Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Due to the lately increased oral nitrate intake of humans and animals the influence of 3% KNO3 in the diet on growth and the thyroid hormone and somatomedin-C-concentration in the serum was to be tested in an experiment with growing pigs in case of different iodine supply. The investigations were undertaken in 3 groups with 9 piglets each. The animals were 6 weeks old: 1. nitrate-exposed, 2. pair-fed to group 1 (without nitrate), 3. ad libitum without nitrate. The mean daily weight gains amounted to 242, 274 and 393 g respectively, after a five-week test period. Compared to the ad libitum control group, the T4-, T3-, rT3- and Sm-C-level of nitrate-exposed animals was significantly lower after 5 weeks. There were no statistically relevant differences between nitrate-exposed and pair-fed animals with regard to the T3- and Sm-C-level. After the 5-week test period with an iodine supply covering the requirement the rations of all 3 groups were supplemented with further 0.8 mg iodine/kg. The T4-, T3- and rT3-levels of the animals of group 1 normalized within one week. The Sm-C-levels of the nitrate-exposed and pair-fed group were still decreased. The investigations show that an increased nitrate intake via food and drinking water influences the thyroid hormone metabolism. It should be taken into consideration in the etiology of endemic struma. Furthermore, excessive nitrate intakes influence the Sm-C-concentration and thus growth due to food intake depression.
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PMID:Effect of chronic dietary nitrate and different iodine supply on porcine thyroid function, somatomedin-C-level and growth. 355 13

There is increasing evidence that constant nitrate plasma levels, as induced by at least three-times-daily ingestions of isosorbide dinitrate in sustained-release form, lead to an attenuation or even complete loss of the anti-ischemic effects (nitrate tolerance). Therefore, the dependence of tolerance development on dosage intervals according to once-daily and twice-daily ingestions was assessed. Tablets of isosorbide dinitrate (80 mg) in sustained-release form were administered once-daily at 8 A.M. (dosage interval 24 hours) or twice-daily at 8 A.M. and 8 P.M. (dosage interval 12 hours), as well as at 8 A.M. and 2 P.M., respectively (maximal dosage interval 18 hours). A total of 34 patients with angiographically proven coronary artery disease, a history of stable, exercise-dependent angina pectoris, and a reproducible, exercise-induced ST-segment depression of at least 0.15 mV (1.5 mm), who initially showed a response to 80 mg of isosorbide dinitrate, were enrolled. The anti-ischemic effects of isosorbide dinitrate on exercise-induced ischemia were objectively determined by the measurement of exercise-induced ST-segment depression before as well as two, six, and 12 hours after the ingestion at the first and the 15th day of the studies. Since the dosage interval of 12 hours resulted in constant plasma levels, the initially beneficial anti-ischemic effects of isosorbide dinitrate were considerably attenuated after two weeks of treatment. In contrast, the once-daily regimen with its intermittent peaks and valleys of nitrate plasma levels showed identical anti-ischemic effects at the 15th day as compared with the first day. Ingestions at 8 A.M. and 2 P.M. also circumvented the development of nitrate tolerance, however, combined with an even more pronounced anti-ischemic effect after 12 hours as compared with the once-daily regimen. Thus, the circumvention of nitrate tolerance requires a daily "nitrate-poor" interval. The best compromise between a maximal possible anti-ischemic effect and the circumvention of tolerance development was found for the "eccentric" dosage regimen in which the tablets were ingested in the morning and early afternoon.
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PMID:Induction and circumvention of nitrate tolerance applying different dosage intervals. 367 93

Adult female Wistar rats were injected with 1 mg/kg body weight of uranyl nitrate (UN). Evaluation of renal function, histopathology studies, and determination of plasma erythropoietin (Ep) titers after exposure to 456 mb for 16 h were performed at 1, 2, 7, 10, 15, and 21 days after drug injection. Plasma urea and creatinine concentrations markedly increased during the first seven days after injection, reaching maximal values on day 7 and decreasing thereafter. Significant increases in urine volume and significant depressions in urine osmolality also were observed; both alterations were most marked on day 7 after injection. A coagulative necrosis of the epithelium of proximal convoluted tubules, desquamation of the necrotic cells, and dilation or collapse of the tubular lumen were observed; the lesions were more marked on day 7. Plasma Ep levels in UN-treated rats exposed to hypobaria were markedly lower than in noninjected controls similarly exposed. Measurements were performed one, two, and seven days after UN injection, with maximal depression observed on day 7. These observations indicate that there is a correlation between the extent of both tubule damage and degree of renal dysfunction and plasma Ep production during exposure to hypoxia in UN-treated rats. This suggests that the renal Ep component is derived primarily from tubular cells.
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PMID:Relationship between severity of renal damage and erythropoietin production in uranyl nitrate-induced acute renal failure. 369 9

Although nitrates are among the oldest drugs in cardiology the problem of tolerance is a scientific challenge of today. We examined and compared the effects of initial and chronic therapy (4 weeks) with 1 X 1 ISDN 120 mg sustained release in 9 patients with coronary heart disease and impaired left ventricular function. At intraindividually identical workloads (average 50 +/- 12 watt) there was a reduction of PCWPm from 32.5 +/- 9.5 to 19.7 +/- 9.8 mm Hg. This reduction of PCWPm during bicycle ergometry was fully achieved in long-term therapy. With the first dose of ISDN cardiac index (CI) at maximum workload increased from 6.0 +/- 1.2 to 6.8 +/- 1.3 l/min/m2; during chronic therapy cardiac index improved from 5.3 +/- 1.3 to 6.6 +/- 1.1 l/min/m2. Exercise capacity during bicycle ergometry in the sitting position increased concomitantly from 414 to 686 watt X min. In long-term therapy there was a further significant improvement to 772 watt X min. ST-segment depression, measured as sum of ST-depression in all 12 standard ECG leads decreased from 0.63 mV before medication to 0.11 mV after the first dose and to 0.16 mV in long-term therapy. The investigation of ventricular function during ventriculography and the investigation of coronary vasomotion during coronary angiography after ergonovine maleate i.v. and ISDN s.l. also demonstrated the full nitrate effect in long-term therapy.
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PMID:[Hemodynamics and coronary dynamics under ISDN long-term therapy]. 379 97

Isometric tetani of single muscle fibers of Rana temporaria were studied as a function of stimulation rate, sarcomere length (1.7-2.3 micron), twitch-to-tetanus ratio, and exposure to twitch potentiators (Zn2+ and NO3-) at 20 degrees C. As the stimulation rate was decreased below a maximal level, tension generation decreased. This depression in tension generation was more pronounced at shorter sarcomere lengths. Therefore the magnitude and shape of the sarcomere length curve was dependent on stimulation rate. Although the depression in tension generation was always accompanied by a noticeable ripple in the tension record in fibers with large twitch-to-tetanus ratios, it could be observed even during well-fused tetani in fibers with low twitch-to-tetanus ratios. In all fibers, however, high stimulation rates or exposure to potentiators resulted in maximum tension generation at each length, and the sarcomere length-tension curve followed that found by Gordon, Huxley, and Julian. This indicates that the fall in tension between sarcomere lengths of 2.0 and 1.7 micron is not due to length-dependent activation but is more likely to be the result of mechanical interference in the force-generating interaction between cross bridges and thin filament sites.
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PMID:Stimulation rate, potentiators, and sarcomere length-tension relationship of muscle. 387 67

Percutaneous isosorbide dinitrate cream and sustained-release tablets were compared in a double-blind randomised crossover trial in 28 patients with coronary artery disease and chronic stable angina pectoris. Twenty-two patients completed the trial. Both preparations significantly increased the mean exercise time to the onset of angina (P less than 0.001) and to termination of exercise (P less than 0.001) compared to the pre-treatment period. There were no significant differences between the cream and tablets with respect to frequency of anginal attacks, glyceryl trinitrate consumption, heart rate and ST segment depression at the onset of angina, ST segment depression at maximal exercise and the double product of heart rate and systolic blood pressure at maximal exercise. Equal numbers of patients expressed preference for cream and tablets. We conclude that in this group of patients isosorbide dinitrate sustained-release tablets have no clinical advantage over isosorbide dinitrate cream which, may, therefore, be of particular value for those patients with angina pectoris who dislike taking tablets or who prefer this form of nitrate preparation.
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PMID:Double-blind randomised crossover trial comparing isosorbide dinitrate cream and oral sustained-release tablets in patients with angina pectoris. 388 83

Molsidomine, similar to nitrates, improves myocardial blood flow in hypoperfused, poststenotic myocardial regions, reduces left ventricular pressure and volumes, and leads to improvement in impaired regional wall motion. In patients with chronic, stable anginal pectoris who underwent long-term treatment with 2 mg of molsidomine three times daily there were reductions in ST segment depression of 45% and 9% at 1 and 3 hours after administration, respectively, and slight but statistically significant reductions in the rates of anginal attacks and nitrate consumption of 16% and 18%. Administration of 3 mg three times daily did not render more significant effects. Doubling the frequency of administration--that is, 2 mg six times daily--led to reductions in the rates of anginal attacks and nitrate consumption of 38% and 36%, respectively, and 4 mg led to a more marked reduction in ST segment depression of 57%. With administration of 8 mg of sustained-release molsidomine, a prolonged antiischemic effect was documented with reductions in ST segment depression of 74% at 1 hour and 31% at 8 hours after medication. In patients with congestive heart failure, 1 hour after administration of 4 mg of molsidomine there were significant reductions in systolic and diastolic pulmonary artery pressures of 25% and 30%, respectively. After 7 days of continuous treatment with 4 mg of molsidomine four times daily, comparable reductions in pulmonary artery pressure were observed. Thus molsidomine, in adequate dosages, elicits an unequivocal anti-ischemic and antianginal effect as well as a salutary reduction in left ventricular filling pressure.
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PMID:Effectiveness of molsidomine in the long-term treatment of exertional angina pectoris and chronic congestive heart failure. 388 33

Systemic administration of angiotensin II (ANG II) (200 micrograms/kg sc) to the rat induced a hypothermic response that was characterized within 12 min by a reduction in the rate of O2 consumption, vasodilation of the tail, and a 1.3 degrees C fall in colonic temperature. Administration of ANG II in doses ranging from 10 to 200 micrograms/kg resulted in a decrease in colonic and an increase in tail skin temperature. Angiotensin I (ANG I) (200 micrograms/kg sc) induced a similar hypothermic response which was abolished by pretreatment with the ANG I-converting enzyme inhibitor, captopril (35 mg/kg ip). The interaction of ANG II with cholinergic and adrenergic pathways was evaluated to determine possible mechanisms. Treatment with ANG II (200 micrograms/kg sc) and propranolol, a beta-adrenoceptor antagonist (6 mg/kg ip), resulted in a greater depression of colonic temperature (Tco) than was observed with ANG II alone but did not affect the increase in tail skin temperature (Tsk) accompanying administration of ANG II. When ANG II was administered in combination with the beta-adrenergic agonist, isoproterenol (50 micrograms/kg ip), Tco remained at control levels, whereas an enhancement of the ANG II-induced increase in Tsk occurred. Administration of ANG II in combination with atropine sulfate (6 mg/kg ip), a muscarinic receptor antagonist which crosses the blood-brain barrier, significantly reduced the extent of the fall in Tco without affecting the increase in Tsk. The combined treatment of ANG II and the quaternary analogue, atropine methyl nitrate (3.25 mg/kg ip), which does not cross the blood-brain barrier, failed to affect the hypothermic responses to ANG II. These results suggest that the hypothermic responses to ANG II may be mediated through a central cholinergic pathway and possibly influenced by an adrenergic component. The inability of both adrenergic and cholinergic blockers to affect the vasodilatory response of the tail of the rat to administration of ANG II suggests that the mechanisms subserving heat production can be blocked independently of those subserving heat loss.
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PMID:Angiotensin II-induced hypothermia in rats. 388 74

Ten patients with angiographically proven coronary heart disease, stable exercise-induced angina pectoris, and reproducible ST-segment depression were treated with isosorbide dinitrate (ISDN) tablets in daily doses of 240 mg (6 X 40 mg) and placebo (PL) for 28 days each on the basis of a randomized double-blind protocol with intraindividual cross-over. ISDN treatment resulted in a sustained reduction of anginal attacks with a weekly mean rate ranging from 1.4 (3rd week) to 3.9 (4th week) as compared to 10.2 (2nd week) to 11.7 (4th week) during placebo treatment (P less than 0.001). Ischemic response during stress testing (sum of ST-segment depressions) was significantly improved during ISDN treatment as compared to placebo. Day 1: 56% (P less than 0.01); day 7: 30% (P less than 0.01); day 28: 49% (P less than 0.001). Heart rate and arterial blood pressure in the upright position were different between ISDN and placebo on day 1 and day 7 of the treatment phases (P less than 0.02), but not on day 28. Nitrate responsiveness with regard to blood pressure and heart rate was restored after a drug-free interval of 2 days. The plasma concentrations for ISDN and the mononitrate metabolites exhibited a constant ratio during the treatment period. Thus, therapy with 6 X 40 mg ISDN per day resulted in a sustained reduction of anginal attacks and preserved improvement of ischemic ST-segment depression during exercise in upright position.
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PMID:[Anti-angina effectiveness of isosorbide dinitrate in an acute trial and following continuous 4-week therapy with 40 mg 6 times a day]. 392 17

This study was undertaken to determine whether an effective antianginal treatment without tolerance development can be carried out with intermittent nitrate administration on a regimen with a single daily dose of 120 mg isosorbide dinitrate (ISDN) in sustained-release form (SR), as well as whether the concomitant administration of 100 mg atenolol or 100 mg atenolol and 20 mg nifedipine renders an additive antiischemic effect. In two independently performed investigations, the duration of action of a single dose of 120 mg ISDN SR was assessed after its initial administration in addition to the anti-ischemic effect during long-term treatment, each according to a randomized, double-blind, crossover, placebo-controlled protocol in a total of 15 patients with angiographically-documented coronary artery disease, stable angina pectoris and reproducible ST-segment depression during exercise. The test phases of four weeks each were separated by one week placebo phases. After completion of the study, for a further eight weeks, 120 mg ISDN SR was given together with 100 mg atenolol in the morning. Exercise testing was carried out after four weeks of treatment in a control period before and at two hours after administration of 120 mg ISDN SR with 100 mg atenolol as well as after another four weeks in a control period before and after concomitant administration of 120 mg ISDN SR, 100 mg atenolol and 20 mg nifedipine in sustained release form.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term therapy of stress angina pectoris by a single daily administration of 120 mg isosorbide dinitrate in retard form. Comparison of monotherapy and combination therapy with atenolol and nifedipine]. 392 13


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