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)

A series of animals was studied to evaluate the effect of commonly used myoneural blockers (curare, succinylcholine, gallamine, and pancuronium) on intracranial physical dynamics. Of this group, only curare alters intracranial pressure. Histamine release secondary to curare administration results in bronchoconstriction with subsequent major alterations in pulmonary ventilation. Resultant hypercarbia along with a decreased cerebral vascular resistance affects intracranial dynamics by alterations in cerebral blood flow; changes in CSF flow patterns passively reflect the alterations in intracranial pressure. These changes can be blocked by prior treatment with antihistamines.
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PMID:The influence of myoneural blockers on intracranial dynamics. 7 91

In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to further characterize respiratory and cardiac anaphylactic events. In guinea pigs, sensitization was produced by subcutaneous application of ovalbumin together with Freund's adjuvant. Fourteen days after sensitization, the effects of an intravenous infusion of ovalbumin were tested in the anesthetized artificially ventilated guinea pigs. The renewed application of the antigen induced an initial increase of left ventricular pressure which was followed by a rapid decrease 5 min after antigenic challenge. Enddiastolic left ventricular pressure increased within 3 min, thus indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, heart rate steadily decreased. All animals died within 15 min. Simultaneously with cardiac anaphylactic malfunction, severe arterial hypoxia and carbon dioxide retention occurred, revealing respiratory distress. Histamine is known as a potent bronchoconstrictor via histamine H1-receptor stimulation. Administration of H1-receptor antagonists to improve respiration may therefore provide further information on the contribution of pulmonary malfunction to anaphylactic cardiovascular shock. Therefore, additional experiments were performed with sensitized guinea pigs pretreated with the histamine H1-receptor blocker mepyramine. In these experiments the antigenic challenge induced a dissociation of cardiac and respiratory manifestation of anaphylaxis. Despite inhibition of hypoxia and carbon dioxide retention, left ventricular pump failure and occurrence of myocardial ischemia were delayed but not suppressed. It is concluded that histamine is an important mediator of anaphylactic respiratory distress. However, vasoactive anaphylactic mediators other than histamine are primarily involved in anaphylactic cardiac malfunction occurring during the later phase of systemic anaphylaxis.
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PMID:Effects of histamine H1-receptor blockade on respiratory and cardiac manifestation of systemic anaphylaxis. 168 6

To determine whether the intensity of dyspnea at a given level of respiratory motor output differs between bronchoconstriction and the presence of an external resistance, we compared the sensation of difficulty in breathing during isocapnic voluntary hyperventilation in six normal subjects. An external resistance of 1.9 cmH2O.1-1.s was applied during both inspiration and expiration. To induce bronchoconstriction, histamine aerosol (5 mg/ml) was inhaled until airway resistance (Raw) increased to a level approximately equal to the subject's control Raw plus the added external resistance. To clarify the role of vagal afferents on the genesis of dyspnea during both forms of obstruction to airflow, the effect of airway anesthesia by lidocaine aerosol inhalation was also examined after histamine and during external resistive loading. The sensation of difficulty in breathing was rated at 30-s intervals on a visual analog scale during isocapnic voluntary hyperpnea, in which the subjects were asked to copy an oscilloscope volume trace obtained previously during progressive hypercapnia. Histamine inhalation significantly increased the intensity of the dyspneic sensation over the equivalent external resistive load at the same levels of ventilation and occlusion pressure during voluntary hyperpnea. Inhaled lidocaine decreased the sensation of dyspnea during bronchoconstriction with no change in Raw, but it did not significantly change the sensation during external resistive loading. These results suggest that afferent vagal activity plays a role in the genesis of dyspnea during bronchoconstriction.
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PMID:Effects of bronchoconstriction and external resistive loading on the sensation of dyspnea. 177 11

We exposed two awake dogs with a chronic tracheostomy and the cervical vagus nerves exteriorized in skin loops to 1.0 ppm of ozone (O3) for 2 h at intervals of 4 wk. We measured ventilatory variables before and after O3 exposure during rest and exercise before and after vagal block. We compared the effects of vagal blockade, exercise, and O3 on the primary determinants of breathing pattern (VT/TI, VT/TE, TI, and TE) in each of three conditions: base line (steady state), during hypercapnia, and after inhalation of 1% histamine. Under base-line conditions, O3 increased respiratory rate and decreased tidal volume (VT) by shortening time of expiration (TE) and time of inspiration (TI) without affecting VT/TI, an indicator of the neural drive to breathing. During progressive hypercapnia, O3 shortened TE and TI by effects both on tonic (nonvolume-related) and on phasic (volume-related) vagal inputs, and only the latter were prevented completely by cooling of the vagus nerves. Histamine-induced tachypnea was increased by O3 and was totally blocked by cooling the vagus nerves. We conclude that O3 shortens the timing of respiration without increasing ventilatory drive, shortens TI and TE through vagal and nonvagal pathways, increases tonic nonvagal and phasic vagal inputs, and stimulates more than one vagal fiber type.
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PMID:Effect of ozone on breathing in dogs: vagal and nonvagal mechanisms. 355 75

In nine greyhound dogs, anaesthetized with chloralose-urethane, total lung resistance, volume of an isolated cervical tracheal segment and resistance of the isolated larynx were simultaneously measured. Three stimuli were tested: inhalation of a CO2-enriched gas mixture; histamine injected intravenously or administered by aerosol to stimulate primarily lung irritant receptors; and intravenous injection of capsaicin to stimulate primarily lung C-fibre receptors. The stimuli were applied in three successive conditions: neurally-intact animals; denervation of the right lung plus cold block of myelinated fibres in the left cervical vagus nerve; and further blockade of non-myelinated fibres in this nerve. Histamine and capsaicin increased lung and laryngeal resistances, and reduced tracheal volume, and the responses after denervation are consistent with the drugs acting by lung vagal reflexes. In neurally-intact animals, hypercapnia increased total lung resistance, decreased tracheal volume and lowered laryngeal resistance. After elimination of conduction in all myelinated fibres, CO2-induced changes in lung resistance and in tracheal volume were still present. However, the dilating effect of hypercapnia on the larynx diminished markedly. Elimination of all vagal pulmonary afferents abolished the residual laryngeal response to hypercapnia, lowered and delayed changes in tracheal volume and greatly reduced the increase in lung resistance. The results indicate that the laryngeal response to hypercapnia depends on vagal integrity, but the tracheobronchial constrictor effect of CO2 is less affected by vagal denervation.
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PMID:Tracheobronchial and laryngeal responses to hypercapnia, histamine and capsaicin in dogs. 407 57

Central histaminergic neurons are distributed in areas of the medulla and pons concerned with respiratory rhythm generation, but their effects on breathing pattern are unknown. We examined breathing pattern during hypercapnic responses in wild type (WT) and H1 receptor knockout (H1RKO) mice at 9-10 weeks of age before and after vagotomy. Minute ventilation increased with PaCO(2) increase equally in both genotypes; respiratory rate response was lower and tidal volume (V(T)) response higher in H1RKO mice than in WT mice. The V(T)-inspiratory time (T(I)) relation during hypercapnia was hyperbolic in both groups, with the curve in H1RKO mice shifted right-upward. After vagotomy, the V(T)-T(I) relation was a vertical line, which shifted right in H1RKO mice. We conclude that alterations of inspiratory off-switch and respiratory rhythm generation change breathing pattern without affecting central chemosensitivity in H1RKO. Histamine might affect breathing pattern centrally via H1 receptors.
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PMID:Central histamine contributes to the inspiratory off-switch mechanism via H1 receptors in mice. 1552