Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A minute ventilation sensing rate responsive pacemaker was implanted in 11 patients with bradycardias. Their mean age was 59 +/- 4 years (mean +/- SEM). The pacemaker measures minute ventilation by sensing intravascular impedance using a standard bipolar electrode. The rate responsive programming was simple: apart from ascribing an upper and lower rate, the only programmable parameter was the slope of rate response. This could be derived approximately by assessing the suggested slope value during an exercise test in the 'adaptive VVI' mode. Compared with exercise in the VVI mode, symptom limited treadmill tests in the rate responsive mode showed a 33% improvement of exercise capacity and a 44% improvement of cardiac output as determined noninvasively by continuous wave Doppler measurements of the ascending aortic blood flow. The pacing rate was appropriately increased during a variety of daily activities such as walking at different speeds and gradients, and ascending and descending stairs. Voluntary interference of the respiratory pattern such as during coughing and hyperventilation increased the pacing rate from a resting rate of 70 bpm to 111 +/- 10 and 86 +/- 4 bpm respectively. Continuous talking during exercise attenuated the expected rate response. The pacemaker can sense activity induced by arm swinging. In conclusion, the Meta pacemaker improved cardiac output and exercise capacity in patients with bradycardias. Its rate response was related to workload. Although voluntary interference affected the pacing rate, excessive rate acceleration was not encountered.
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PMID:Reliability of minute ventilation as a parameter for rate responsive pacing. 246 42

Clinical evaluation and prolonged esophageal pH monitoring were performed before and during treatment with cisapride (0.3 mg/kg t.i.d.) for 1 month in 19 children with reflux-associated bronchopulmonary disease. Results (mean +/- SEM) show that cisapride significantly decreases the frequency of long duration (greater than 5 min) reflux episodes (from 9.7 +/- 0.7 to 5.7 +/- 1.2), the percentage of total time pH was less than 4 (from 15.9 +/- 2.5 to 7.7 +/- 1.1%), the percentage of time pH was less than 4 at night (from 18.0 +/- 3.9 to 4.9 +/- 1.5%), the duration of the longest reflux episodes (from 44.5 +/- 6.4 to 19.7 +/- 2.7 min), as well as the duration of reflux at night (from 100.1 +/- 28.0 to 28.2 +/- 10.1 min). The frequency of reflux episodes, however, remains unaffected by cisapride. Cough fits at night disappeared completely in 12 out of 13 children. We conclude that cisapride given for 1 month significantly decreased gastroesophageal reflux as well as cough episodes at night.
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PMID:Effect of cisapride on esophageal pH monitoring in children with reflux-associated bronchopulmonary disease. 270 65

In 1981 to 1982, we reported that many (19/43) asymptomatic dairy farmers, especially those with positive serum precipitins, had a lymphocytic alveolitis. We reevaluated, six and seven years later, 33 of the initial 43 farmers to verify their outcome. The restudied group included 31 men and 2 women between 24 and 67 years of age. In both studies, 24 were nonsmokers and 9 were exsmokers. Each farmer answered a questionnaire, had a physical examination, blood withdrawal for precipitin analysis, a chest roentgenogram, and pulmonary function tests (forced expiratory flows and diffusion capacity). At restudy, one subject had developed symptoms suggestive of sub-acute farmer's lung and now had inspiratory crackles; six had chronic morning cough and sputum production. Serum precipitins were positive in 10 subjects, whereas 16 had been positive at the initial study. Precipitins reverted from positive to negative in eight subjects and from negative to positive in six. Chest roentgenograms were normal in 23 subjects, while discrete interstitial abnormalities were noted in nine. One subject had significant pulmonary infiltrates. Results of current pulmonary function tests were (% predicted, mean +/- SEM) DL(CO) 114.8 +/- 3.0, FEV1 108.1 +/- 2.4, FVC 105.4 +/- 1.1. No correlations were found between these data and the lymphocytes or mast cells found in the bronchoalveolar lavage (BAL) at the initial study of 1981 and 1982. We conclude that bronchoalveolar lavage cell counts of asymptomatic farmers have no long-term clinical significance.
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PMID:Predictive value of bronchoalveolar lavage cells and serum precipitins in asymptomatic dairy farmers. 281 2

We investigated the antitussive effect of fenoterol in 40 patients (34 males) undergoing bronchofiberscopy for diagnostic purposes. The patients were randomly allocated into two groups, one receiving two puffs (400 micrograms) of fenoterol and the other two puffs of placebo, from a metered-dose inhaler in a double-blind fashion. The following procedure was used: premedication with 0.5 mg atropine sulfate and 100 mg hydroxyzine administered intramuscularly; 50 min later, aerosol administration; 10 min after aerosol administration, a standardized topical anesthesia was performed. As soon as the bronchofiberscope had entered the trachea, sounds were recorded for a 5-min period, while the tracheobronchial tree was systematically inspected. Additional lidocaine (2% solution, 2 ml boluses) was injected into the airways if troublesome cough occurred. The two groups did not differ significantly in terms of age, sex ratio, and smoking history. In contrast, both the number of coughs and the volume (ml) of additional lidocaine were significantly smaller in the fenoterol group than in the placebo group: m +/- SEM: 35.0 +/- 5.5 versus 51.6 +/- 6.5, p less than 0.01 and 1.9 +/- 0.5 versus 3.3 +/- 0.4, p less than 0.01, respectively. Thus, fenoterol exhibits antitussive properties and can usefully be administered before bronchofiberscopy.
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PMID:Attenuation of bronchofiberscopy-induced cough by an inhaled beta 2-adrenergic agonist, fenoterol. 290 78

Uncomplicated colonic diverticula have been regarded as weak points in the bowel wall which have a predisposition to rupture during colonoscopy. We attempted to prove or disprove this assumption. Eleven segments of diverticula-containing sigmoid colon were insufflated via a colonoscope and the rupture pressure manometrically recorded. The mean +/- SEM pressure causing serosal tear was 202 +/- 15 mm Hg and mucosal rupture 226 +/- 14 mm Hg. No diverticular blowouts occurred. Intraluminal sigmoid pressures were measured manometrically in 15 patients with and 15 patients without colonic diverticula during routine colonoscopy. The pressure recordings were read in a blinded fashion, and the values were then grouped and analyzed in those patients with and without sigmoid colon diverticula. Intrarectal, sigmoid, peak sigmoid, peak sigmoid with cough, and peak sigmoid with Valsalva pressures were similar in both groups. Furthermore, the pressure levels generated during colonoscopy were much lower than those required for colonic rupture in the cadaver colons. We conclude that the reason most colonic perforations occur in the sigmoid area is not due to diverticular blowout. Rather, excluding instances where electrocautery is used, we feel it is due to instrument trauma. Less commonly, excessive air insufflation can result in serosal laceration and mucosal rupture, whereas diverticular blowout is probably limited to the setting of acute diverticulitis.
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PMID:Diverticular rupture during colonoscopy. Fact or fancy? 642 26

Patients with respiratory disease commonly report that their sleep is disrupted by nocturnal cough. We have recorded cough during the night in 10 patients with severe chronic bronchitis and emphysema (forced expiratory volume in one second, 1.0 +/- SEM 0.1/L) who complained of nocturnal cough and correlated cough with electroencephalographic sleep stage and arterial oxygenation. Cough was recorded using a directional microphone and an auto-editing tape recorder system. Each cough was subsequently verified by a listener. There was a mean of 14.6 +/- 4.5 bouts of coughing per patient per night, each bout lasting on average 3.9 +/- 0.2 s. Eighty-five percent of coughing bouts occurred during electroencephalographically confirmed wakefulness (p less than 0.02 versus sleep), and coughs during true sleep were rare, with only 1 patient coughing during rapid eye movement sleep and none during Stages 3 and 4 sleep. Cough was only once followed by arousal. There was no correlation between cough and either apneas or hypoxemia during sleep. We conclude that spontaneous cough is suppressed during sleep and only rarely awakens patients.
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PMID:Nocturnal cough in patients with chronic bronchitis and emphysema. 650 20

Within 15 minutes of terminating general anaesthesia, progressive recovery of consciousness, spontaneous ventilation and cough, and limb movements were assessed in 60 young children (age range 0-5 years, mean +/- SEM; 2.83 +/- 0.34; weight 13.86 +/- 0.41 kg). All patients were ASA physical status class I-III, received a standard intravenous induction (atropine 0.02 mg X kg-1, thiopental sodium 5 mg X kg-1, diazepam 0.2 mg X kg-1), were intubated with an orotracheal tube following the administration of metocurine, 0.4 mg X kg-1, and were maintained under general anaesthesia with nitrous oxide and oxygen in a 70:30 mixture administered by a T-piece circuit. They were ventilated mechanically to maintain normal blood-oxygen tension and normocarbia. The patients were assessed in three equal groups according to the anaesthetic supplement they received. Group I received intravenous infusions of morphine sulfate (loading dose 60 micrograms X kg-1 administered over 5 minutes followed by a continuous intravenous infusion of 2 micrograms X kg-1 X min-1. Patients in Groups II and III had 0.5 per cent halothane and 1.0 per cent isoflurane respectively added to the nitrous oxide/oxygen fresh gas mixture rather than morphine sulphate infusions. By the end of the study period, there was no significant difference in the degree of recovery between the morphine and the isoflurane groups but the patients in the halothane group had recovered to a lesser degree. Generally, the patients in the morphine group were awake but not crying, while those in the other two groups were less sedated.
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PMID:Assessment of immediate post-anaesthetic recovery in young children following intravenous morphine infusions, halothane, and isoflurane. 669 77

The minimal alveolar concentrations for halothane, enflurane, and isoflurane in the domestic cat were found to be 1.19 +/- 0.05 (SEM)%, 2.37 +/- 0.06%, and 1.61 +/- 0.04%, respectively. During the potency studies, it was observed that enflurane and isoflurane resulted in shorter wake-up times, compared with halothane. However, enflurane and isoflurane produced electroencephalographic (EEG) and clinical signs of CNS irritability (EEG spiking, myoclonus) in normocapnic or mildly hypocapnic cats. In addition, enflurane and isoflurane caused greater airway irritability (coughing, salivation) than did halothane.
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PMID:Minimal alveolar concentrations for halothane, enflurane, and isoflurane in the cat. 686 22

To determine whether anaesthesia of the intrathoracic airways would attenuate the development of exercise-induced asthma, we studied eight symptomless asthmatic patients by cycle ergometry after saline or lignocaine pretreatment while they were breathing air at 24 degrees C with 9.1 mg of H2O/l. Pulmonary mechanics were measured before and after the administration of each agent, and again five minutes after cessation of exercise. Sufficient lignocaine was administered to abolish the gag reflex and the cough response to aerosols of citric acid. Before exercise there were no significant differences for any lung function variable between the saline and lignocaine results. Equally, there were no significant differences between these agents for minute ventilation (VE) during exercise (VE lignocaine = 71.0 +/- 7.4 (SEM) l/min; VE saline 67.2 +/- 8.1 l/min;), or in the severity of the subsequent bronchospastic response (for example, the FEV1 with saline was 22.6 +/- 2.9% decrease, and with lignocaine 23.6 +/- 8.5%). Thus these results do not support the idea that there are thermally sensitive neural receptors in intrathoracic airways that play a role in the pathogenesis of exercise-induced asthma.
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PMID:Controlled-analysis of the effects of inhaled lignocaine in exercise-induced asthma. 715 12

Recent observations indicate that angiotensin-converting enzyme (ACE) inhibition corrects renal transplant erythrocytosis (RTE). The mechanism for this association is not known. We examined the effect of ACE inhibition on hematocrit, erythropoietin (EPO), and renin substrate. ACE inhibition has been reported to suppress renin substrate, which is known to stimulate EPO and erythropoiesis. In 15 patients with RTE, hematocrit dropped from 52.8 +/- 0.6 (SEM) to 45.8 +/- 1.4% after 8 weeks of treatment with Enalapril, 2.5-20 mg/day. Serum EPO (normal range: 9-30 mU/ml) was high in one, normal in seven, and low in seven patients. ACE inhibition reduced EPO in patients with initial high or normal levels but induced no change in patients with initial low levels. ACE inhibition had no significant effect on renin substrate. In one patient who rejected his first graft, erythrocytosis recurred following a second, successful transplant. Treatment was discontinued because of cough in two patients and symptomatic drop in blood pressure in one patient. We conclude RTE is not caused by hypererythropoietinemia. In patients with normal circulating EPO, erythrocytosis may result from an increase sensitivity to EPO, and ACE inhibition lowered hematocrit by further reduction of this hormone. However, the finding of erythrocytosis in half our patients with suppressed EPO, suggests the participation of non-EPO-mediated mechanism(s). The recurrence of RTE in a patient after a second transplant raises the additional possibility of patient-specific factors in the pathogenesis of this disorder. In contrast to other reports, we documented side-effects (cough, hypotension) in three (20%) of our patients. Our clinical experience, coupled with prior reports of spontaneous resolution of RTE in some patients, suggests that intermittent courses of ACE-inhibition may be the optimal strategy in the use of this form of therapy for RTE.
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PMID:Angiotensin-converting enzyme inhibition in the treatment of renal transplant erythrocytosis. Clinical experience and observation of mechanism. 762 54


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