Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant hyperthermia is a rare but severe complication of modern anesthesia, induced by halothane and succinylcholine. The syndrome is characterized by a rapid sustained and extreme rise in body temperature associated with muscular rigidity, tachycardia, tachypnoea and cyanosis. The lethality is about 60%. The present paper describes the histological, histochemical and electron microscopical findings performed on muscle biopsies of 3 patients with malignant hyperthermia (1 patient died) and a so called risk patient. In all patients morphological findings consistent with a pre-existent myopathy were found. Histologically there were acute necrotic muscular fibers as well as in types I and II, variations in the fiber diameter and centralization of the nuclei. In two cases even fibers that had a normal aspect in HE slides, showed a pathologic pattern after phosphorylase reaction. In addition to acute rhabdomyolysis, electron-microscopic investigations revealed cystic expansion of the cisterns of the sarcoplasmic reticulum with a peculiar proliferation of the sarcolemma. In a degenerating mitochondrium, a crystalline inclusion was identified. These findings support the pathogenetic concept of Britt and coworkers of a functional defect in the calcium release or binding mechanism of sarcoplasmic reticulum. Since it is known that malignant hyperthermia has a familial predilection, it seems very important that clinical, biochemical, and morphological investigations be performed such as CPK estimations and muscular biopsies not only of the patients but also of the relatives in order to rule out this type of latent myopathy.
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PMID:[Histological, histochemical, and ultrastructural findings in malignant hyperthermia (author's transl)]. 80 99

Single dose toxicity studies of T-3761 were carried out in mice, rats and dogs, and the following results were obtained. 1. The approximate lethal dose of T-3761 were more than 5,000 mg/kg for mice and rats, more than 2,000 mg/kg for dogs with oral administration, and more than 5,000 mg/kg for mice and rats with subcutaneous injection. LD50 values with intravenous injection were 783 mg/kg for male mice, 832 mg/kg for female mice, 341 mg/kg for male rats, and 403 mg/kg for female rats. Two dogs given 200 mg/kg did not die but one of the two treated with 400 mg/kg died after intravenous injection. The approximate lethal dose for dog was 400 mg/kg. 2. Neither abnormal symptoms and macroscopic findings nor deaths were observed in mice and rats treated orally. Granuloma around precipitates of T-3761 at the injection site was seen in mice and rats injected subcutaneously. Slight increase of white blood cell count, serum GOT, CPK and urea nitrogen were transiently found in dogs treated orally. Neither abnormal macroscopic findings nor deaths were observed in dogs treated orally. 3. Decreased motor activity and irregular breathing were observed in mice and rats injected intravenously. In dying animals, tonic or clonic convulsions were observed. Vomiting, hyperemia of ophthalmic mucosa, edema of face, decrease of motor activity, salivation and decrease in body temperature were observed in dogs injected intravenously. At higher doses, scream and tachypnea were observed while injecting. Hematological examinations disclosed that increases in red blood cell count, white blood cell count, hematocrit and hemoglobin were found transiently. In biochemical examinations, increases in serum GOT, GPT, urea nitrogen and creatinine were found transiently. One dog intravenously injected 400 mg/kg, showed tonic convulsion and died.
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PMID:[Single administration toxicity studies of T-3761 in mice, rats and dogs]. 766 80

This paper is a review of the patients with pulmonary thromboembolism hospitalized at General hospital in Teanj starting from the first case recorded in 1980 till now and 172 patients were subjects of this study. Thromboembolism was a direct cause of death in 43.7% (75 patients). Clinical and laboratory records, etiology, chest radiography, ECG data of 89 patients hospitalised and treated in the last five years were analyzed in detail. The most frequent symptoms were dyspnea and tachypnea, often accompanied with other symptoms (84.2%), chest pain (65.2%), cough (52.4%), tachycardia (40.5%), hemoptysis (25.8%). At 74% of patients with pulmonary thromboembolism a significant simultaneous increase of all examined enzymes, except CPK was found. Pulmonary insufficiency (global or partial) was found at 75% of patients. According to our results, in 57.2% of the subjects the pathologic changes on Radiography (infiltrates of the lung, with or without affection of the pleura and changed position of diaphragm) were found, and 70.9% had changes on the ECG.
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PMID:[Clinical aspects of pulmonary thromboembolism]. 1032 Oct 63

Acute lung embolism is an uncommon but recognised complication of deep venous thrombosis. The parameters RTG, ECG, PaO2, PaCO2, LDH, CPK, SGOT, SGPT and pulmonary ventilation/perfusion scan have been examined in 200 patients with pulmonary thromboembolism. For that purpose discrimination values of synopticly relevant RTG findings, arterial blood gas and enzymes analysis results and pulmonary ventilation/perfusion scintigraphy, were observed in a comparative analysis of numerous data that could be integrated as an unique finding in sense of qualitative diagnosis. The most frequent symptom was dyspnea and tachypnea, often accompanied with other symptoms (84%), chest pain (65%), cough (53%), tachycardia (41%), hemoptysis (26%). In 74% of patients pulmonary thromboembolism the significant simultaneous increase of all the mentioned enzymes, except CPK, was found 75%. However, according to the results in 58% of the examined persons the pathologic changes on RTG (infiltrates of the lung, with or without affection of the pleura and changed position of diaphragma) were found, and 71% on ECG. Pulmonary ventilation/perfusion scintigraphy is the precise examination for acute lung embolia. For the routine clinical examination measurement of PaO2, PaCO2, LDH, ECG, x-rays is sufficient (correlation test + 0.56). In this paper we have presented our own diagnostic-therapeutic protocol in of lung emboly.
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PMID:[Diagnosis and treatment of acute pulmonary embolism]. 1054 64

Transitory myocardial ischemia (TMI) is seen as a complication of severe asphyxia. Its presentation is variable, ranging from tachypnea to cardiogenic shock, and it is often masked by the predominant disease. The objective of this study was to detect TMI secondary to perinatal asphyxia in a population of asphyxiated newborns (NB) in comparison with asphyxiated NB with no evidence of TMI. From April 1996 to December 1997, 43 asphyxiated (stressed) NB were studied. Three were excluded. Patients were placed into two groups: Group A with TMI (n = 33) and Group B without TMI (n = 7). No significant differences were found in gestational age, birth weight, extrauterine age, Apgar score, or total creatine phosphokinase values between the two groups. Differences were found in CPK-MB levels and in ischemic electrocardiographic changes and blockages, especially for Group A. In this group, only 24 (72.7%) were cardiovascularly symptomatic. We conclude that TMI secondary to perinatal asphyxia is more frequent than has been reported. Thus, it would be useful in all asphyxiated NB to measure CPK-MB isoenzyme activity and patients can then be submitted to an electrocardiogram for detection in order to offer opportune treatment when required.
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PMID:Detection of transitory myocardial ischemia secondary to perinatal asphyxia. 1106 79