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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanical and hemodynamic components of a cardiogenic hypertensive chemoreflex were studied in 50 dogs. Within 6 seconds after a single injection of serotonin (100 microgram/ml) into the left atrium, mean pressure (mm Hg) rose in the aorta from 103 to 197 and in the pulmonary artery from 21 to 34. Left ventricular dp/dt virtually doubled. There was an increase (75%) in peripheral vascular resistance that returned to control within 10 seconds. There was no significant change in pulmonary vascular resistance. Aortic and pulmonary arterial hypertension were associated with a profound depression (82%) in atrial force. Atropine transformed this negative inotropic effect on the atria into a positive inotropic action that averaged 65%. In contrast, ventricular force was always sharply increased, more in the right (95%) than in the left ventricle (50%). Bilateral stellectomy did not eliminate the reflex but it completely abolished the initial increase of cardiac contractility; a delayed increase in contractility persisted and was due exclusively to release of catecholamines from the adrenal glands. This cardiogenic hypertensive chemoreflex uses the vagus for its afferent neural traffic and both the sympathetic and the vagus nerves for its efferent route. The brief and intense systemic vasoconstriction concomitant with an increase in cardiac contractility might represent a kind of "aortic cough." Some possible clinical implications are discussed.
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PMID:Hemodynamic components of a cardiogenic hypertensive chemoreflex in dogs. 61 94

The safety of outpatient surgery depends mainly on patient selection, the type of operation, and the anesthetic technique. Subjects of this study were 500 women who as outpatients underwent tubal electrocoagulation through a laparoscope. After an interval of 1 week to 4 months postoperatively, each was sent a questionnaire regarding postanesthetic complications. The questionnaire was returned by 418 patients (83.6%). Several anesthetic agents had been used. Premedication was given only to very nervous patients (18%). Atropine .4 mg was given to all just before the operation. The trachae of all patients were untubated after a dose of succinylcholine and in 60% of cases 3-6 mg of D-tubocurare. There were no immediate anesthetic complications. Most patients were discharged within 3 hours. Postanesthetic complications were common. Muscle pains occurred in 45%, many lasting 2-5 days. Sore throat followed in 28.2% but was usually mild. Headache, nausea, vomiting, cough, and sputum were noted in 8-17%. A mild dizziness was sometimes a complaint. Inability to concentrate was experienced by 30% of patients for over 2 days. In 32.9 %, return to usual work took up to 48 hours; in 57.9%, it was 2-5 days w hile the others required over 5 days. 81% of the patients reported that they would accept the procedure again, while 16.7% would refuse. Return to preoperative mental status usually took several days and in a few over 5 days. Too early use of alcoholic beverages or driving an automob ile were warned against. Most patients considered that the advantage of having the operation as outpatients made up for the discomforts.
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PMID:Anaesthetic complications in surgical out-patients. 115 42

The purpose of this study was to investigate the nature of the serotonin-induced coronary chemoreflex in the conscious monkey. Ten chronically prepared and four acute monkeys were used in this study. Five chronically prepared animals had catheters in the left atrium, ascending aorta, descending aorta, and, bilaterally, in the common carotid arteries. In addition, Silastic catheters were placed next to both vagi to permit vagal block with 2% lidocaine. Serotonin was injected (12-200 micrograms/kg) into the left atrium, ascending aorta, descending aorta, or, bilaterally, into the carotid arteries while blood pressure, heart rate, and respiratory movements were recorded. Injections of serotonin were associated with hypertension and bradycardia followed by tachycardia, all of which were preceded by a cough response. Atropine blocked the bradycardia, whereas atropine and phentolamine eliminated the cardiovascular components of the reflex. Vagal blockade eliminated the bradycardia but otherwise did not alter the response to left atrial serotonin. Three monkeys were prepared with aortic and left atrial catheters. Subsequently, they were subjected to sinoaortic deafferentation. Serotonin injected into these animals did not alter blood pressure or respiration. The results of this study show that serotonin injected into the left atrium of the conscious monkey produces respiratory and cardiovascular alterations by its effect on aortic and carotid chemoreceptors, and that there is no coronary chemoreflex in the conscious monkey.
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PMID:Is there a serotonin-induced hypertensive coronary chemoreflex in the nonhuman primate? 640 20

The modification of cough reflex by contraction and relaxation of the peripheral airway was investigated in anesthetized dogs. For administration of the drugs directly into the peripheral airway, an arterial cannula was chronically implanted in the right bronchial artery via the right intercostal artery. The cough reflex was induced by electrical stimulation of the upper tracheal mucosa by means of an electrode-cannula. Evaluation of the cough response was made by changes in frequency and amplitude of coughs. Drug solutions were infused for 5 min at a rate of 0.17 ml/min into the right bronchial artery. Intraarterial infusion of isoproterenol, 1-3 mu g/min, reduced the amplitude, but had no effect on the frequency of coughs, while that of histamine, 3-10 mu g/min, increased the frequency and amplitude of coughs. Atropine, 100 mu g/min, caused no significant changes in amplitude and frequency, respectively. Benzonatate, 0.85 mg/min, reduced the frequency, but had no effect on the amplitude. Thus, the tonus of the peripheral airway, in particular the airway contraction, may the increase the frequency of cough reflex by lowering the threshold of the airway receptors.
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PMID:[Effects of peripheral airway response on the cough reflex (author's transl)]. 727 38

Atropine is routinely used as part of the premedication regimen for fibreoptic bronchoscopy. This study was performed, firstly, to evaluate the effect of anticholinergic agents on the ease of bronchoscopy, haemodynamic parameters and patient comfort during the procedure; and secondly, to compare atropine with glycopyrrolate, a newer acetylcholine antagonist which is claimed to cause less tachycardia and sedation, whilst suppressing salivation more effectively. One hundred and ninety consecutive patients were randomly allocated to three treatment groups: diazepam 5 mg; diazepam 5 mg + atropine 600 micrograms; and diazepam 5 mg + glycopyrrolate 300 micrograms. Diazepam was given orally one hour before bronchoscopy, and glycopyrrolate/atropine intramuscularly 30 min before bronchoscopy. All patients received thalamonal intravenously, lignocaine gel into one nostril, and lignocaine by transtracheal injection just prior to the procedure. The incidence of bronchoscopy related haemodynamic problems was similar in all three groups. Troublesome coughing, as observed by the operator, was less frequent with glycopyrrolate (control 51%, atropine 42%, glycopyrrolate 30%), as was patient movement (40%, 32%, 19%, respectively). Uncomfortable dryness of the mouth was most common with glycopyrrolate (37%, 32%, 66%, respectively), but overall assessment of discomfort, and the number of patients who would agree to a repeat bronchoscopy (73%, 76%, 70%, respectively) were very similar in all three groups. In conclusion, the differences between the three groups were slight. Glycopyrrolate made the bronchoscopy slightly easier for the operator because of significantly improved cough and movement suppression, though atropine was marginally preferable in terms of patient comfort.
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PMID:Anticholinergic premedication for fibreoptic bronchoscopy. 804 91

1. Pentamidine is routinely used to reduce the incidence of Pneumocystis carinii pneumonia in patients infected with human immunodeficiency virus, but it has been described as inducing pulmonary adverse effects, such as cough and bronchospasm. 2. In this paper we have investigated the effects of pentamidine on guinea-pig isolated main bronchi and human isolated bronchi. Pentamidine induced a concentration-dependent contraction in both preparations with pD2 values of 9.64 +/- 0.07 (n = 8) and 9.73 +/- 0.06 (n = 8) and a maximal effect (Emax) of 40 +/- 4% and 34 +/- 5% of the response to acetylcholine (1 mM) in guinea-pig and human bronchi respectively. Atropine (0.01 to 0.1 microM) and the muscarinic M3 receptor antagonist, hexahydro-siladiphenidol (0.1 and 1 microM) inhibited pentamidine-induced concentration-responses in both preparations in a non-competitive manner, whereas only high concentrations of the M1 receptor antagonist pirenzipine (1 microM) inhibited pentamidine concentration-response curves. 3. The cholinesterase inhibitor, tacrine (1 microM), potentiated the effect of pentamidine; in contrast, morphine inhibited pentamidine-induced responses. 4. The bronchoconstrictor effect of pentamidine on guinea-pig and human isolated bronchi was not modified by the H1 histamine receptor antagonist, mepyramine, by indomethacin or by the neurokinin NK1 and NK2 receptor antagonists, CP-96,345 and SR 48969 respectively, suggesting that neither histamine receptor stimulation, arachidonic acid derivative formation, nor tachykinin release are involved in pentamidine-induced contraction of human and guinea-pig airways. 5. Our overall results suggest that pentamidine induces contraction of guinea-pig and human isolated bronchi through prejunctional cholinergic nerve stimulation.
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PMID:Indirect muscarinic receptor activation by pentamidine on airway smooth muscle. 893 15

1. We studied the effects of an intraperitoneal (i.p.) administration of atropine on bronchomotor tone induced by carbachol aerosols in anaesthetized and ventilated guinea-pigs and on the sensitivity of cough reflex to capsaicin aerosols in awake guinea-pigs. 2. The intraperitoneal administration of atropine (10(-8)-10(-6) M kg(-1)) reduced carbachol (8 mg ml(-1); 1 min)-induced increases in pulmonary insufflation pressure and a complete inhibition was achieved at a dose of 10(-6) M kg(-1) in anaesthetized guinea-pigs. 3. In awake guinea pigs, capsaicin aerosols (10(-5)-10(-3) M) caused dose-dependent increases in the number of coughs. Atropine (10(-7)-10(-6) M kg(-1) i.p.) shifted the dose-response curves to capsaicin to the right in a dose-dependent fashion. Carbachol aerosols, at the maximal concentration (2 mg ml(-1)) that did not cause bronchoconstriction, shifted them to the left compared with the control. 4. Atropine (10(-6) M kg(-1) i.p.) significantly increased the provocative concentration of capsaicin that caused five coughs (P < 0.01) and carbachol aerosols (2 mg ml(-1)) significantly decreased it (P < 0.01). 5. We conclude that cholinergically mediated airway tone regulates cough sensitivity in awake guinea pigs.
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PMID:Cholinergic influence on the sensitivity of cough reflex in awake guinea-pigs. 983 Dec 25

1. Although monumental efforts have been made to define the action sites of cough, the importance of neurotransmitter systems in the cough reflex has received limited attention. We studied the roles for four major neurotransmitters [acetylcholine, histamine, serotonin (5-hydroxytryptamine, 5-HT) and dopamine] in the modulation of the cough reflex. 2. Atropine (muscarinic cholinergic blocking agent), pyrilamine maleate (PM, histamine H1 blocker), cimetidine (histamine H2 blocker), 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT, specific 5-HT1A receptor agonist) and SCH-23390 (selective dopamine D1 receptor antagonist) were examined on the cough response to inhaled capsaicin in conscious guinea-pigs. 3. All the drugs significantly decreased the number of capsaicin-induced coughs in a dose-dependent manner. To compare the sensitivity of these drugs on cough response, we calculated the effective doses for 50% inhibition of cough (ED50) when the animals were exposed to 3 x 10-4 m capsaicin. The ED50 values were 0.03 microm kg-1 for atropine, 0.2 microm kg-1 for 8-OH-DPAT, 6.2 microm kg-1 for SCH-23390, 8.5 microm kg-1 for PM and 13.9 microm kg-1 for cimetidine. 4. These findings indicated that all these four neurotransmitters may be involved in the regulation of the cough reflex. Multiple changes of these neurotransmitters in disorders of the central nervous system might synergically affect the cough reflex.
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PMID:Neurochemical regulation of cough response to capsaicin in guinea-pigs. 1242 27

Gastro-oesophageal acid reflux may cause airway responses such as cough, bronchoconstriction and inflammation in asthmatic patients. Studies in humans or in animals have suggested that these responses involve cholinergic nerves. The purpose of this study was to investigate the role of the efferent vagal component on airway microvascular leakage induced by instillation of hydrochloric acid (HCl) into the oesophagus of guinea-pigs and the subtype of muscarinic receptors involved. Airway microvascular leakage induced by intra-oesophageal HCl instillation was abolished by bilateral vagotomy or by the nicotinic receptor antagonist, hexamethonium. HCl-induced leakage was inhibited by pretreatment with atropine, a non-specific muscarinic receptor antagonist, and also by pretreatment with either pirenzepine, a muscarinic M(1) receptor antagonist, or 4-DAMP, a muscarinic M(3) receptor antagonist. Pirenzepine was more potent than atropine and 4-DAMP. These antagonists were also studied on airway microvascular leakage or bronchoconstriction induced by intravenous administration of acetylcholine (ACh). Atropine, pirenzepine and 4-DAMP inhibited ACh-induced airway microvascular leakage with similar potencies. In sharp contrast, 4-DAMP and atropine were more potent inhibitors of ACh-induced bronchoconstriction than pirenzepine. Methoctramine, a muscarinic M(2) receptor antagonist, was ineffective in all experimental conditions. These results suggest that airway microvascular leakage caused by HCl intra-oesophageal instillation involves ACh release from vagus nerve terminals and that M(1) and M(3) receptors play a major role in cholinergic-mediated microvascular leakage, whereas M(3) receptors are mainly involved in ACh-induced bronchoconstriction.
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PMID:Muscarinic receptors involved in airway vascular leakage induced by experimental gastro-oesophageal reflux. 1836 13

BACKGROUND AND PURPOSE Airway sensory nerves play a key role in respiratory cough, dyspnoea, airway hyper-responsiveness (AHR), all fundamental features of airway diseases [asthma and chronic obstructive pulmonary disease (COPD)]. Vagally mediated airway reflexes such as cough, bronchoconstriction and chest tightness originate from stimulation of airway sensory nerve endings. The transient receptor potential vanilloid 1 receptor (TRPV1) is present on peripheral terminals of airway sensory nerves and modulation of its activity represents a potential target for the pharmacological therapy of AHR in airway disease. EXPERIMENTAL APPROACH As guinea pig models can provide some of the essential features of asthma, including AHR, we have established the model with some classical pharmacological agents and examined the effect of the TRPV1 antagonists, SB-705498 and PF-04065463 on AHR to histamine evoked by ovalbumin (OA) in unanaesthetized sensitized guinea pigs restrained in a double chamber plethysmograph. Specific airway conductance (sGaw) derived from the airflow was calculated as a percentage of change from baseline. KEY RESULTS Cetirizine and salbutamol significantly inhibited OA-evoked bronchoconstriction [sGaw area under the curve (AUC): 70 and 78%, respectively]. Atropine, SB-705498 and PF-04065463 significantly inhibited OA-evoked AHR to histamine in unanaesthetized, OA-sensitized guinea pigs (sGaw AUC: 94%, 57% and 73%, respectively). Furthermore, this effect was not related to antagonism of histamine's activity. CONCLUSION AND IMPLICATIONS These data suggest that TRPV1 receptors located on airway sensory nerves are important in the development of AHR and that modulation of TRPV1-receptor activity represents a potential target for the pharmacological therapy of AHR in airway disease.
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PMID:Inhibition of airway hyper-responsiveness by TRPV1 antagonists (SB-705498 and PF-04065463) in the unanaesthetized, ovalbumin-sensitized guinea pig. 2232 Jan 81


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