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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.
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PMID:Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle. 401 39

Thirteen infants and children with adenovirus type 7 infection proved by virus isolation are described. High fever, cough and dyspnea were the most frequent findings; in infants under 1 year of age wheezing was common. Four patients required artificial ventilation. Lobar collapse, consolidation and hyperinflation were frequent radiologic findings. None of the symptoms responded to antibiotic therapy or bronchodilator drugs. Three patients died (mortality rate of 23%). Pathologic findings were compatible with adenovirus type 7 pneumonia, and were characterized by a necrotizing bronchitis and bronchiolitis, patchy alveolar fibrinopurulent exudate and hyaline membrane formation. Some intra-alveolar epithelial cells showed strikingly abnormal nuclei and rare typical halo-outlined intranuclear inclusions were seen. Only one of eight survivors had evidence of significant chronic chest disease.
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PMID:An outbreak of adenovirus type 7 infection in children in Montreal. 434 82

This paper discusses causes, hemodynamics, symptoms, and signs of pulmonary embolism. Severe cases obstruct at least 60 percent of the pulmonary vascular bed. Small or moderate cases may be easily overlooked. Symptoms may be only slight chest pain or dyspnoea, fever, giddiness, or irregular heart beat. In the author's experience with 35 cases of acute massive pulmonary embolism at the Bromptom Hospital oral contraceptives were considered a predisposing factor in 5 cases (14 percent), pregnancy was a possible cause in 2 (6 percent), a recent operation in 24 (68 percent). No other recognized factor was thought to have predisposed more than a single case. Clinical features included cyanosis, collapse, sever chest pain, dyspnoea, sweating, rapid heart rate, falling blood pressure, and occasional coughing up of blood. Electrocardiograms sometimes gave helpful information. Chest x-ray was usually not helpful except to exclude other causes. Heart catheterization and pulmonary arteriography have been done to assess the extent of the embolism. Emergency surgical pulmonary embolectomy is recommended for extreme cases. Fibrinolytic agents such as streptokinase may be adequate for less severe cases who have not had a recent operation of do not suffer from a hemorrhagic disorder.
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PMID:Pulmonary embolism. 535 32

Certain patients receiving hemodialysis experience recurrent chest pain, dyspnea, and hypotension during exposure to new cuprophane-membrane dialyzers (the "first-use syndrome"). Because activation of complement may be involved in these events, we examined in vivo complement activation with new cuprophane membranes and in vitro activation by zymosan in 6 such patients, and compared them with 10 patients who did not have symptoms during dialysis. All patients with the first-use syndrome had maximal complement activation 10 minutes after initiation of dialysis, with C3a des-arginine (desArg), the stable metabolite of C3 activation, equal to 8533 +/- 157 ng per milliliter (mean +/- S.E.M.). In asymptomatic patients the maximal C3a desArg value occurred at 15 minutes and was only 2907 +/- 372 ng per milliliter (P less than or equal to 0.0001). At a concentration of 3.8 x 10(-5) g of zymosan per milliliter, patients with the first-use syndrome had a C3a desArg level of 29.6 +/- 1.4 micrograms per milliliter, whereas it was only 16.6 +/- 2.3 micrograms per milliliter in asymptomatic patients (P less than or equal to 0.0001). Two other patients, who experienced cardiopulmonary collapse during the first two minutes of dialysis, had a C3a desArg level of 18,900 and 7800 ng per milliliter, respectively. We conclude that the occurrence of adverse symptoms associated with new cuprophane-membrane dialyzers correlates with complement activation.
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PMID:Complement activation and hypersensitivity reactions to dialysis membranes. 633 76

A retrospective review was undertaken to determine the influence of the St John Ambulance life support units on the the incidence of sudden cardiac death during a 12 month period in Auckland. In 65 instances subjects who collapsed with either ventricular fibrillation or cardiac arrest were resuscitated and transported alive to a hospital accident and emergency department in the Auckland area. Twenty patients died within 24 hours of admission and a further 14 died in hospital. There were seven late deaths and 24 survivors (37%). Ten patients are asymptomatic and the remainder are troubled by angina or breathlessness. Only three of the surviving patients have suffered severe cerebral damage as a result of their collapse.
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PMID:Sudden cardiac death: results of resuscitation begun outside hospital. 634 35

Though tracheal injuries often appear only superficial, exploration may reveal severe lacerations or fractures of the cartilaginous rings. A thorough physical examination and thoracic radiographs should precede tracheal surgery. Severe tracheal trauma is best repaired by partial resection and primary end-to-end anastomosis. Tension-relieving sutures aid healing of the anastomotic area, which is closed with synthetic absorbable sutures with extraluminal knots. Tracheal collapse, which primarily occurs in small or toy breeds, causes inspiratory dyspnea and can be corrected with polypropylene prostheses. Permanent tracheostomy may be required with laryngeal paralysis or irreparable tracheal injuries.
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PMID:Tracheal surgery in dogs: a review. 639 Jan 66

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

This article reports a case of acute pancreatitis in a patient taking the oral contraceptive pill. A 32 year old mother had been on combined contraceptive pills since 1975. In 1978 she started having upper abdominal and retrosternal pain. She became critically ill with peripheral circulatory collapse, dyspnoea and cyanosis. A superficial thrombophlebitis was noted on the medial aspect of the right thigh. The diagnosis of pancreatitis was considered with history of recurrent abdominal pain. After several tests and supportive therapy (intravenous fluids, antibiotics, steriods), the woman started showing improvements in 48 hours and recovered in 10 days. This case differs from previously described cases in that the cholesterol and triglyceride levels were normal. The hypoglycemia has not been described previously.
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PMID:Contraceptive pills and acute pancreatitis. 732 5

The clinical picture and the electrocardiographic and rheopneumographic findings were compared with the data obtained during operation or angiopneumography in 31 patients with embolism of the pulmonary artery. In massive embolism of the pulmonary artery, the dominating clinical symptoms were sudden dyspnea, tachycardia and cyanosis. Collapse and cardiac arrest were encountered in most patients. Moderate embolism is characterized by advancing dyspnea but cyanosis and tachycardia are inconsistant symptoms. The results of electrocardiography and rheopneumography are in correlation with the data obtained in catheterization of the heart, angiopneumography and during embolectomy.
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PMID:[Diagnosis of acute pulmonary artery embolism]. 735 8

The history and physical examination were assessed in 215 patients with acute pulmonary embolism uncomplicated by preexisting cardiac or pulmonary disease. The patients had been included in the Urokinase Pulmonary Embolism Trial or the Urokinase-Streptokinase Embolism Trial. Presenting syndromes were (1) circulatory collapse with shock (10 percent) or syncope (9 percent); (2) pulmonary infarction with hemoptysis (25 percent) or pleuritic pain and no hemoptysis (41 percent); (3) uncomplicated embolism characterized by dyspnea (12 percent) or nonpleuritic pain usually with tachypnea (3 percent) or deep venous thrombosis with tachypnea (0.5 percent). The most frequent symptoms were dyspnea (84 percent), pleuritic pain (74 percent), apprehension (63 percent) and cough (50 percent). Hemoptysis occurred in only 28 percent. Dyspnea, hemoptysis or pleuritic pain occurred separately or in combination in 94 percent. All three occurred in only 22 percent. The most frequent signs were tachypnea (respiration ate 20/min or more) (85 percent), tachycardia (heart rate 100 beats/min or more) (58 percent), accentuated pulmonary component of the second heart sound (57 percent) and rales (56 percent). Signs of deep venous thrombosis were present in only 41 percent and a pleural friction rub was present in only 18 percent. Either dyspnea or tachypnea occurred in 96 percent. Dyspnea, tachypnea or deep venous thrombosis occurred in 99 percent. As a group, the identified clinical manifestations, although nonspecific, are strongly suggestive of acute pulmonary embolism. Conversely, acute pulmonary embolism was rarely identified in the absence of dyspnea, tachypnea or deep venous thrombosis.
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PMID:History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. 746 69


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