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)

Parathyroid hormone and calcitonin, two major calcium-regulating hormones, were measured in the plasma of five experimental groups of rats to evaluate postflight calcium homeostasis after the 14-day COSMOS 2044 flight. Parathyroid hormone values were slightly higher in the flight animals (F) than in the appropriate cage and diet controls (S) (44 +/- 21 vs. 21 +/- 4 pg/ml, P less than 0.05), but they were the same as in the vivarium controls (V), which had different housing and feeding schedules. Neither V nor S showed the increase in plasma creatinine phosphorus and magnesium found in F, features of early renal insufficiency. F showed the lowest mean plasma calcitonin that was statistically different from V only. This difference in F and V (22 +/- 11 vs. 49 +/- 16 pg/ml, P less than 0.05) was most likely due to failure of circulating calcitonin in F to show the normal age-dependent increase we demonstrated in age-matched controls in a separate experiment. Basal values for parathyroid hormone and calcitonin were unchanged after 2 wk of hindlimb suspension, a flight simulation model, in age-matched and younger rats. From a time course experiment serum calcium was higher and parathyroid hormone lower after 4 wk than in ambulatory controls. Postflight circulating levels of parathyroid hormone appear to reflect disturbances in calcium homeostasis from impaired renal function of undetermined cause, whereas levels of calcitonin reflect depression of a normal growth process.
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PMID:Circulating parathyroid hormone and calcitonin in rats after spaceflight. 152 47

Data are given on the study of functional correlations of the pairs of organs (kidneys-liver and kidneys-lungs) that participate in provision of the functional system of secretion. The correlation of these pairs of organs contribution to the total secretion of metabolites as renal insufficiency grows is characterized by the S-shaped dependence, i.e. by a compensatory increase of the conjoined functions at the early stages and its depression at the graver stages of renal insufficiency. This approach makes it possible to determine the character, terms and significance of the participation of various organs in provision of metabolic homeostasis maintenance long before its failure and to reveal the main links in the pathogenesis of functional disorders of secretion.
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PMID:[Functional system of secretion in renal tuberculosis]. 152 26

Acute causes and chronic risk factors for the development of acute renal failure were analyzed in prospective acquired data of 261 patients in a medical ICU. The population was divided into a group requiring dialysis treatment for established renal failure (n = 95) and a collective maintaining mild renal insufficiency (n = 166). Bivariate and linear discriminant analyses revealed that, above all, variables related to bacterial infections (sepsis and administration of antibiotic agents) and pancreatitis contributed to the discrimination, followed by bleeding, volume depletion, and chronic liver disease in the discriminant function. Bivariate analysis also yielded significant results for mechanical ventilation, CNS depression, and surgery. The importance of the nephrotoxic properties of aminoglycosides may be outweighed by their role as an indicator of severe infectious disease. The overall correct classification rate of the discriminant function was 78.5%, which reflects the importance of the predictor variables, but does not allow individual predictions.
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PMID:Impairment of renal function in medical intensive care: predictability of acute renal failure. 218 66

We review the English-language literature on antibiotic-associated adverse reactions in patients with renal insufficiency in order to highlight this important but often overlooked clinical problem. Because many adverse reactions to antibiotics are not dependent on renal function, we have attempted to review only those reactions that are believed to be associated with renal insufficiency or that have been reported in patients with impaired renal function. Adverse effects of antibiotics in this setting can be divided into six major categories: neurologic toxicity, coagulopathy, nephrotoxicity, hypoglycemia, hematologic toxicity, and aminoglycoside inactivation by penicillins. Neurologic toxicity can be further divided into central nervous system toxicity consisting primarily of encephalopathy and seizures, ototoxicity, peripheral neuropathy, and neuromuscular blockade/respiratory depression. We explore the factors in uremia that may contribute to the susceptibility of patients with renal insufficiency to the adverse effects of antibiotics. Moreover, we make general recommendations regarding the use of the discussed antibiotics in patients with compromised renal function.
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PMID:Adverse antibiotic effects associated with renal insufficiency. 192 3

The mechanisms responsible for renal insufficiency in septic shock (SS) have not been well characterized. We therefore investigated renal hemodynamics and the renal excretion of prostaglandin E2 (PGE2) in a nonhuman primate model of severe, low systemic vascular resistance (SVR) SS. In 18 cynomolgus monkeys, SS was induced by an infusion of 3 x 10(10) live Escherichia coli per kg; five saline-treated animals served as nonseptic controls. Systemic and renal hemodynamics, and urine PGE2 concentrations were determined over the 3 h after the induction of sepsis. The septic group demonstrated a significant (p less than .001) and sustained depression in both mean arterial pressure and SVR. Septic animals also had significantly lower effective renal plasma flow (ERPF) (p less than .01) and glomerular filtration rate (GFR) (p less than .01) compared to controls. Furthermore, the renal hemodynamic response to SS was biphasic, with significant increases in ERPF and GFR in the second hour postsepsis, followed by a pronounced decrease in the third postseptic hour. The septic group also demonstrated an increase in the renal excretion of PGE2 (p less than .001) that was temporally associated with the transient recovery in renal hemodynamics during the second postseptic hour. These sepsis-induced renal alterations may be important in the pathogenesis of renal insufficiency complicating clinical SS.
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PMID:Renal hemodynamics and prostaglandin E2 excretion in a nonhuman primate model of septic shock. 240 7

In this study, background factors were determined in 108 surgical patients who showed depression in phagocytic and bacteriocidal activity with nitroblue tetrazolium reduction test. Control subjects consisted of 4 healthy males and 4 healthy females whose age ranged from 25 to 38 years. The background factors associated with the depressed neutrophil phagocytic and bacteriocidal activity in surgical patients were renal insufficiency, liver cirrhosis, hypoproteinemia, diabetes mellitus, long-term administration of steroids and immunosuppressants, obesity, anemia, aging and malignant tumors. These depression factors closely resembled those generally considered to be involved in increased susceptibility to infections.
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PMID:Depression factors of neutrophil bactericidal activity with nitroblue tetrazolium reduction test in surgical patients. 297 37

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

The disposition and pharmacologic activities of morphine, meperidine, methadone, propoxyphene, dihydrocodeine, and codeine are reviewed. Dose-related toxicities of these opioid analgesics include mental obtundation, respiratory depression, and hypotension. Furthermore, convulsions have been associated with normeperidine and cardiac toxicities with norpropoxyphene. Hepatic metabolism is the primary route of elimination, except for methadone, for which there is also significant renal excretion. Although the pharmacokinetics of morphine are unchanged in renal insufficiency, accumulation of active metabolites may lead to narcosis. Similar accumulation of normeperidine and norpropoxyphene, metabolites of meperidine and propoxyphene, respectively, as well as propoxyphene itself, and dihydrocodeine and codeine may explain reports of adverse reactions in patients with impaired renal function. A high index of suspicion of opioid-induced toxicities should be maintained in patients who have renal dysfunction and receive opioids.
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PMID:Effects of renal insufficiency on the pharmacokinetics and pharmacodynamics of opioid analgesics. 332 55

The activity of the renin-angiotensin-aldosterone system (RAAS), excretion of renal prostaglandins, renal hemodynamics, water-electrolyte balance were studied in 110 patients with chronic nephritis with arterial hypertension: 47 with hypertonic nephritis and 63 patients at the stage of renal insufficiency. Some investigations, the results of data processing, an analysis of the results of cross-group comparative studies, and the use of captopril (a drug that inhibits the activity of angiotensin-converting enzymes) confirmed the RAAS involvement in the pathogenesis of arterial hypertension in nephritides. Pathophysiological features of arterial hypertension in nephritides are the following: disturbances of physiological interrelationships between renin plasma activity and the state of water-electrolyte balance; hyperaldosteronism and depression of renal prostaglandin synthesis revealed both in unchanged and lowered renal function. The peculiarity of arterial hypertension at the stage of marked renal insufficiency is invariability of renin production resulting from structural reserves of the renal juxtaglomerular apparatus.
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PMID:[Pathophysiological features of arterial hypertension in chronic nephritis]. 332 85

Hexamethylene bisacetamide (HMBA), a potent differentiating agent, was tested in patients with refractory, solid tumors. Twenty patients received 25 evaluable courses. HMBA was given by continuous i.v. infusion for 5 consecutive days with courses repeated every 4 wk, provided there was acceptable, reversible toxicity. The starting dose was 4.8 g/m2/day for 5 days with escalations in subsequent cohorts of patients to 43.2 g/m2/day for 5 days. The patients included 12 females and eight males with median age of 56 yr (range 35 to 75 yr) and a median performance status of 80% (range, 60 to 100%). All except two patients had received prior chemotherapy, radiation therapy, or both. Metabolic acidosis and neurotoxicity, consisting of agitation, hallucinations, confusion, and alteration of consciousness, were dose dependent and dose limiting. The one patient treated with 43.2 m/m2/day became acidotic, agitated, and disoriented but recovered to his previous mental and electrolyte status by 8 days after the end of the HMBA infusion. One patient treated with 33.6 g/m2/day became severely acidotic (pH 7.07) and obtunded and also developed myocardial and cerebral infarctions during the HMBA infusion. The other two patients treated with 33.6 g/m2/day became mildly agitated during drug infusion. Six patients were treated at 24 g/m2/day without neurotoxicity. Transient renal insufficiency was seen in the two patients with severe neurotoxicity and in three other patients. Dose-related, mild to moderate nausea and vomiting were observed in ten patients. Four patients developed cutaneous herpes infections during treatment. White blood cell depression was not dose related, and at 24 g/m2/day, the median white blood cell nadir was 4,500/microliter (range, 2,000 to 7,900/microliter). Thrombocytopenia was dose related. At 24 g/m2/day, the median platelet count nadir was 207,000/microliter (range, 66,000 to 542,000/microliter). No objective tumor regressions were noted. HMBA pharmacokinetics was studied at all dosages. Plasma and urine samples from 20 patients were analyzed by gas-liquid chromatography for parent compound. HMBA plasma steady-state concentrations (Css) were achieved in all patients by 12 to 24 h into infusion. Once Css was achieved, daily variation was generally less than or equal to 10% from the mean Css. HMBA plasma Css increased linearly with dose, but there was variation in the Css achieved in individual patients at each dose. Doses of 24 to 33.6 g/m2/day consistently produced plasma HMBA Css of 1 to 2 mM matching concentrations required for differentiation in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Phase I clinical and pharmacokinetic study of hexamethylene bisacetamide (NSC 95580) administered as a five-day continuous infusion. 379 Dec 46


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