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)

Eighty patients admitted to hospital between 1975 and 1980 for "non-transmural" myocardial infarction (72 men, 8 women, mean age 56 +/- 9 years) were studied. The diagnosis was based on a severe attack of pain of over 30 minutes duration, increased serum cardiac enzyme levels (CKMB greater than 24 U; SGOT greater than 60 U), pyrexia and signs of inflammation. The patients were divided into two groups according to their ECG changes: Group A: "rudimentary" infarction with prolonged T wave inversion from V1 to V5, narrow transient Q waves and reduction of R wave amplitude in the corresponding leads; Group B: persistant prolonged, intercritical ST depression greater than 2.5 mm (subendocardial infarct). All patients underwent selective coronary angiography and left ventriculography in the RAO projection within 15 days of admission. The angiographic data (coronary score, ejection fraction, alinetic perimeter) were compared to those of 2 randomly chosen control groups: Group C: 30 inferior wall infarcts with coronary angiography and regularly followed-up; Group D: 30 transmural anterior infarcts with coronary angiography, regularly followed-up. Four factors were analysed during follow-up: the incidence of death after discharge from hospital, transmural infarction, unstable angina and cardiac failure. All patients were treated medically (nitrate derivatives, betablockers, calcium antagonists). Sixteen patients in Group A (p less than 0,025) were operated and excluded from the prognostic study. The angiographic data showed a high incidence of isolated, severe LAD disease in Group A (59.2% of cases) and that multivessel disease was commoner in Group B (78.4%). A collateral circulation revascularising the LAD was observed in 42% of patients in Group A. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called rudimentary or nontransmural myocardial infarction. Coronary lesions, course and prognosis]. 643 44

A 42 year old woman presented with resting and effort angina. During an attack of chest pain, ST-T wave depression was recorded in the anterior chest leads. Coronary angiography showed spontaneous spasm of the left main stem, relieved by nitrate derivatives. The coronary arteries were angiographically normal between attacks of angina. Thallium 201 myocardial scintigraphy showed anterior wall hypofixation at maximal effort. A good therapeutic result was obtained with calcium antagonists. The site of coronary spasm is the special feature of this case, which may be grouped with other rare reported cases of spontaneous spasm or spasm on effort. We confirm that spasm-induced myocardial ischaemia may cause ST depression on the surface ECG.
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PMID:[Rest and exercise angina caused by spasm of the left coronary artery. Apropos of a case with angiographically normal coronary arteries]. 643 63

An open, multi-centre clinical trial was carried out in 537 hospital patients and 2138 general practice patients to evaluate the efficacy and tolerance of isosorbide 5-mononitrate in the treatment of angina pectoris. Prior to entry into the trial, angina attack frequency and acute glyceryl trinitrate consumption were assessed during previous, in most cases unsatisfactory, anti-anginal therapy. After a treatment-free washout period of 3 days, graded multi-stage exercise testing was performed and then treatment started with 20 mg isosorbide mononitrate 3-times per day. Exercise testing was repeated after 14 days' therapy and, in the case of the hospital patients, also 4 to 5 hours after the first dose of isosorbide mononitrate. At the end of the 14-day treatment period, angina attack frequency and glyceryl trinitrate consumption were again assessed. Similar results were obtained for both hospital and general practice patients. Changing to isosorbide mononitrate resulted in a marked reduction in angina frequency, with complete elimination of angina attacks in approximately half of the patients; nocturnal angina, present in approximately 20% of the patients during previous therapy, virtually disappeared during isosorbide mononitrate therapy. Exercise tolerance and performance improved in the majority of patients, with a marked increase in the number of patients able to exercise to the level at which some symptom other than angina pectoris caused them to stop. ST-depression during exercise and exercise-induced arrhythmias also showed clear reductions during isosorbide mononitrate therapy. Tolerance to isosorbide mononitrate was good, the expected 'nitrate headaches' being the only common side-effect reported. The results were such that continuation of treatment with isosorbide mononitrate after the trial was recommended by the attending physician in 77% of the hospital patients and 87% of the general practice patients.
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PMID:Treatment of coronary heart disease with isosorbide mononitrate ('Elantan' 20): a multi-centre study in hospital and general practice. 644 49

1. The chronotropic and inotropic effects of the anti-anginal agent SG-75 (2-nicotinamidoethyl nitrate) and 1-verapamil were investigated in isolated blood-perfused canine atrial preparations. The compounds were administered via the cannulated sinus node artery. 2. SG-75 induced a selective negative inotropic as opposed to a chronotropic effect. Verapamil showed no selective negative chronotropic or inotropic activity. 3. Effects of SG-75 and 1-verapamil on the frequency-force relationship were studied. SG-75 produced a uniform depression of the developed tension at all frequencies tested which the depression with 1-verapamil was greater at higher than at lower frequencies.
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PMID:Differential chronotropic and inotropic effects of 2-nicotinamidoethyl nitrate (SG-75) in the dog isolated atrium. 644

The clinical course of 59 patients with coronary artery spasm and no fixed severe coronary obstruction was analyzed for an average of 5.9 years. The study group consisted of 27 men and 32 women. Angina at rest was the predominant symptom in 93% of the patients. Myocardial infarction occurred in 19% and syncope during angina in 27%. During spontaneous anginal episodes, 64% of the patients showed ST segment elevation, 17% ST segment depression and 15% no electrocardiographic changes. Major arrhythmias during angina occurred in 24% of the patients. Permanent pacemakers were required in 10% of the patients. Stress tests were positive in 32% of the patients. Long-acting nitrate therapy controlled symptoms in only 31%, and calcium antagonist agents controlled symptoms in 83% of the patients unresponsive to nitrates. Spontaneous remission of angina for at least 1 month while receiving no medical treatment occurred in 39% of the patients. Fifteen percent of patients had an indefinite remission with no recurrence of symptoms for at least 2 years. There were no cardiac deaths. The natural history of medically treated patients with pure coronary spasm is characterized by recurrent angina at rest, frequent spontaneous remission, a poor response to long-acting nitrate therapy and a good response to calcium antagonists. Although myocardial infarction and major arrhythmias are common, cardiac mortality is low in medically treated patients.
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PMID:Natural history of pure coronary artery spasm in patients treated medically. 660 22

The efficacy of nifedipine in relieving recurrent ischemic episodes following acute myocardial infarction was studied in 11 patients a mean of 9.2 days post infarction (range 2-42 days). Prior to infarction, all of the patients had a history of exertional angina only, yet following the infarction, episodes of recurrent ischemia occurred at rest in spite of maximal medical management with beta-blockers and/or nitrate preparations, which lowered the heart rate to a mean of 65 beats/min, and the blood pressure to a mean of 109/70 mmHg. Ischemic episodes were associated with ST-segment elevation in 7 patients and ST-segment depression or T-wave inversion in 4 patients. Coronary angiography was performed in 8 patients, and demonstrated multivessel coronary disease in 7. The episodes of rest ischemia were prevented in all but one patient by the addition of nifedipine (mean daily dose 60 mg, range 40-120 mg) without causing a change in heart rate or blood pressure. Two patients continued to have myocardial ischemia with minimal exertion, although rest pains were abolished, and they underwent coronary bypass surgery for relief of exertional pain. Only one patient continued to have episodes of ischemia at rest, although the frequency of ischemic episodes was decreased, and bypass surgery was necessary for pain relief. The other 8 patients have been managed medically for a mean of 5.4 months (range 1-12 months) and have remained pain free on combined regimens of nifedipine, beta blockers, and/or nitrate preparations. We conclude that nifedipine may be efficacious for the relief of recurrent myocardial ischemia at rest following acute infarction. In some patients nifedipine may eliminate the need for coronary artery bypass surgery and in others it may provide clinical stability prior to operation.
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PMID:Nifedipine therapy for recurrent ischemic pain following myocardial infarction. 708 48

The ability of physostigmine to antagonize the respiratory depressant effect of morphine was studied in conscious rabbits and ketamine-anaesthetized dogs pretreated with atropine methyl nitrate. Morphine 4 mg kg-1 increased PaCO2 in the rabbit from 3.43 +/- 0.16 to 4.95 +/- 0.28 kPa, decreased arterial pH from 7.45 +/- 0.01 to 7.31 +/- 0.01 and decreased respiratory frequency by 36%. Physostigmine 0.1 mg kg-1 reduced PaCO2 to control values within 10 min and significantly increased arterial pH and respiratory frequency. There was no antagonism of the analgesic effect of morphine. Neostigmine 0.1 mg kg-1 did not reverse the respiratory depressant effect of morphine. In dogs anaesthetized with ketamine, morphine 15 mg kg-1 caused loss of consciousness and marked analgesia, decreased the respiratory frequency by 47%, and increased PaCO2 by 47%. Physostigmine 0.1 mg kg-1 antagonized the effect of morphine on respiration and restored consciousness in the dogs, but did not impair analgesia. It is concluded that physostigmine reverses morphine-induced respiratory depression by prolonging the effect of acetylcholine released from brain-stem neurones. The possibility should be considered of replacing opiate antagonists by physostigmine to reverse postoperative respiratory depression and drowsiness induced by opiates.
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PMID:Physostigmine antagonizes morphine-induced respiratory depression but not analgesia in dogs and rabbits. 744 96

Nitric oxide (NO) generation in a series of 20 burn patients was studied with a novel anion exchange high-performance liquid chromatographic method for the simultaneous determination of nitrite (NO2-) and nitrate (NO3-), the stable metabolic endproducts of NO. The NO values within our survivor group (n = 17) were significantly altered at days 1, 6, and 12 postburn in contrast to controls (n = 23) (p < or = 0.03). NO2- values were significantly depressed in both plasma and urine, whereas NO3- values were significantly elevated in contrast to control values (p < or = 0.03). The ratio of NO2-:NO3- was significantly lower for burn patients versus controls in both plasma and urine (p < 0.01). The NO generation seemed in part to be dependent on the percentage of total body surface area burn, most dramatically elevated in patients with burns of 10 to 40% total body surface area. In subjects who did not survive beyond 36 hours postinjury because of irreversible shock (n = 3), the production of NO was significantly depressed in contrast to survivors and controls (p < 0.0001). However, the NO2-:NO3- ratio (0.001) was relatively unchanged, with reflection of a global depression in NO formation with no change in the individual component release. Burn injury resulted in an increased release/production of NO that in the first postburn week is maximally elevated immediately postinjury. NO release, although decreased at day 6 relative to the day 1 values, remained elevated into the second week postinjury when there was evidence for a further increase in NO production. The enhanced NO3- formation may well result from NO reacting with oxygen-free radicals counteracting superoxide anion-induced destruction of tissue, thereby potentially functioning as a protectant molecule.
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PMID:Burn-induced nitric oxide release in humans. 747 2

To evaluate the efficacy of anipamil, a phenylalkylamine calcium antagonist, in treatment of stable angina pectoris, we performed a randomized, double blind placebo-controlled, cross-over study. Inclusion criteria were (a) stable angina pectoris for at least 2 months, (b) an exercise test with > or = 0.1-mV horizontal or downsloping ST-segment depression limited by angina, and (c) at least 10 attacks of angina pectoris in a single-blind 3-week run-in period. Nineteen patients were randomized to enter the study. In 3-week periods, they received either anipamil 80 mg once daily (o.d.), anipamil 160 mg o.d., or placebo. At the end of each period, an exercise test was performed. The number of angina pectoris attacks was significantly reduced during treatment with anipamil 80 mg (p < 0.05) and anipamil 160 mg (p < 0.001) as compared with placebo. Glycerol nitrate consumption was significantly reduced during treatment with anipamil 80 mg (p < 0.01) and 160 mg (p < 0.001) as compared with placebo. During exercise testing, the load (W) at start of angina was significantly increased during treatment with anipamil 80 mg (p < 0.01) and 160 mg (p < 0.05) as compared with placebo. Heart rate (HR) at 0.1 mV ST-segment depression was increased during treatment with anipamil 80 mg (p < 0.001). Few adverse events were reported.
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PMID:Efficacy of anipamil, a phenylalkylamine calcium antagonist, in treatment of angina pectoris. 753 63

Uranyl nitrate (UO2(NO3)2) has been shown to be capable of increasing transmitter release from the motor nerve accompanied by the potentiation of nerve evoked muscle contraction. In this paper, we have demonstrated that UO2(2+) induced an initial twitch depression followed by a later twitch potentiation in low (0.35 mM) Ca2+ medium. Although UO2(2+) has been identified as a K(+)-channel blocker, we have found it only partially blocked the fast K(+)-current (IK(f) as recorded in the perineurial sheath of the mouse triangularis sterni preparation. Increasing the concentration of UO2(2+) to a high concentration of 0.4 mM did not further inhibit IK(f) but markedly prolonged the duration of the outward current of the nerve terminals. From the time course of its appearance together with the specific inhibition by 4-aminopyridine, dendrotoxin and beta-bungarotoxin, which has been shown to be capable of blocking the K(+)-current of the motor nerve terminal, it was proposed that UO2(2+) prolonged the duration of the nerve terminal spikes by an enhancement of an IK(s)-like current, which was further characterized by its susceptibility to be enhanced by low K+, low Ca2+ and Cd2+ but attenuated by high K+ and high Ca2+. These cation effects not only supported UO2(2+)-induced IK(s) current but also excluded the possibility of an enhancement of Ca(2+)-activated K(+)-current induced by UO2(2+) plus TEA. The significance of this enhancement of IK(s) induced by UO2(2+) has been elucidated by the finding that dendrotoxin inhibited but tetraethylammonium potentiated not only UO2(2+)-induced IK(s) but also UO2(2+)-induced twitch depression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement of a slow potassium current component by uranyl nitrate and its relation to the antagonism on beta-bungarotoxin in the mouse motor nerve terminal. 761 42


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