To investigate the change in myocardial phospholipids after the administration of isoproterenol and its prevention by pretreatment with phospholipase inhibitors and calcium antagonists, we determined the phospholipid species in the heart of female Wistar rats. Isoproterenol (40 mg/kg) was administered 24 h before excising the heart, and chlorpromazine, mepacrine (phospholipase inhibitors), nifedipine, verapamil (calcium antagonists) and propranolol (beta-adrenoceptor blocker) were injected intraperitoneally 30 min prior to isoproterenol administration. The phospholipid species were quantified using silica gel precoated thin-layer rods and the hydrogen flame ionization method. Isoproterenol induced significant increases in heart/body weight ratio, myocardial protein/heart weight ratio and lysophosphatidylcholine (LPC), and significant decreases in myocardial total phosphorus, creatine kinase (CK) activity, phosphatidylethanolamine and phosphatidylcholine (PC). The significant decrease in PC and increase in LPC indicated the degradation of myocardial phospholipids. Pretreatment with nifedipine (30 mg/kg), verapamil (50 mg/kg) or propranolol (20 mg/kg) completely prevented the occurrence of myocardial injury through the preservation of myocardial phospholipid composition, total phosphorus, CK activity and heart/body and protein/heart weight ratios. On the other hand, chlorpromazine (30 mg/kg) and mepacrine (50 mg/kg) partially prevented myocardial damage through the preservation of myocardial phospholipid composition, total phosphorus and CK activity. Results suggest that not only calcium influx but also phospholipase activation plays an important role in the development of myocardial injury induced by isoproterenol.

Animals↗

PubMedDate not supplied

Rifampin-induced hypothyroidism.

Three euthyroid patients with Hashimoto's thyroiditis developed hypothyroidism after the administration of rifampin. We studied 67 patients with tuberculosis. All of them were treated with rifampin. Of the 67 patients, 42 had negative tests for anti-thyroid antibodies (ATA) and 25 had positive tests for ATA. The diagnosis of Hashimoto's thyroiditis was made on the basis of positive tests for ATA. After the administration of rifampin, TSH levels were not significantly altered in all of the former 42 ATA-negative patients and in 22 of the latter 25 ATA-positives, but TSH levels increased in the other three (Patients 1, 2 and 3) of the latter 25 ATA-positives. Three euthyroid Hashimoto's patients (Patients 1, 2 and 3) developed hypothyroidism after the administration of rifampin. This rifampin-induced hypothyroidism resolved in each, once rifampin was discontinued. A) Patient 1: a 62-yr-old man with lymphoma had pulmonary tuberculosis. After the administration of rifampin, serum TSH increased to 170 mU/l; B) Patient 2: a peritoneal-biopsy specimen containing Langhans' giant cells led to a diagnosis of tuberculous peritonitis in a 66-yr-old woman with ascites. After the administration of rifampin, TSH increased to 12.4 mU/l; C) Patient 3: a 56-yr-old woman with a liver abscess and lymphadenopathy underwent lymph-node biopsy that showed Mycobacterium tuberculosis with caseating granulomas. After the administration of rifampin, TSH increased to 21.3 mU/l. After its administration, Patients 1, 2 and 3 developed hypothyroidism, and received T4. When rifampin was discontinued, the hypothyroidism resolved. After the course of rifampin-therapy had been completed, T4 was discontinued. At-risk patients who receive rifampin may become hypothyroid.

Aged↗

PubMedDate not supplied

Chronic neurobehavioral and central and autonomic nervous system effects of Tokyo subway sarin poisoning.

To evaluate delayed (prolonged) neurobehavioral and neurophysiological effects of acute sarin poisoning, nine male and nine female patients of the Tokyo subway sarin poisoning in Japan were examined by neurobehavioral tests, posttraumatic stress disorder (PTSD) checklist, brain evoked potentials, computerized static posturography, and electrocardiographic R-R interval variability, 6-8 months after the poisoning. Their serum cholinesterase activities on the day of the poisoning (March 20, 1995) were 13-131 (mean 72.1) IU/L. The results suggested delayed effects on psychomotor performance, the higher and visual nervous system and the vestibulo-cerebellar system with psychiatric symptoms resulting from PTSD.

Autonomic Nervous System Diseases↗

PubMedDate not supplied

Chronic neurobehavioral effects of Tokyo subway sarin poisoning in relation to posttraumatic stress disorder.

Chronic neurobehavioral effects of acute sarin poisoning were evaluated in 9 male and 9 female patients who were exposed to sarin poisoning in the Tokyo subway incident in Japan. The investigators used nine neurobehavioral tests, as well as a posttraumatic stress disorder checklist, 6-8 mo after the poisoning occurred. Serum cholinesterase activity in patients on the day of poisoning (i.e., March 20, 1995) ranged from 13 to 131 IU/l (mean=72.1 IU/l). The results of analysis covariance, in which age, education level, alcohol consumption, and smoking status (covariates) were controlled in 18 sarin cases and in 18 controls, showed that the score on the digit symbol (psychomotor performance) test was significantly lower in the sarin cases than in controls. Nonetheless, the scores for the General Health Questionnaires, fatigue of Profile of Mood States, and posttraumatic stress disorder checklist were significantly higher in the sarin cases than controls. The investigators added posttraumatic stress disorder to the covariates, and only the score on the digit symbol test was significantly lower in sarin cases. In addition, the results of stepwise multiple regression analysis in 18 sarin cases revealed that scores for the General Health Questionnaires, fatigue of Profile of Mood States (i.e., fatigue, tension-anxiety, depression, and anger-hostility)-together with the paired-associate learning test-were associated significantly with posttraumatic stress disorder. The association did not remain significant for the digit symbol test score. Perhaps a chronic effect on psychomotor performance was caused directly by acute sarin poisoning; on the other hand, the effects on psychiatric symptoms (General Health Questionnaire) and fatigue (Profile of Mood States) appeared to result from posttraumatic stress disorder induced by exposure to sarin.

Adult↗

PubMedDate not supplied

An important effect of TSH on prostacyclin concentration in porcine thyroid cells.

Fresh thyroid slices obtained from normal pigs contained prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha) and prostacyclin (PGI2, measured as the end metabolite, 6-keto PGF1 alpha), but the concentrations of PGI2 exceeded those of PGE2 and PGF2 alpha. A preferential increase of PGI2 was produced when the slices were exposed to a large dose of TSH (thyroid-stimulating hormone). When thyroid cells were isolated and cultured in the absence of TSH, thyroidal concentrations of PGI2, PGE2 and PGF2 alpha were about equal. When the cells were acutely exposed to a large dose of TSH, intrathyroidal concentration of prostaglandin increased significantly, but the relative concentrations of prostaglandins were not markedly altered. When thyroid cells were cultured in the presence of a small dose of TSH, relative concentrations of thyroidal prostaglandins were comparable to those of fresh thyroid slices, as a result of a preferential increase of PGI2 and decreases of PGE2 and PGF2 alpha. Further increase of PGI2 was induced when the cells cultured with TSH were acutely exposed to a large dose of TSH. It is concluded that although cells contain PGE2, PGF2 alpha and PGI2, a preferential accumulation of PGI2 is found only when thyroid cells are chronically stimulated by TSH.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Late complications in traumatic coronary artery fistula: report of a case requiring surgical repair after 8 years.

We report the unusual case of a patient with traumatic coronary artery fistula who had been free of symptoms for more than 4 years, but who ultimately required surgical repair 8 years after the trauma due to late complications including angina pectoris, atrial flutter and fibrillation, congestive heart failure, and tricuspid regurgitation. Our findings suggest that early surgical repair should be undertaken in cases of traumatic coronary artery fistula, even if the shunt is minimal and early symptoms are mild. The persistence of, or a slow increase in, shunt flow over the years greatly increases the risk of the ultimate development of life-threatening complications.

Angina Pectoris↗

PubMedDate not supplied

Evaluation of the I L B G electrolytes.

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Blood Chemical Analysis↗

PubMedDate not supplied

Evaluation of the Ciba Corning 634 ISE calcium/pH analyzer.

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Calcium↗