessed by calculating changes in dynamic compliance and by measuring the relaxation lung volume at the completion of experiments. Visualization of the airways by tantalum bronchography showed constriction of segmental bronchi with relative sparing of more proximal airways. Hypocapnia-induced bronchoconstriction was prevented by prior administration of salbutamol aerosol. Three experimental interventions were used to investigate the role of TKs in HIBC: 1) repeated capsaicin injections to deplete airway sensory nerves of TKs, 2) treatment with phosphoramidon, an inhibitor of enkephalinase, the main enzyme responsible for TK inactivation, and 3) topical airway anesthesia. Capsaicin pretreatment markedly attenuated the hypocapnia-induced changes in dynamic compliance (P less than 0.0005) and relaxation lung volume (P less than 0.0002), whereas phosphoramidon augmented these changes (P less than 0.02, P less than 0.03, respectively). Topical anesthesia of airways with lignocaine postponed the onset of bronchoconstriction, whereas the longer-acting, more lipid-soluble local anesthetic, bupivacaine, almost completely prevented HIBC. We conclude that, in the guinea pig lung, HIBC is mediated by TKs that are released after the activation of bronchial axonal reflexes.
 ...
PMID:Tachykinins mediate hypocapnia-induced bronchoconstriction in guinea pigs. 251 77

Bilateral carotid occlusion (BCO) was performed in pentobarbital anesthetized adult rats neonatally treated with capsaicin (50 mg/kg, sc, CNT rats). Pressor and ventilatory responses to BCO in CNT rats were compared with those of littermate controls injected with a same volume of solvent (olive oil, 0.1 ml). Capsaicin was used in order to produce partial degeneration of unmyelinated C fibres related to baroreflexes and peripheral chemoreflexes. In control rats, BCO provoked in less than 5 s, hyperventilation, hypocapnia and hyperoxia. Systemic arterial hypertension and tachycardia developed more slowly. They were maximum at 65 s. At this time, ventilation was returned to control values. Hyperventilation results from the stimulation of the carotid chemoreceptors by stagnant asphyxia generated by the blood flow stop. Hypertension and tachycardia are provoked by an increase in the orthosympathetic outflow when carotid baroreceptors are unloaded. In a first time, chemoreceptors stimulation tends to oppose to the increase of heart rate in normal rats. In a second one, development of hypertension is autolimited by the stimulation of the aortic baroreceptors particularly effective in rats. Simultaneously the hyperoxic inhibition from aortic chemoreceptors, the central hypocapnia and the reperfusion of the carotid bodies lead to the suppression of hyperventilation. As hyperventilation decreases when hypertension develops, even in rats with vago-sympathetic section at low cervical level, the part of aortic baroreceptors effects is probably reduced except for the fibres travelling through superior laryngeal nerves. Carotid bodies reperfusion seems to predominate. Before any manipulations, CNT rats had lower heart rate and systemic blood pressure than controls. During BCO, initial hyperventilation was moderately prolonged as hypertension slowly developed.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Bilateral carotid occlusion in the rat neonatally treated with capsaicin]. 800 42