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At least 1,171 records · Page 65Linked to original sources
PubMed1980

Long-lasting hyperventilation induced by almitrine: evidence for a specific effect on carotid and thoracic chemoreceptors.

In anesthetized dogs, almitrine (0.5-3 mg/kg i.v.) induced a dose-dependent increase in respiratory rate and ventilation. The aortic and carotid chemoreceptors were involved in the effects of almitrine. Section of both carotid sinus nerves and vagus nerves abolished the effects of the drug on respiration. The respiratory response did not occur in dogs with bilateral lesions of the nucleus of the solitary tract. The electrical activity of chemoreceptor fibres was increased. Perfusion of almitrine into the carotid artery stimulated respiration. Inhalation of pure oxygen shifted the dose-response curve of the respiratory effect towards the right. Almitrine slightly stimulated ventilation in dogs with bilateral section of carotid sinus nerves and aortic nerves and this disappeared when both vagus nerves were cut indicating that this effect was mediated through some chemoreceptor fibres present in the vagus nerves or through afferent vagal fibres.

Animals↗
PubMed1975

Hyperoxic hyperventilation in carotid-deafferented cats.

Ventilation when breathing air and during exposure to hyperoxia (PAO2 equal to 400-450 mm Hg) was studied in unanesthetized cats before and after carotid sinus nerve section (chemo-deafferentation). Chemo-deafferentation resulted in lowered values of measured ventilation, tidal volume, and respiratory frequency, during air breathing PACO2 increased by an average of 7.9 mm Hg. In intact animals, ventilation after 10 minutes of exposure to hyperoxia was similar in magnitude and pattern to that measured during air breathing. Exposure of chemo-deafferented animals to hyperoxia resulted in an increased ventilation, due entirely to augmented tidal volume. Increased ventilation was accompanied by a decrease in PACO2. This response to hyperoxia developed gradually duringa 3-4-minute period, the rise in ventilation and fall in PACO2 invariably stabilizing by 5 minutes. It is concluded that carotid body chemoreceptor activity is essential for the maintenance of normal values of ventilation and PACO2 in unanesthetized cats. In addition, central mechanisms responsible for tidal volume production may, in the absence of carotid body afferent input, be depressed by the PO2 characteristic of normal arterial blood. The significance of these findings to the chemical control of breathing is discussed.

Air↗
PubMed1977

Patterns of bulbar respiratory neurons during and after artifical hyperventilation.

Single bulbar respiratory unit activity was recorded in urethane-anesthetized rabbits. During artificial ventilation, reflex contractions of the diaphragm were elicited by the forced deflations of the respirator. Out of 44 neurons, four I, one E and two EI units exhibited a shift of their discharge relative to the contractile phase of the diaphragm, compared to normal respiration. During hypocapnic apnea, some I, IE and E neurons became silent. Other cells belonging to all phase types, however, continued to fire tonically at a rate less than the peak rate in normal bursts. When rhythmic respiration resumed after termination of the apneic pause, five (I, IE and E) units exhibited a transient phase shift of their burst discharge compared to normal respiration. The results of simultaneous recordings of two neurons belonging to different phase types are compatible with the assumption that inspiratory units are periodically inhibited by inspiratory-expiratory cells.

Animals↗
PubMed1984

Exercise and isocapnic hyperventilation-induced bronchoconstriction in asthma: relevance of circulating basophils to measurements of plasma histamine.

The relationship of airway cooling during exercise to changes in airway caliber, plasma histamine levels, and circulating basophils was investigated in eight allergic asthmatic and eight normal subjects. In asthma matched RHE during exercise and ICH produced almost identical bronchoconstriction with maximum falls in SGaw of 61.0 +/- 4.5% and 57.9 +/- 5.2%, respectively. A similar RHE in normal subjects was associated with a 7.9 +/- 3.3% fall in SGaw. The resting plasma-histamine levels were higher in the asthmatic (0.52 +/- 0.06 ng/ml) than in the normal (0.31 +/- 0.07 ng/ml, p less than 0.05) subjects. No significant change in plasma histamine occurred after exercise in either group nor in the asthmatic subjects with ICH. In contrast, exercise but not ICH stimulated an increase in leukocytes, basophils, and total blood histamine in parallel with the airway response that reached a maximum at 2 to 5 min in both normal and asthmatic subjects. There was a positive correlation between basal plasma and total blood-histamine levels (r = 0.67, p less than 0.01) in normal and asthmatic subjects suggesting that basophils contribute significantly to plasma histamine. The spontaneous basophil release of histamine was greater in asthmatic (13.4 +/- 2%) than in normal subjects (6.46 +/- 7%, p less than 0.005), which is consistent with the higher resting plasma-histamine levels in the asthmatic subjects. These findings suggest that plasma-histamine changes with exercise in asthma but not ICH may be related to the associated basophilia and sample handling rather than intrapulmonary mast cell degranulation.

Adult↗