Search

Objectives: To investigate the role of oxidative stress in left ventricular function after acute myocardial infarction., Methods: We studied 41 patients with acute myocardial infarction (30 men and 11 women, mean age 61.7 +/- 11.6 years) with Thrombolysis in Myocardial Infarction grade 3 recanalization of occluded coronary arteries within 12 hr after onset. Cardiac catheterization was performed at the time of admission and before discharge. Three markers for oxidative stress were measured: plasma lipid hydroperoxide, plasma creatol and whole arterial blood glutathione at the time of admission., Results: Mean time from onset to recanalization was 5.2 +/- 0.6 hr. The patients were divided into two groups according to the changes in left ventricular wall motion (LVWM); patients who showed improvement in LVWM and those without improvement. There were no significant differences in age, sex, coronary risk factors, severity of coronary artery disease, time from onset to recanalization or ejection fraction between two groups. Maximum creatine kinase and C-reactive protein levels in patients without LVWM improvement were significantly higher than in patients with improvement. Plasma levels of lipid hydroperoxide and creatol did not differ significantly between two groups. On the other hand, reduced glutathione/oxidized glutathione ratio in arterial blood in patients without LVWM improvement was significantly lower than in patients with LVWM improvement (69.8 +/- 3.4 vs 85.5 +/- 2.9, p < 0.05)., Conclusions: Our results suggest that whole arterial blood glutathione is more oxidized in acute myocardial infarction patients without LVWM improvement than in patients with improvement. Redox state of arterial blood can be a predicting factor for left ventricular function after acute myocardial infarction.

A 49-year-old woman had a right adrenalectomy for pheochromocytoma in April 1989. In May 1990 she underwent an operation to remove paraaortic lymph nodes, and the lymph nodes showed pheochromocytoma. Twenty-two months after the first operation, metastases to the left cervical nodes, lung, and liver occurred. Her blood pressure was 172/104 mmHg; fasting plasma glucose (FPG), 342 mg/dl; urinary noradrenaline (NA), more than 2000 micrograms/day; and plasma NA, 17.28 ng/ml. Treatment with the CVD regimen (cyclophosphamide, 750 mg/m2 on day 1; vincristine, 1.4 mg/m2 on day 1; dacarbazine, 600 mg/m2 on days 1 and 2, every 21 days) was begun on February 14, 1991. After 3 cycles of the CVD regimen her blood pressure was 140/82 mmHg; FPG, 157 mg/dl; urinary NA, 917 micrograms/day 1; and plasma NA, 4.54 ng/ml. The size of the metastatic lesions in the liver had decreased. Treatment with the CVD regimen was continued until May 1992. After that she did not go to the hospital for about 2 months. Metastatic lesions progressed gradually and treatment with the CVD regimen was repeated again. She was admitted to the hospital on February 17, 1993 because of appetite loss and nausea. Her blood pressure was 188/94 mmHg; FPG, 197 mg/dl; HbA1c, 9.5%; urinary NA, 18265.3 micrograms/day; and plasma NA, 47.20 ng/ml. She was treated with the CVD regimen in 2 repeated cycles (28th cycle of treatment with the CVD regimen) but there was no effect. She died following hemoptysis on March 15, 1993.(ABSTRACT TRUNCATED AT 250 WORDS)

A 70-year-old woman was admitted because of disturbance of her consciousness. Physical examinations and laboratory data suggested hypothyroidism. Primary hypothyroidism was subsequently confirmed with endocrinological examinations. Antidiuretic hormone (ADH) levels were elevated despite severe hyponatremia. On admission, urinary sodium concentration was 10mEq/l. The patient was treated with saline intravenously; serum sodium level increased from 120 to 125mEq/l and urinary sodium concentration increased from 10 to 54mEq/l. Mental confusion developed and serum sodium level dropped with urinary sodium concentration above 20mEq/l when thyroid replacement was started with the cessation of saline infusion. The patient's state of consciousness, elevated ADH levels, decreased serum sodium level and urinary sodium concentration were improved by thyroid replacement together with hydrocortisone therapy. Effects of acute water loading were abnormal with the administration of iodothyronine (T3) alone but were normalized with the administration of hydrocortisone together with T3. On discharge she was treated with the oral administration of levothyroxine alone. Pituitary hormones were normal. These results suggest that the patient was in a state of hypoadrenocorticism. Impaired water excretion in a state of hypoadrenocorticism due to hypothyroidism may give rise to an inappropriate secretion of ADH thereby resulting in hyponatremia, which in turn leads to hypotonic dehydration induced by water intoxication.

We measured total cholesterol (TC) and triglyceride (TG) in 78 pregnant women with obvious hypercholesterolemia (TC greater than or equal to 300 mg/dl) in pregnancy, measuring the concomitant effects of age, grade of obesity prior to pregnancy, total weight gain and degree of weight gain during pregnancy. After delivery the body weight was measured until TC was below 250 mg/dl, and then the average weekly weight loss was calculated. Age, the grade of obesity prior to pregnancy, total weight gain or degree of weight gain during pregnancy did not influence TC or TG in pregnancy. TC or TG in pregnancy had no effects on the birth weight of the newborn. There was significantly positive correlation between TC or TG at the 13th-16th week of pregnancy and the maximal level of TC or TG in pregnancy. In 22 of the 25 subjects, whose average weekly weight loss was 1.0 kg or over, TC was below 250 mg/dl by the 8th week postpartum. In pregnancy many factors including weight changes might influence TC or TG; however, the effects of weight changes postpartum on TC or TG such as weight reduction in obesity might appear.

The changes of serum total cholesterol (TC), HDL-cholesterol (HDL-C), Atherogenic Index [TC-HDL-C)/HDL-C, AI) and body weight in postpartum were studied in 58 normal women with obvious hypercholesterolemia (TC greater than or equal to 300 mg/dl) during pregnancy. They were divided into two groups: Groups A (n = 33) and B (n = 25), according to the maximal levels of TC (TCmax) in pregnancy, (Group A: TCmax less than 350mg/dl, Group B: TCmax greater than or equal to 350mg/dl). These groups were divided into four subgroups according to the length of time during which TC was below 250mg/dl) after delivery. In Groups A1 (n = 20) and B1 (n = 12) TC reached 250mg/dl within 10 weeks postpartum, and in Groups A2 (n = 13) and B2 (n = 13) after more than 11 weeks postpartum. TC in Group A was significantly higher than in Group B within 6 weeks postpartum. In Group A AI was significantly lower than in Group B at the same period. HDL-C in Group B1 was significantly higher than in Group B2. AI in Group B1 was significantly lower than in Group B2. In Group A TC reached 250mg/dl more rapidly than in Group B. The average weekly weight loss in postpartum in each Group A1 or B1 was significantly greater than each Group A2 or B2. The degree of hypercholesterolemia in pregnancy might influence the changes of serum lipids in postpartum. Rapid weight loss in postpartum might bring rapid recovery from abnormal metabolism of serum lipids in pregnancy.