Biomedical subjects
D Leak
Publications and source records attributed to D Leak.
Exhaled ethane is elevated in cystic fibrosis and correlates with carbon monoxide levels and airway obstruction.
Ethane is produced from lipid peroxidation and can be measured in the exhaled air. Cystic fibrosis (CF) is characterized by recurrent respiratory infections, release of reactive oxygen species by inflammatory cells, and increased oxidative stress. We measured exhaled ethane in 23 CF subjects (mean age +/- SEM, 21 +/- 4 yr; 10 male, FEV(1) 62 +/- 4%) and compared it with two other noninvasive markers of oxidative stress and inflammation, carbon monoxide (CO) and nitric oxide (NO). Exhaled ethane was collected during a flow and pressure-controlled exhalation into a reservoir discarding dead space air contaminated with ambient air. A sample (2 ml) of the expired air was analyzed by chromatography. Ethane levels were elevated in patients not on steroids (n = 13, 1.99 +/- 0.20 ppb) compared with steroid-treated patients (n = 10, 0.67 +/- 0.09 ppb, p < 0.01) and with 14 nonsmoking control (8 men, age 33 +/- 2.8 yr) subjects (0.82 +/- 0.40 ppb, p < 0.05). In patients not on steroid treatment ethane was correlated to airway obstruction as assessed by the ratio of residual volume to total lung capacity (RV/ TLC) (r = 0. 66, p < 0.05) and exhaled CO (r = 0.65, p < 0.05). CO concentrations were also higher in patients not on steroid treatment (3.4 +/- 0.2 ppm) than in steroid-treated patients (2.6 +/- 0.1 ppm, p < 0.05), whereas NO concentrations were not influenced by steroid treatment (3.0 +/- 0.4 ppm and 2.9 +/- 0.2 ppm, p > 0.05) and were lower than in a control group (7.0 +/- 0.4 ppb, p < 0.05). Exhaled ethane is elevated in CF, reduced in steroid-treated patients and correlates with CO and RV/TLC; therefore, it may be a useful noninvasive marker of oxidative stress.
Exhaled ethane, a marker of lipid peroxidation, is elevated in chronic obstructive pulmonary disease.
Ethane is a product of lipid peroxidation and can be measured in the exhaled air as an index of oxidative stress. Oxidant/antioxidant imbalance is important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Therefore, we measured exhaled ethane in 22 patients with COPD (mean age +/- SEM, 59 +/- 8 yr; 19 male) and compared it with other noninvasive markers of oxidative stress and inflammation such as carbon monoxide (CO), measured electrochemically, and nitric oxide (NO), measured by chemiluminescence. Exhaled ethane was collected during a flow and pressure-controlled exhalation into a reservoir, discarding dead space air contaminated with ambient air. A sample of the collected expired air was analyzed by chromatography. Compared with normal subjects (n = 14; eight men; age, 33 +/- 2.8 yr), patients with COPD not on steroid treatment (n = 12; FEV(1), 58 +/- 6%) had elevated levels of exhaled ethane (2.77 +/- 0.25 and 0.88 +/- 0.09 ppb, respectively, p < 0.05), CO (5.96 +/- 0.50 and 2.8 +/- 0.25 ppm, p < 0.05) and NO (11.86 +/- 0.53 and 6.77 +/- 0.50 ppb, p < 0.05) levels. Ethane was correlated to FEV(1) (r = -0.67, p < 0.05). Patients receiving steroid treatment (n = 10; FEV(1), 56 +/- 2%) had lower levels of ethane (0.48 +/- 0.05 ppb) than did steroid-treated patients, whereas CO (5.99 +/- 0.63 ppm) and NO (9.11 +/- 0.53 ppb) levels were similar in the two treatment groups. Exhaled ethane is elevated, correlates with FEV(1), and is significantly lower in patients treated with steroids, so it may be complementary to the use of NO and CO in assessing and monitoring oxidative stress in COPD.
Amiodarone for control of recurrent ventricular tachycardia secondary to cardiac metastasis.
Metastatic tumors of the ventricles may cause symptomatic ventricular tachycardia such as described in this 66-year-old man, who presented with recurrent presyncope. The tumor may be readily diagnosed by 2-dimensional echocardiography, ultrafast computed tomography, or magnetic resonance imaging. Such tumors usually indicate an advanced stage of disease, and curative treatment is rarely possible. However, in this patient, effective control of the arrhythmia was achieved with a moderate dosage of oral amiodarone (600 mg daily for 4 weeks, then 400 mg daily), and he had no further episodes of presyncope. This report shows that the effectiveness of amiodarone in the control of symptomatic ventricular tachycardias may also extend to those that are probably secondary to metastatic tumors of the heart.
Absence of cross-reaction between lisinopril and enalapril in drug-induced lupus.
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Effects of cocaine on canines' coronary arteries.
Nine canines were anesthetized with pentobarbital and studied by both selective and semiselective coronary artery angiography following intravenous bolus doses of 1,3,5,8, or 10 mg/kg of cocaine. Catheterization was accomplished with a 5 Fr catheter over a 0.035 inch guidewire under fluoroscopic control, and angiograms were obtained by injection of a diatrizoate solution. Digital subtraction angiography (DSA) was performed prior to cocaine administration and at minutes 0.5, 1, 1.5, 3, 5, and, in some cases, minutes 10 and 15 after cocaine administration. The 1 and 3 mg/kg doses of cocaine had no effect on the coronary arteries. The 5 mg/kg dose significantly dilated the coronary arteries. The 8 mg/kg dose produced significant dilation at 30 seconds after cocaine but nonsignificant dilation of the coronary arteries at all other times. The 10 mg/kg dose produced significant dilation at 30 seconds, nonsignificant dilation at 60 seconds followed by significant constriction at 90 seconds after cocaine, which led to immediate death in most animals. The coronary dilation and constriction produced by 10 mg/kg of cocaine could be prevented by either preadministration or postadministration of naloxone, but this did not prevent subsequent death.
Nifedipine therapy of phenylpropanolamine-induced hypertension.
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Amiodarone for refractory cardiac arrhythmias: 10-year study.
Over a 10-year period 130 patients with drug-resistant cardiac arrhythmias associated mainly with coronary artery disease and its complications were treated with amiodarone. The drug controlled all the tachyarrhythmias associated with the Wolff-Parkinson-White syndrome, 95% of the ventricular arrhythmias, including recurrent ventricular tachycardia and fibrillation, and 92% of the supraventricular arrhythmias. The maximum duration of therapy was 111 months and the mean 34 months. Side effects occurred in 34% of the patients, and there was one withdrawal from therapy per 15.3 patient-years of treatment. The commonest cause of withdrawal was nausea, which was significantly related (p less than 0.01) to a drug interaction with digoxin and diuretics. Reversible neurologic complications occurred in eight patients (6%), and acute myositis was recognized for the first time. Pulmonary infiltration developed in four patients (3%), who were receiving 600 mg of amiodarone per day. The rates of side effects and of withdrawal from therapy differed significantly between the patients whose maintenance doses were 600 and 200 mg/d, at 59% v. 6% (p less than 0.01) and 32% v. 0% (p less than 0.05) respectively. Thus, amiodarone is a very effective antiarrhythmic that can be administered over long periods with acceptable rates of side effects and withdrawal provided the minimal effective dose is used; 400 mg/d or less is desirable.
Intravenous amiodarone in the treatment of refractory life-threatening cardiac arrhythmias in the critically ill patient.
Eleven critically ill patients with life-threatening cardiac arrhythmias refractory to currently approved antiarrhythmic drugs were treated with intravenous amiodarone. Two patients had acute myocarditis, five had acute myocardial infarction, two had left ventricular failure secondary to ischemic heart disease, one had Wolff-Parkinson-White syndrome, and one manifested postoperative atrial fibrillation. Eight of the patients had severe cardiac failure and five had hypotension requiring intravenous dopamine. Five patients were treated for recurrent ventricular fibrillation, two for recurrent ventricular tachycardia, and four for recurrent atrial arrhythmias. Six patients had repeated cardioversions. The arrhythmias had lasted a mean of 88.3 hours resistant to a mean of 2.7 different intravenous antiarrhythmic drugs. The ventricular arrhythmias did not recur after commencing intravenous amiodarone, but some minor atrial arrhythmias occurred for 24 hours. One patient died of intractable left ventricular failure, chronic obstructive lung disease, and respiratory arrest during treatment. The dose of amiodarone was 150 mg over 5 minutes, followed by 600 mg/24 hr for 3 to 4 days; one patient on total parenteral nutrition required intravenous amiodarone for 20 days. Hypotension, cardiac failure, and bradyarrhythmias were not induced by this treatment. Intravenous amiodarone can be used safely in critically ill patients with impaired left ventricular function to control life-threatening refractory cardiac arrhythmias.
Toxoplasmic infection in cardiac disease.
In 18 patients who presented in less than 2 years with heart disease characterized by arrhythmias (including atrial fibrillation, ventricular arrhythmias and heart block), atypical chest pain, pericarditis and cardiac failure, extensive investigation revealed no cause for the disease except for evidence of toxoplasmic infection. One patient had acute toxoplasmosis; the other 17 patients had chronically increased titers, higher than the expected level in the community and also higher than in a control series of patients with well defined heart disease. Toxoplasmosis is probably a fairly common cause of heart disease in this community. The source of infection appeared to be cats, uncooked meat and congenital infection. Patients received chemotherapy with either pyrimethamine and sulfadiazine or tetracycline. Serious relapse occurrred in three patients and embolic complications in two. Experimental myocarditis occurs when toxoplasmic cysts rupture within the heart; therefore clinical symptoms may occur sporadically during a chronic infection.
Control of refractory cardiac arrhythmias with amiodarone.
Amiodarone hydrochloride was used to treat 19 patients with symptomatic arrhythmias refractory to quinidine sulfate, procainamide hydrochloride, disopyramide phosphate, antazoline hydrochloride, lidocaine hydrochloride, bretylium tosylate, propranolol hydrochloride, phenytoin sodium, and practotol acetanilide given to the limit of tolerance. In 17 patients, attacks were completely controlled. Arrhythmias treated successfully included recurrent supraventricular tachycardias, recurrent supraventricular tachycardias with Wolff-Parkinson-White syndrome, and refractory ventricular arrhythmias including recurrent ventricular tachycardia and ventricular fibrillation complicating acute coronary heart disease. Control was confirmed by continuous ECG monitoring both in the hospital and when ambulatory and was maintained for up to four years. Attacks of supraventricular tachycardia were reduced from 7.9/mo to one attack every 53.5 months on amiodarone. Hospital admissions for arrhythmias were reduced from 34 the year before treatment to none the year after. Therefore, amiodarone is an excellent drug for control of many refractory arrhythmias, but two patients with recurrent atrial fibrillation were refractory to this treatment.
An assessment of intermediate coronary care.
The effect of intermediate coronary care, with and without ECG monitoring, was compared with general medical ward care on the basis of mortality, resuscitation, and detection and treatment of arrhythmias from days 3 to 14 after admission in 2,095 cases of acute coronary heart disease. Mortality was significantly reduced (P less than .02), and number of successful resuscitations for ventricular fibrillation was increased (P less than .05) but only in the unit with monitoring. Number of arrhythmias detected was significantly increased, particularly incidence of ventricular ectopics and heart block (P less than .02). Number of arrhythmias corrected to sinus rhythm was increased, but not significantly. Death from pulmonary embolism fell (P less than .01). Review of causes of death and autopsies showed an increased proportion of deaths due to intractable heart failure and cardiogenic shock. Not only specially trained nurses, but also ECG monitoring, were necessary to obtain the benefits of this treatment.
Management of pheochromocytoma during pregnancy.
To reduce the high maternal and fetal mortality in pheochromocytoma of pregnancy, therapy is advocated with phenoxybenzamine and propranolol to obtain adequate alpha- and beta-adrenergic receptor blockade. In early pregnancy control of symptoms may be difficult, but the patient may be carried to term with such medical therapy. Delivery should be by cesarean section before the onset of labour, with, if possible, simultaneous removal of the tumour. Additional preoperative preparation with phenoxybenzamine and propranolol and careful intraoperative management are essential. During her third pregnancy a 29-year-old woman was found to have a pheochromocytoma of the left adrenal gland. After the medical therapy and preparation described, the infant was delivered by cesarean section and the mother's left adrenal gland excised. Eight-year follow-up, including during a fourth pregnancy, showed no recurrence of tumour in the mother and only mild hypertension. The infant developed normally.
Management of pheochromocytoma during pregnancy.
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Acute appendicitis complicating myocardial infarction with heart block.
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Correlation between psychic and endocrinological responses to emotional stress.
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A taxonomic study of physiological responses to a psychological stress.
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Symposium--hypertension. 1. What is hypertension?
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