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At least 865 records · Page 48Linked to original sources
PubMed1995

Chronic cough and hoarseness in patients with severe gastroesophageal reflux disease. Diagnosis and response to therapy.

Gastroesophageal reflux may be responsible for atypical symptoms such as chronic cough and hoarseness. Our aim was to evaluate and treat patients with severe gastroesophageal reflux and chronic cough or hoarseness with intensive antireflux therapy. Twenty-seven patients with typical heartburn symptoms in addition to significant cough or hoarseness were treated with aggressive antireflux therapy. We recorded the response of each symptom to the antireflux therapy. Two patients were lost to follow-up. Twenty of the 25 (80%) patients showed some improvement in cough or hoarseness, nine (36%) had no atypical symptoms at follow-up. The response of heartburn to therapy was strongly predictive of successful therapy for the atypical symptoms. Cough and hoarseness improved in only two of the five patients with residual heartburn symptoms compared to 18 of 20 patients with no heartburn (P < 0.04). Only patients with no heartburn symptoms at follow-up had complete resolution of atypical symptoms. There were no important differences on ambulatory pH monitoring between partial and complete responders. Improvement in atypical reflux symptoms, such as chronic cough and hoarseness, is common with aggressive antireflux therapy. There are no findings on ambulatory esophageal pH monitoring that uniquely identify patients who are likely to respond to antireflux therapy.

Case-Control Studies↗
PubMed1996

Terbutaline inhalation suppresses fentanyl-induced coughing.

PURPOSE: To study the suppressive effect of inhalation of a selective beta 2-adrenergic bronchodilator terbutaline, and the effect of an intravenous anticholinergic, atropine, on fentanyl-induced coughing. METHODS: We studied 131 ASA class I patients, aged 16-45 yr, scheduled for elective surgery, randomized into four groups. Fifteen minutes before bolus fentanyl (5 micrograms.kg-1, iv), patients inhaled either normal saline (4 ml; Group I, n = 30) or terbutaline (5 mg in 2 ml normal saline; Group 2, n = 34) via a jet nebulizer. After inhalation of normal saline, patients in Group 3 (n = 32) received sterile water iv instead of fentanyl. Patients in Group 4 (n = 35) were pretreated with atropine (0.01 mg.kg-1, iv) 10 min before iv fentanyl bolus. The onset, frequency and intensity of cough were observed immediately by an anaesthetist blinded to the study. RESULTS: The cough frequency was higher in Groups I (43%) and 4 (46%) than in Groups 2 (3%) and 3 (0%) (P < 0.05). The onset time and intensity of cough showed no difference among groups. No truncal rigidity was observed in patients receiving fentanyl bolus iv. The blood pressure, heart rate, and peripheral oxygen saturation did not change in Groups 1, 2, and 3, while patients in Group 4 showed an increase in heart rate (25.5 +/- 15.2%). CONCLUSIONS: The inhalation of a selective beta 2-adrenergic bronchodilator, terbutaline, effectively inhibited fentanyl-induced cough, whereas atropine, an antimuscarinic vagolytic, had no efficacy. Our results suggest that bronchoconstriction may underlie the mechanism on fentanyl-induced cough.

Administration, Inhalation↗
PubMedDate not supplied

Intravenous lidocaine and ephedrine, but not propofol, suppress fentanyl-induced cough.

PURPOSE: The aim of this study was to evaluate the effectiveness of lidocaine, propofol and ephedrine in suppressing fentanyl-induced cough. METHODS: One hundred and eighteen patients were randomly assigned into four groups and the following medications were given intravenously: patients in Group I (n = 31) received normal saline 2 mL, Group II (n = 29) received lidocaine 2 mg.kg(-1), Group III (n = 30) received propofol 0.6 mg.kg(-1) and Group IV (n = 28) received ephedrine 5 mg. At one minute after the study medication, fentanyl 2.5 microg.kg(-1) was given intravenously within two seconds. The occurrence of cough and vital sign profiles were recorded within two minutes after fentanyl bolus by an anesthesiologist blinded to study design. RESULTS: Sixty-five percent of patients in the placebo group had cough, whereas the frequency was significantly decreased in Groups II (14%) and IV (21%). Although a numerically lower frequency of cough was noted in Group III (37%), it was not statistically different from that of the placebo group. SpO(2) decreased significantly in patients of Group III compared to placebo; one patient experienced hypoxemia necessitating mask ventilation. Patients in Group III showed a decrease in heart rate and systolic blood pressure (2 beats.min(-1) and 8 mmHg vs baseline). Patients in Group IV showed an increase in both measurements (5 beats.min(-1) and 8 mmHg vs baseline). No truncal rigidity was observed throughout the study. CONCLUSIONS: Intravenous lidocaine 2 mg.kg(-1) or ephedrine 5 mg, but not propofol 0.6 mg.kg(-1), was effective in preventing fentanyl-induced cough. The results provide a convenient method to decrease fentanyl-induced cough.

Adult↗
PubMedDate not supplied

Comparative study of effects of angiotensin II receptor antagonist, KD3-671, and angiotensin converting enzyme inhibitor, enalaprilat, on cough reflex in guinea pig.

Angiotensin converting enzyme (ACE) inhibitor prevents the inactivation of bradykinin by inhibiting ACE activity, leading to side effects such as dry cough and angioedema. KD3-671 is a novel nonpeptide angiotensin II antagonist which is expected to exhibit persistent hypotensive action without these side effects. In this study, we investigated the relationship between the pharmacokinetics and cough-inducing effect of this drug in guinea-pig, compared with that of an ACE inhibitor, enalaprilat. KD3-671 was not significantly different from the vehicle treatment in the ability to induce coughing, whereas enalaprilat significantly enhanced coughing compared with the vehicle treatment. Thus, as expected from its mechanism of pharmacological action, KD3-671 did not induce coughing. We suggest that the citric acid-induced guinea pig coughing model will be useful in preclinical studies to examine the effect of drug on pulmonary function.

Angiotensin II↗
PubMed1992

Effects of inhaled alpha 2-adrenoceptor and GABAB receptor agonists on citric acid-induced cough and tidal volume changes in guinea pigs.

The effects of alpha 2-adrenoceptor and GABA receptor agonists on citric acid-induced cough and increased tidal volume were investigated in conscious guinea pigs. Inhalation of low doses of B-HT 920 (5-allyl-2-amino 5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]azepine dihydrochloride), and xylazine significantly inhibited citric acid-induced cough and tidal volume increases. Intraperitoneal administration of higher doses of B-HT 920 than those given by aerosol were ineffective. The inhibitory effects of B-HT 920 were antagonised by prior intraperitoneal administration of yohimbine, but not atropine. Inhalation of GABA or baclofen inhibited tidal volume increases, but had no effect on cough. Inhaled alpha 2-adrenoceptor or GABA agonists had no effect on the reduced respiratory rate after citric acid inhalation. It is concluded that alpha 2-adrenoceptor agonists inhibit cough via a mechanism which may not be related to their ability to reduce citric acid-induced tidal volume increases, since GABA and baclofen inhibited tidal volume increases but not cough. We suggest that alpha 2-adrenoceptor agonists may have therapeutic potential in the treatment of cough.

Acetylcholine↗
PubMedDate not supplied

Hemodynamics of cough cardiopulmonary resuscitation in a patient with sustained torsades de pointes/ventricular flutter.

A 43-year-old female with old myocardial infarction and stenosed bypass grafts developed sustained Torsades de Pointes/ventricular flutter (rate = 300-400 beats per minute) during coronary arteriography after contrast injection to the diagonal graft. Cough-CPR (rate = 37/min) was started within 5 s of dysrhythmia initiation and continued through two defibrillation attempts (200 and 360 joules), and IV lidocaine was administered until return of spontaneous circulation 62 s later. The patient never lost consciousness during this very rapid dysrhythmia. Certain cardiac arrest resuscitation measures (namely, initial defibrillation attemps, IV lidocaine administration) can thus be initiated in a patient while performing cough-CPR and maintaining adequate cerebral perfusion. During the dysrhythmia with Cough-CPR: (a) aortic systolic pressures averaged 100 mmHg--this has commonly been observed in other reports, and (b) aortic diastolic pressures were always > or = 50 mmHg and averaged 63 mmHg, which has seldom been this high during cough-CPR. Dysrhythmia reversion occurred 4 s after the second defibrillation attempt and 80 msec after the peak of the highest cough-generated aortic pressure pulse (128 mmHg). Cough-induced ventricular tachycardia reversion has previously been reported; this may have acted in concert with electrical defibrillation to facilitate dysrhythmia reversion. The patient recovered without incident.

Adult↗
PubMed1992

Peripheral site of action of levodropropizine in experimentally-induced cough: role of sensory neuropeptides.

The mechanism of action of levodropropizine has been investigated in different models of experimentally-induced cough in guinea-pigs. In particular it has been demonstrated that the antitussive drug has a peripheral site of action by injecting the drug intracerebroventricularly (i.c.v.). In these experiments levodropropizine (40 micrograms/50 microliters i.c.v.) did not prevent electrically-induced cough. On the other hand, codeine (5 micrograms/50 microliters i.c.v.) markedly prevented coughing. A difference in the potency ratio of levodropropizine and codeine has been demonstrated in capsaicin-induced cough; after oral administration, codeine was about two to three times more potent than levodropropizine. However, after aerosol administration the two compounds were equipotent. These data might suggest a peripheral site of action for levodropropizine which is related to sensory neuropeptides. Further support for the role of sensory neuropeptides in the mechanism of action of levodropropizine comes from the results obtained in capsaicin-desensitized animals. In this experimental model levodropropizine failed to prevent the vagally elicited cough in neuropeptide-depleted animals, whereas codeine did not differentiate between control and capsaicin-treated animals. In conclusion, our results support the suggestion that levodropropizine has a peripheral site of action. In addition, the interference with the sensory neuropeptide system may explain, at least in part, its activity in experimentally-induced cough.

Animals↗
PubMed2005

[Action to be taken when facing one or more cases of whooping-cough].

The evolution of the epidemiology of pertussis, new licensed macrolides and vaccines, new recommendations for vaccination among adolescents and adults need an update of the French guidelines for prevention of the disease around one or grouped cases of the disease. A particular attention should be raised to the diagnosis of whooping cough in adults who are presently the main reservoir of Bordetella pertussis. Whooping cough in adults presents as an unexplained prolonged cough with nocturnal exacerbation witch accounts for most of the contaminations of young infants. A bacteriological confirmation of pertussis should be provided before implementation of preventive measures: culture and PCR are presently the gold standard for the diagnosis of pertussis in infants, children and even adults who have been coughing for less than 20 days. Later on, serology (Elisa, immuno-empreinte) is the only technique available, but cannot be interpreted if the patient has been vaccinated less than one year ago. Infants under three months should be admitted to hospital and every case submitted to respiratory isolation. Eviction from the community should be pronounced within the five first days following the onset of an effective antibiotic treatment. New macrolides should be favoured: clarithromycin for seven days or azithromycin for five days. Household contacts should be given the same prophylactic antibiotic treatment: children and adolescent not correctly immunized, parents of the index case as adults parents of not or not completely immunized infants. The vaccination program of the household should be updated. The same measures should be applied in case of grouped cases (at least two contemporary or consecutive cases in the same area). In that case, the Public Health System doctors should be involved in the investigation and the classification of the cases. The close contacts not or not completely immunized should be prescribed and antibiotic prophylaxis and an update of their vaccination program. Among the occasional contacts, high-risk people only should be treated. In the day care centres an antibiotic prophylaxis should be given to children who have received less than four vaccine shots against pertussis and to the personnel contact to the cases as well. In the schools, the antibiotic prophylaxis should be prescribed to all children of the classroom(s) not completely vaccinated and to the teacher(s) as well. In the boarding schools and institutions with handicapped children, antibiotic prophylaxis could be applied to every member if the pertussis vaccine coverage is at less than 50%. In hospitals, coughing personnel should wear masks and investigations towards pertussis should be performed in people with a more than seven day unexplained cough. Preventive measures should be applied in case of confirmation of pertussis.

Adult↗
PubMed2004

Effect of a novel NK1 receptor selective antagonist (NKP608) on citric acid induced cough and airway obstruction.

The effects of an orally administered novel and selective NK1 antagonist, NKP608, on cough and airway obstruction, induced by citric acid in guinea pigs, were investigated. Guinea pigs were pre-treated with 0.03, 0.3 and 1 mg kg(-1) of NKP608, the NK2 antagonist, SR48968 or both 2 h prior to challenge with citric acid (0.6 M) for a 10 min period. Guinea pigs pre-treated with 0.03, 0.3 and 1mgkg(-1) of NKP608 exhibited a significant reduction of 77, 74 and 79%, respectively, in the numbers of cough compared to vehicle pre-treated animals (P<0.05). SR48968, 10 mg kg(-1), alone did not significantly affect the citric acid-induced cough but when co-administered with 1 mg kg(-1) of NKP608, there was a significant 90% reduction in cough. NKP608 did not significantly reduce the citric acid-induced increase in Penh at any of the doses used. SR48968 significantly reduced the citric acid induced airway obstruction by about 50%. However, when SR48968 was co-administered with NKP608, there was a greater (73%) decrease in the airway obstruction compared with SR48968 alone. These data show that NKP608, a selective NK1 receptor antagonist, is a potent inhibitor of citric acid induced cough in guinea pigs and may therefore have value in the therapy of clinical cough.

Airway Obstruction↗
PubMed2004

Plasticity of central mechanisms for cough.

Cough is associated with plasticity of putative cough afferent fibres, but whether plasticity in the brainstem network contributes is less well understood. A key site in the CNS network is the nucleus tractus solitarius (NTS), the first synaptic contact of the primary afferent fibres. We sought to develop a conscious guinea pig model to detect enhanced cough, to focus on the NTS as a potential site for plasticity, and to test a role for substance P in the NTS since the neuropeptide has been implicated in plasticity of the vagal afferent fibres. Guinea pigs were exposed to second-hand tobacco smoke (SHS) or filtered air (FA) from 1-6 weeks of age. At 5 weeks, cannulae were implanted in the NTS. At 6 weeks, either vehicle or a neurokinin 1 (NK-1) receptor antagonist was injected into the NTS of the conscious guinea pigs who were then exposed to citric acid aerosol. SHS exposure significantly enhanced citric acid-induced cough (56%, P<0.05), an effect attenuated by NTS NK-1 receptor blockade (P<0.05). The findings suggest that one possible mechanism for plasticity in cough is related to substance P effects in the NTS. Future studies will be required to investigate the possible mechanisms underlying the role of substance P as well as other mechanisms in generating SHS-induced cough.

Animals↗
PubMed2004

Cough induced by airway vibration as a model of airway hyperreactivity in patients with acute upper respiratory tract infection.

Patients with acute upper respiratory tract infection (URTI) have been shown to be hyperreactive to inhaled tussigens such as citric acid and capsaicin, and the authors propose that this may be due to an increased sensitivity of airway receptors that mediate cough. In recent studies we have demonstrated that cough may be induced by vibration of the airway at the level of the throat or chest in patients with URTI but that the same stimuli induce little or no cough in healthy subjects. The difference between the patients with URTI and healthy subjects in their response to airway vibration may be explained on the basis of hyperreactivity of airway sensory receptors. We propose that the model of cough induced by airway vibration may be useful for studies on the pathophysiology and pharmacology of airway hyperreactivity in acute cough. The airway vibration model of cough may have some advantages over inhaled tussigens as the stimulus is easily controlled and the method is safe for use in children.

Acute Disease↗
PubMed2004

Cough in children with congenital central hypoventilation syndrome.

Congenital central hypoventilation syndrome (CCHS) is defined as failure of the chemical (autonomic) control of breathing causing alveolar hypoventilation in the absence of pulmonary, cardiac, neuromuscular or patent brainstem lesions. Hypoventilation is predominant in non-rapid-eye-movement sleep, during which breathing is primarily under chemical control. Failure of the central integration of chemosensory inputs is proposed as the putative defect. A genetic basis for CCHS is supported by lines of evidence. In some diseases of the central nervous system there is more or less complete depression of the cough reflex, whereas spontaneous ventilation is generally preserved. Little is known regarding cough in CCHS patients. Parents consistently report that their children cough 'normally' during airway infections; in contrast, experimental lines of evidence suggest that CCHS children lack a cough response following inhalation of a tussigenic agent. Although several factors may account for the discrepancy, the possibility of a weakened or even absent cough reflex remains to be fully ascertained. Conceivably, a defective cough reflex, in conjunction with the well established lack of perception of respiratory discomfort, might result in an increased risk of potentially serious respiratory complications in CCHS patients.

Central Nervous System Diseases↗
PubMed2005

The effects of nasal histamine challenge on cough reflex in healthy volunteers.

UNLABELLED: The aim of the study was to investigate the effects of nasal histamine on the intensity of cough reflex and the effects of intensified nasal breathing following the nasal histamine challenge on cough sensitivity (CS) in humans. 20 volunteers (mean age 23, nonsmokers, no history of nasal or respiratory system diseases and atopy) were recruited to the study. Baseline CS was determined in all subjects. 2 days later the subjects (n = 20) were challenged with nasal histamine (8 mg/ml, 0.1 ml) and the number of coughs was determined after four consecutive single-breath inhalations of capsaicin C2 concentration during the period of the most intensive nasal symptoms (sneezing, itching of the nose). The same capsaicin C2 challenge was performed after nasal saline challenge two days later. One week later CS was determined after nasal histamine challenge with subsequent 10 min of intensified breathing (5-6 sniff-like aspirations to total lung capacity per minute) through the nose and mouth in randomized order in ten volunteers, and with a two-day interval between the challenges. The same manoeuvres after intranasal saline challenge were performed in volunteers of the control group (n = 10). The number of coughs after nasal histamine was significantly higher than that after intranasal saline challenge (8(6-10) vs 5(3-7); p = 0.038(. CS was not significantly different between the baseline challenge and challenges after nasal histamine followed by the intensified nasal and mouth breathing ((2.21 (1.8-2.62) vs 2.04 (1.57-2.51) vs 2.05 (1.6-2.5) log(10) of capsaicin concentration in mumol.l(-1); p = 0.09). CONCLUSIONS: During the period of maximum nasal symptoms after nasal histamine challenge the cough response to inhaled capsaicin was enhanced. Capsaicin cough sensitivity measured after a 10-min. intensified nasal breathing after nasal histamine challenge, compared to a previous measurement of CS, remain unchanged.

Administration, Intranasal↗
PubMed2006

Clinical assessment of chronic cough severity.

The assessment of cough severity solely through consultation with the patient is limited by its subjective nature and variability of physician judgement. The assessment of cough has been hampered by a paucity of objective tools, those available have been poorly validated, non-standardized and are impractical for clinical use. Recent developments have overcome some of these problems and a variety of tools can now be used to assess cough that include visual analogue scales (VAS), quality-of-life questionnaires, cough reflex sensitivity measurement and automated cough frequency monitors. These tools can be used to validate the presence of cough and assess response to therapy. They will also have an important role in clinical trials.

Automation↗
PubMed2004

Pontine respiratory group neuron discharge is altered during fictive cough in the decerebrate cat.

A network of neurons in the rostral dorsal lateral pons and pons/mescencephalic junction constitute the pontine respiratory group (PRG) and is essential for reflex cough. As a next step in understanding the role of the PRG in the expression of the cough reflex, we examined neuron firing rates during fictive cough in cats. Decerebrated, thoracotomized, paralyzed, cycle-triggered ventilated adult cats were used. Extracellular activity of many single neurons and phrenic and lumbar neurograms were monitored during fictive cough produced by mechanical stimulation of the intrathoracic trachea. Neurons were tested during control periods for respiratory modulation of firing rate by cycle-triggered histograms and statistical tests. Most respiratory modulated cells were continuously active with various superimposed respiratory patterns; major categories included inspiratory decrementing (I-Dec), expiratory decrementing (E-Dec) and expiratory augmenting (E-Aug). There were alterations in the discharge patterns of respiratory, as well as, non-respiratory modulated neurons during cough. The results suggest an involvement of the PRG in the configuration of the cough motor pattern.

Action Potentials↗
PubMed2005

Cough determinants in patients with neuromuscular disease.

Neuromuscular disease leads to cough impairment. Cough augmentation can be achieved by mechanical insufflation (MI) or manually assisted coughing (MAC). Many studies have compared these two methods, but few have evaluated them in combination. In 155 neuromuscular patients, we assessed determinants of peak cough flow (PCF) using stepwise correlation. Maximal inspiratory capacity contributed 44% of the variance (p<0.001), expiratory reserve volume 13%, and maximal expiratory pressure 2%. Thus, augmenting inspiration seems crucial. However, parameters dependent on expiratory muscles independently influence PCF. We measured vital capacity and PCF in 10 neuromuscular patients during cough augmentation by MI, MAC, or both. MI or MAC significantly improved VC and PCF (p<0.01) as compared to the basal condition and VC and PCF were higher during MI plus MAC than during MAC or MI alone (p<0.01). In conclusion, combining MAC and MI is useful for improving cough in neuromuscular patients.

Adolescent↗
PubMed2005

Mechanisms of the placebo effect of sweet cough syrups.

The review discusses the large placebo effect associated with cough medicines and speculates on the observation that most cough medicines are formulated as sweet syrups rather than capsules or tablets. The review proposes that the major benefit of cough medicines for treatment of cough associated with common cold is related to the placebo effect rather than the pharmacological effect of an active ingredient. The placebo effect is discussed in terms of physiological effects of cough syrups associated with the taste of the medicine and true placebo effects associated with belief in the therapy. The idea is developed that a sweet taste may modulate cough at the level of the nucleus tractus solitarius, possibly by influencing the production of endogenous opioids.

Animals↗
PubMed2006

Clinical cough and its mechanisms.

Cough is the commonest symptom of clinical importance and the most frequent reason for new consultations with a doctor. Although therapy directed at any underlying cause for cough can be effective there is a clinical need for new treatments specifically directed at the cough itself. A major obstacle to the development of such therapy has been an imprecise understanding of the pathophysiological mechanisms responsible for cough. In this article, we review the important clinical aspects of both acute and chronic cough, offer practical insight into the existing treatment options, highlight the current understanding of cough pathophysiology and identify important areas for future research effort.

Animals↗