Showing papers in "Respiration in 1997"

Survival and cause of death among elderly chronic obstructive pulmonary disease patients after first admission to hospital

Abstract: Those patients with chronic obstructive pulmonary disease (COPD) who require hospital treatment are severely ill. We have studied the survival and cause of death among COPD patients in Finland after their first admission to hospital due to COPD. COPD-related treatment periods in all hospitals during 1972-1992 were collected from the national discharge register, and a subgroup was defined consisting of 2,237 patients aged 65-69 years who had their first admission during 1986-1990. Survival and causes of death were analysed for this group using the data contained in the national mortality statistics. The mortality data were recorded up to the end of 1993. By the end of 1993, 1,070 persons (48%) in the study group had died. The median survival time was 5.71 years (95% CI 5.27-6.15). Female COPD patients had a more favourable prognosis than males. COPD had been certified as the main cause of death for 33.3% of the women and 29.4% of the men. The proportion of COPD as main cause of death increased with an increasing number of treatment periods prior to death. In conclusion, the first hospital admission for COPD indicates a poor prognosis. A high incidence of pulmonary cancer contributes to the poor outcome in the case of men. COPD is obviously underrated on death certificates as the cause of death among COPD patients.

Modafinil in obstructive sleep apnea-hypopnea syndrome: a pilot study in 6 patients.

Abstract: We studied the effects of modafinil, a vigilance-enhancing drug, on excessive daytime sleepiness, memory, night sleep and respiration in 6 patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) using a double-blind random cross-over design with 24-hour polysomnography, verbal memory test and a 5-week sleep-wake diary kept by the patients. There were two 2-week treatment periods in which either modafinil or placebo was used; they were separated by a 1-week wash-out period. Our results show that modafinil reduces daytime sleep duration, lengthens the duration of subjective daytime vigilance and improves long-term memory in patients with OSAHS without modifying night sleep and respiration events.

Control of breathing at high altitude.

Abstract: Ventilatory acclimatization to high altitude has been discussed in a chronologic fashion, i.e. the acute, prolonged, and chronic or lifelong phases, and the integration of exercise ventilation as it relates to each of these phases has been outlined. Unanswered questions in each of these areas have been posed as fertile grounds for future investigation.

High altitude pulmonary edema.

Abstract: Altitude, speed and mode of ascent and, above all, individual susceptibility are the most important determinants for the occurrence of high-altitude pulmonary edema (HAPE). This illness usually occurs only 2-5 days after acute exposure to altitudes above 2,500-3,000 m. Chest radiographs and CT scans show a patchy predominantly peripheral distribution of edema. Wedge pressure is normal at rest, and there is an excessive rise in pulmonary artery pressure (Ppa) which precedes edema formation. Bronchoalveolar lavage in patients with advanced HAPE shows evidence of inflammatory response with increased capillary permeability. There are, however, no prospective data indicating whether the inflammatory response is a primary cause of HAPE or a consequence of edema formation. Excessive rise in Ppa appears to be a crucial pathophysiologic factor for HAPE. Recent observations of high Ppa in HAPE-susceptible sujects who did not develop pulmonary edema after rapid ascent to high altitude suggest either that Ppa does not necessarily reflect capillary pressure in these individuals or else that additional factors, such as an inflammatory response and/or a decreased fluid clearance from the lung, are necessary for the development of pulmonary edema. The treatment of choice is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible.

Nocturnal respiratory failure as an indication of noninvasive ventilation in the patient with neuromuscular disease.

Abstract: Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. Diagnosis of obstructive, central and mixed apneas, hypopneas, and hypoventilation is best made using polysomnography. Therapeutic options include noninvasive ventilation such as continuous positive airway pressure, bilevel positive airway pressure, intermittent positive pressure ventilation and, rarely, tracheostomy, oxygen, or protriptyline. Evaluation by a sleep specialist should be initiated in any neuromuscular patient with nocturnal symptoms such as air hunger, intermittent snoring or breathing, orthopnea, cyanosis, restlessness, and insomnia. Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.

Bronchial Asthma and Airway Hyperresponsiveness at High Altitude

Abstract: The mountain climate can modify respiratory function and bronchial responsiveness of asthmatic subjects. Hypoxia, hyperventilation of cold and dry air and physical exertion may worsen asthma or enhance bronchial hyperresponsiveness while a reduction in pollen and pollution may play an important role in reducing bronchial inflammation. At moderate altitude (1,500-2,500 m), the main effect is the absence of allergen and pollutants. We studied bronchial hyperresponsiveness to both hyposmolar aerosol and methacholine at sea level (SL) and at high altitude (HA; 5,050 m) in 11 adult subjects (23-48 years old, 8 atopic, 3 nonatopic) affected by mild asthma. Basal FEV1 at SL and HA were not different (p = 0.09), whereas the decrease in FEV1 induced by the challenge was significantly higher at SL than at HA. (1) Hyposmolar aerosol: at SL the mean FEV1 decreased by 28% from 4.32 to 3.11 liters; at 5,050 m by 7.2% from 4.41 to 4.1 liters (p 1,600 micrograms (p < 0.005). In 3 asthmatic and 5 nonasthmatic subjects plasma levels of cortisol were also measured. The mean value at SL was 265 nmol and 601 nmol at HA (p < 0.005). We suppose that the reduction in bronchial response might be mainly related to the protective role carried out by the higher levels of cortisol and, as already known, catecholamines.

Heavy snorer disease: from snoring to the sleep apnea syndrome--an overview.

Abstract: This short review discusses the clinical, pathophysiological and epidemiological aspects of heavy snorer disease. Snoring and obstructive apneas constitute the end points of the same syndrome, i.e. an enhancement in upper airway resistance during sleep. Obstructive apneas, and possibly snoring, are risk factors of chronic arterial hypertension.

Clinical and physiological improvement after inhalation of low-dose beclomethasone dipropionate and salbutamol in wheezy infants.

Abstract: Twenty-nine of initially 42 infants with recurrent wheeze (20 male and 9 female) with an age range of 2.1-25.2 months were randomly assigned to receive either 100 µg beclomethasone dipropionate (BDP)

Predictive diagnostic value of clinical assessment and nonlaboratory monitoring system recordings in patients with symptoms suggestive of obstructive sleep apnea syndrome.

Abstract: Obstructive sleep apnea syndrome (OSA) is of increasing importance because of its high prevalence and danger of morbidity to untreated patients. Diagnostic procedures need simplification. We evaluated the qualitative value of a stepwise diagnostic approach using clinical assessment and a home-based screening device according to current recommendations. Methods: We investigated 114 patients with symptoms suggestive of obstructive sleep apnea syndrome by means of their clinical features, questionnaire responses, four-channel nonlaboratory monitoring (NLM) and full polysomnography. Operative indices in the diagnosis of OSA were calculated. Results: A significant correlation (r = 0.7; p Conclusion: Home-based monitoring provides reasonable negative predictive values in the diagnosis of OSA syndrome in symptomatic patients. It therefore qualifies as a screening method. Combined with clinical features and questionnaires it provides high positive predictive values and may therefore prove useful in simplifying diagnostic procedures.

Death due to asthma at workplace in a diphenylmethane diisocyanate-sensitized subject.

Abstract: Total cases of fatal asthma in the occupational setting reported in the literature are reviewed and the case of a 39-year-old foundry worker who died at work is described. A diagnosis of occupational asthma induced by diphenylmethane diisocyanate (MDI) had been assessed 5 years in advance through a 0.005-ppm exposure inhalation challenge. Postmortem microscopic examination of the lung showed epithelial desquamation, eosinophilic/neutrophilic infiltration of the mucosa, dilatation of bronchial vessels, edema, hypertrophy and disarray of smooth muscle. Fatal asthma attack in a MDI-sensitized individual, to our knowledge, has not been previously described.

Cosinor Analysis of Circadian Peak Expiratory Flow Variability in Normal Subjects, Passive Smokers, Heavy Smokers, Patients with Chronic Obstructive Pulmonary Disease and Patients with Interstitial Lung Disease

Abstract: Peak expiratory flow (PEF) presents a circadian rhythm with a maximum in the afternoon, and a significant variability in its diurnal variations has been reported in normal subjects and in chronic obstructive pulmonary disease (COPD). In order to investigate whether passive smoking, active tobacco smoking, COPD and interstitial lung disease (ILD) are associated with changes in the circadian rhythm of PEF, five groups of adult male subjects, comparable for age, weight and height, were studied: group A: 30 clinically healthy subjects who never smoked, group B: 30 subjects passively exposed to tobacco smoking, group C 30 heavy smokers (> 20 cigarettes daily for at least 5 years), group D: 30 patients with nonasthmatic COPD (emphysema and/or chronic bronchitis), and group E: 15 patients with ILD (pneumoconiosis). Active tobacco smoking and exposure to passive smoking were assessed by the determination of the urinary cotinine concentration. A portable spirometer was used to measure PEF over a whole day, at 0.00, 6.00, 8.00, 10.00, 12.00, 14.00, 16.00, 18.00, 20.00, 22.00, and 24.00 h, all subjects leading a normal life. The 'mean cosinor' method was used for statistical analyses; the PEF variability was evaluated by the amplitude percent mesor (daily mean). All groups showed diurnal fluctuations in PEF values with significant (p 0.05) differences between the groups. The cosinor mean was significantly (p < 0.05) lower in heavy smokers, in passive smokers, and in COPD patients than in controls. Controls, passive smokers, heavy smokers, COPD and ILD patients presented a PEF amplitude percent mesor (95% confidence limits) of 6.26% (range 4.57-7.95), 7.79% (range 5.07-10.51), 12.60% (range 7.61-17.59), 17.19% (range 10.18-23.50), and 3.98% (range 2.09-5.87), respectively, with significant differences (p < 0.05) between all groups, except between controls and passive smokers. These data suggest that tobacco smoke, both passive and active, does not modify the circadian peak of PEF, but modifies significantly its mesor and amplitude. In this respect, heavy smokers have the same pattern of COPD: lower mesor and greater amplitude; passive smokers present an intermediate situation. An increased diurnal variability in PEF could be considered as an early index of tobacco smoke damage and of developing COPD. When studying diurnal PEF variability, active and passive smoking habits should be considered.

Respiratory Function at Different Altitudes

Abstract: For the evaluation of a respiratory test at high altitude, several factors must be taken into account: the decreased barometric pressure, the decreased density of air and the degree of acclimatization

50 endobronchial tuberculosis cases based on bronchoscopic diagnosis.

Abstract: Endobronchial tuberculosis (ETB) is most often a complication of primary pulmonary tuberculosis in children, although it may also occur in adults. Bronchoscopically, mass lesion (polypoid and ulcerous

Pulmonary Circulation at High Altitude

Abstract: Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance is seen in normal subjects during hypoxic breathing at sea level, in acclimatized lowlanders and in high-altitude natives. Hypoxic pulmonary hypertension in all these circumstances is most generally moderate, except in high-altitude natives at exercise. Pulmonary hypertension may become severe during high-altitude pulmonary edema, during infantile or adult forms of subacute mountain sickness, and during chronic mountain sickness. Subacute and chronic mountain sickness may be associated with a right heart failure that would be the human counterpart of brisket disease described in cattle. Subjects susceptible to high-altitude pulmonary edema present with a slight increase in pulmonary vascular resistance at rest and at exercise, and often with an enhanced pulmonary vascular reactivity to hypoxia. However, compared to unselected controls, the overlap is great, so that noninvasive echo-Doppler studies of the pulmonary circulation at sea level are of little predictive value of tolerance to altitudes on an individual basis.

Changes in Arterial and Transcutaneous Oxygen and Carbon Dioxide Tensions during and after Voluntary Hyperventilation

Abstract: The purposes of our study were (1) to investigate whether a 3-min short-term hyperventilation leads to posthyperventilatory hypoxemia and (2) to assess the role of transcutaneous blood gas measurement

Late Resolution of Hepatopulmonary Syndrome after Liver Transplantation

Abstract: We report a 38-year-old patient with hepatopulmonary syndrome related to posthepatitis C liver cirrhosis. After liver transplantation, hypoxemia initially worsened markedly, then resolved completely 14 months after transplantation. Liver transplantation may be a reliable treatment of hepatopulmonary syndrome, but clinicians should be aware that the correction of hypoxemia may be delayed and that transient deterioration is possible.

Idiopathic pulmonary fibrosis and pulmonary fibrosis in diffuse systemic sclerosis: two fibroses with different prognoses

Abstract: Idiopathic pulmonary fibrosis and diffuse cutaneous systemic sclerosis (dSSc) involve the lung by a fibrotic process. In recent years, there has been increasing awareness that the natural history of these two types of pulmonary fibrosis might be different. The purpose of this study was to compare lung involvement in these two diseases in a prospective fashion in order to address differences in their clinical course. Forty-three consecutive patients, 18 with lone interstitial pulmonary fibrosis (lone IPF) and 25 with dSSc-IPF were evaluated clinically, radiologically and physiologically at the entry into the study and the evolution of their disease was contrasted by survival analysis. Patients with lone IPF compared with dSSc-IPF were characterized by male predominance (p < 0.001), older age at disease onset (p < 0.001), shorter disease duration (p < 0.001), more frequent crackles on auscultation and clubbing (p < 0.001 and p < 0.0001, respectively), more severe dyspnea (p < 0.0001) and more advanced radiological involvement (p < 0.0001). Functional indices presented comparable values and did not reach statistically significant differences except for the values of single breath CO diffusing capacity (p < 0.0001) and the PaO2 (p < 0.01) which was worse in patients with lone IPF. Finally 12 of the 18 patients with lone IPF died in 2.66 +/- 1.18 years from the onset of respiratory symptoms, while none of the dSSc-IPF patients had died 5.6 +/- 4.25 years from the first ever appearance of respiratory involvement (p < 0.001). In conclusion, although the two groups of patients were not at an absolutely comparable stage of their disease, a worse prognosis for patients with lone IPF seems to emerge from this study.

The Value of a Risk Factor Analysis in Clinically Suspected Deep Venous Thrombosis

Abstract: Background: The value of a risk factor analysis in the presence of a clinically suspected deep venous thrombosis (DVT) has been assessed mainly in inpatient populations. The aim of this prospective study was to evaluate the potential association between DVT and acquired circumstances suspected as risk factors, in a cohort of outpatients with a clinically suspected DVT. Methods: Consecutive outpatients referred for a clinically suspected DVT, with recent clinical signs, not exceeding 1 week, were included. Before venography, all patients were interviewed by a trained physician to detect the presence of risk factors. Results: from March 1992 to February 1994, 277 patients were included; venography was positive in 162 (58.4%). Five independent variables were significantly associated with the occurrence of DVT; in a multivariate analysis, 64.7% of patients were correctly classified; odds ratios for having DVT in the presence of these underlying conditions were respectively: 1.75 for age over 65 years, 1.68 for prior history of venous thromboembolism, 1.69 for high risk circumstances (any type of surgery or leg trauma within the past 3 months), 5.59 for malignancy, and 2.56 for varicose veins. Conclusion: In outpatients referred for a clinically suspected DVT, recognition of associated conditions might increase the certainty of the diagnosis.

Pulmonary microlithiasis. Report of two cases

Abstract: Pulmonary alveolar microlithiasis (PAM) is a rare disease characterized by widespread localization of calcispherites in the alveolar spaces. The patients are symptomless for a long time. Nevertheless, this disease slowly develops into pulmonary fibrosis and cardiac failure. The chest X-rays and high-resolution computed tomography strongly point towards a diagnosis of PAM. As for therapeutic approaches, repeated broncho-alveolar lavages (BAL) have been performed with improvement of symptoms but without recovery, and a new oral drug treatment is still under way. We report 2 familial cases of PAM. Both patients underwent chest X-ray examination showing diffuse bilateral micronodular opacities of calcific density. After 5 years, in May 1993, one of them developed exertional dyspnoea, cyanosis, dry cough and was admitted to our Division. Cardiokinetic and diuretic drugs as well as oxygen were administered with satisfactory results. Then repeated BAL were performed. The chest X-ray after 6 months of sodium etidronate (300 mg t.i.d.) administration was unchanged.

Long-Term Augmentation Therapy in Twenty Patients with Severe Alpha-1-Antitrypsin Deficiency – Three-Year Follow-Up

Abstract: The purpose of this uncontrolled, prospective study was to evaluate the influence of long-term augmentation therapy with plasma-derived α1-antitrypsin (AAT) on lung function parameters in p

Blood gas transport at high altitude

Abstract: As a model of human hypoxia, exposure to high altitude causes a number of ventilatory, circulatory and hemopoietic adaptations. A review of the literature on blood gas transport responses to hypoxia i

Upper airway resistance syndrome.

Abstract: Obstruction of the upper airway may cause arousals resulting in daytime sleepiness and cardiovascular disturbances. The upper airway resistance syndrome may easily be overlooked because conventional measurements of oronasal airflow and thoracic and abdominal efforts are not sensitive enough. By measuring esophageal pressure even small disturbances can be detected, but the esophageal gauge may disturb sleep. We conclude that other, less invasive methods like measurements of impedance by forced oscillation technique, or flattening of the inspiratory flow contour could be valid alternatives in the diagnosis of the upper airway resistance syndrome. Other methods, such as measurements of the pulse transit time, phase angle, or systolic blood pressure profile are promising, but need further evaluation.

A case report of a double-blind, randomized trial of inhaled steroids in a patient with lung transplant bronchiolitis obliterans.

Abstract: Lung transplant bronchiolitis obliterans syndrome (BOS) is the most significant long-term cause of morbidity and mortality after lung transplantation. Although augmented immunosuppression is used by most centers, reported on treatment to reverse BOS are largely anecdotal. We performed a double-blind, randomized, controlled trial (RCT) with ten treatment pairs of 2 weeks duration each comparing inhaled fluticasone propionate (2 x 1,000 micrograms/day) with placebo in a patient with BOS grade 2 who previously showed an improvement in lung function after inhaled steroids. The Baseline Dyspnea Index and the Modified Medical Research Council Dyspnea Scale showed a significant improvement during fluticasone treatment compared with the placebo period (2.7 +/- 0.2 vs. 2.0 +/- 0.3; p = 0.043; and 1.7 +/- 0.2 vs. 2.4 +/- 0.2; p = 0.043). The patient correctly identified fluticasone and placebo, respectively, in eight of ten trial pairs (p = 0.016). The values of forced expiratory volume in 1 s were significantly higher during the fluticasone period (1,207 +/- 10 ml; 95% confidence interval, CI, 1,187-1,227 ml) compared to the placebo period (1,150 +/- 6 ml; 95% CI 1,138-1,162 ml; p = 0.0012). In conclusion, this n-of-1 RCT suggests the efficacy of high-dose inhaled fluticasone in our patient with lung transplant BOS. We propose to conduct a multicenter RCT of high-dose inhaled steroids. Until further data are available, this treatment modality should be offered to patients with lung transplant BOS.

Serum neuron-specific enolase as a tumor marker in the diagnosis and follow-up of small-cell lung cancer.

Abstract: Serum samples for the determination of neuron-specific enolase (NSE) levels were collected at diagnosis, after induction of chemotherapy and at relapse in order to assess the value of NSE in the diagnosis and management of small-cell lung cancer (SCLC). At diagnosis, 47 of 64 patients with SCLC (73%) had abnormal NSE values (i.e. NSE > 12.5 micrograms/l). Mean NSE values were significantly higher in patients with extensive disease compared to limited disease. Patients with other malignancies or benign lung diseases presented with elevated NSE levels in approximately 15 and 4% of cases. Sensitivity, specificity and predictive value of positive results of NSE at diagnosis were 74, 83 and 71%, respectively, for a cutoff value of 12.5 micrograms/l. In responders mean NSE dropped significantly from 46.1 micrograms/l before chemotherapy to 17.0 micrograms/l after three cycles of chemotherapy. Nonresponders as a group showed a nonsignificant drop. At relapse mean NSE increased from 6.5 micrograms/l at the time of response to 51.9 micrograms/l at the time of progression, but in 5 of the 18 evaluable patients normal levels persisted. Thus, evolution of NSE in patients receiving chemotherapy correlated well with tumor volume in patients who responded, but often failed to predict a therapeutic outcome in patients with apparently chemoresistant tumor (i.e. some nonresponders showed a decrease in NSE levels). A similar lack of correlation between NSE levels and tumor volume was seen at the time of relapse. We conclude that the determination of NSE levels is of doubtful utility in the diagnosis and follow-up of SCLC patients.

Central Sleep Apnea

Abstract: A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting

Beta-2-agonists have antioxidant function in vitro. 2. The effect of beta-2-agonists on oxidant-mediated cytotoxicity and on superoxide anion generated by human polymorphonuclear leukocytes.

Abstract: Therapeutic agents which may be able to enhance the antioxidant screen of the epithelial surface of the lung have the potential to influence the progression of lung inflammation. This study evaluates the efficacy of a variety of antiasthma drugs to reduce oxidant-mediated cytotoxicity and to inhibit superoxide anion generated by human polymorphonuclear leukocytes. We quantified in vitro the prevention of H2O2-mediated cytotoxicity (lactate dehydrogenase release assay) using the antiasthma drugs as follows: ipratropium bromide, salbutamol (salbutamol base), fenoterol (fenoterol hydrobromide), terbutaline (terbutaline sulfate), isoproterenol, prednisolone (prednisolone hydrogensuccinate), beclomethasone (17,21-beclomethasone dipropionate) and reduced glutathione. Furthermore, fenoterol and isoproterenol were evaluated ex vivo to reduce superoxide anion (O2-) generated by freshly isolated polymorphonuclear cells (PMN) from smokers with chronic obstructive lung disease (n = 10). Using a concentration of 10-4M, reduction of cytotoxicity was quite different among β2-agonists: fenoterol (97.8%) > isoproterenol (67.6%) > salbutamol (41.8%) > terbutaline (30.5%) > ipratropium bromide (18.1%). Corticosteroids and theophylline had no antioxidant effect. The cellular O2- production of freshly isolated PMN was significantly (p -7M) reduced with fenoterol and isoproterenol at concentrations ≧ 10-7M. Propranolol had no inhibitory effect on antioxidant properties of β2-agonists. We hypothesize that the antioxidant function of β2-agonists is related to the number and formation of hydroxyl groups of the phenol rings within their molecular structure. These results demonstrate that β2-agonists have in part a good intrinsic scavenger function on reactive oxygen species when used in micromolar concentrations. However, to achieve this effect supratherapeutic concentrations were necessary. Thus, the conceivable benefit of β2-agonists in the treatment of high oxidant burden in vivo seems doubtful.

Pulmonary Capillary Haemangiomatosis as a Cause of Pulmonary Hypertension in Takayasu’s Aortoarteritis

Abstract: Pulmonary hypertension is known to occur in Takayasu's aortoarteritis. It may be either due to pulmonary arterial involvement or elevated left ventricular end diastolic pressure, or both. In our case, the cause of pulmonary hypertension was a recently described rare lesion termed pulmonary capillary haemangiomatosis. This entity has a very distinct histopathologic picture. Although 19 cases have been reported in the English literature, this is the first report on pulmonary capillary haemangiomatosis producing pulmonary hypertension in Takayasu's aortoarteritis.

Fatal Diffuse Alveolar Damage from Bird Fanciers’ Lung

Abstract: A 68-year-old man, who had continuing exposure to budgerigars, developed fatal acute respiratory failure following years of slowly progressive pulmonary deterioration. His lung function was characterized first by mild airflow obstruction and later by progressive loss of lung volume. Computed tomography showed progressive development of pulmonary fibrosis and honeycombing. His serum disclosed precipitins to pigeon antigen. During his final illness his chest radiograph showed widespread patchy consolidation. At autopsy, his lungs revealed left lower lobe bronchopneumonia, fibrosis and honeycombing at the bases and widespread evidence of diffuse alveolar damage with organized exudate in some alveoli. To our knowledge, this is the second reported fatality due to acute alveolar injury in bird fanciers' lung.

Vasoactive Intestinal Peptide Causes Nitric Oxide-Dependent Pulmonary Vasodilation in Isolated Rat Lung

Abstract: Vasoactive intestinal peptide (VIP) is one of the chief neurotransmitters of nonadrenergic noncholinergic nerve fibers. In this study, we investigated the effect of VIP on the pulmonary circulation in isolated perfused rat lungs. Baseline pressures of the pulmonary artery for the isolated rat lungs were not affected by 3 x 10(-8) M VIP. VIP caused dose-dependent pulmonary vasodilation when the pulmonary vascular bed was constricted with 20 mM KCl. This vasodilative effect of VIP was inhibited by 1 x 10(-6) M L-n omega-nitro-arginine, an endothelium-derived relaxing factor (nitric oxide) inhibitor, and was restored by the addition of 10(-4) M L-arginine, a substrate of nitric oxide. VIP also caused suppression of the ANG II pressor response, and this VIP-induced suppressive effect was reduced when L-N omega-nitro-arginine or 3 x 10(-6) M meclofenamate was added to the perfusate. These results indicate that VIP causes pulmonary vasodilation in isolated rat lung and suggest the possible involvement of NO and/or cyclooxygenase metabolites in VIP-induced pulmonary vasodilation.