Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anticholinergics (in particular, ipratropium bromide [Atrovent]) are first-line therapy in patients with chronic obstructive pulmonary disease (COPD). Although more studies are needed to support the use of combination therapy, adding an inhaled beta agonist to the therapeutic regimen is reasonable in patients who remain symptomatic and need quick relief. Patients frequently receive inadequate amounts of drug with standard doses delivered by metered-dose inhalers, often as the result of improper technique, so symptomatic patients may require higher doses. Caution is recommended when the dose of inhaled sympathomimetics is increased in COPD patients with ischemic heart disease or tachyarrhythmias. The addition of an oral sympathomimetic is seldom necessary. Theophylline may be considered in outpatients who remain symptomatic despite their use of inhaled bronchodilators, but heart disease, seizure disorders, and gastroesophageal reflux are contraindications. Corticosteroid therapy remains controversial but can be helpful in patients who still have severe disease despite maximum bronchodilator therapy. Antibiotics can be of benefit in COPD patients undergoing an exacerbation who have increasing dyspnea, cough, and phlegm production.
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PMID:Drug treatment of COPD. Controversies about agents and how to deliver them. 134 54

Although numerous studies have implicated accelerated phospholipid catabolism during myocardial ischemia as an important contributor to ischemic membrane dysfunction, no information is currently available on the subcellular distribution, physical properties, or kinetic characteristics of human myocardial phospholipase A2. In this report, we demonstrate that the overwhelming majority (98%) of total phospholipase A2 activity in human myocardium (obtained from transplant recipients) is calcium independent, plasmalogen selective, and is distributed between the microsomal (60-70% of total activity) and cytosolic (30-40% of total activity) fractions. Both human myocardial microsomal and cytosolic phospholipase A2 enzymes 1) preferentially hydrolyze plasmalogen molecular species containing arachidonic acid at the sn-2 position, 2) are recalcitrant to chemical inactivation by the indole-reactive agent parabromophenacyl bromide, 3) are irreversibly inhibited by covalent modification of an essential thiol residue by 5,5'-dithio-bis(2-nitrobenzoic acid) (DTNB), and 4) are exquisitely sensitive to mechanism-based inhibition by (E)-6-(bromomethylene)tetrahydro-3-(1-naphthalenyl)-2H-pyran-2-one (bromoenol lactone). In sharp contrast, human mitochondrial phospholipase A2 1) accounts for only a diminutive amount of total myocardial phospholipase A2 activity (1-2%), 2) is augmented by calcium ion, 3) exhibits a higher reaction velocity using phosphatidylcholine in comparison with plasmenylcholine substrate, and 4) is not substantially inhibited by either DTNB or bromoenol lactone. Collectively, these results demonstrate that the majority of phospholipase A2 activity in human myocardium is catalyzed by a novel class of calcium-independent plasmalogen-selective phospholipases A2 and underscore the potential importance of this class of enzymes in mediating membrane dysfunction during myocardial infarction in humans.
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PMID:Identification and characterization of human myocardial phospholipase A2 from transplant recipients suffering from end-stage ischemic heart disease. 153 86

A 63-yr-old man weighing 56kg was scheduled for pharyngoplasty under general anesthesia. The patient had no history of ischemic heart disease. Preoperative ECG showed incomplete right branch block. We administered thiopental and succinylcholine for intubation. Anesthesia was maintained with enflurane, nitrous oxide, oxygen and pancuronium bromide. Thirty minutes after the start of incision, the patient developed a severe hypotension and ECG revealed ST elevation and complete AV block. We administered ephedrine hydrochloride, phenylephrine hydrochloride and atropine sulfate. The ECG returned to sinus rhythm but ST segment was depressed this time. We considered it due to coronary spasm, so we started continuous intravenous administration of nitroglycerin (0.5 microgram. kg-1. min-1). One hour later, ST segment returned to normal. ECG showed no remarkable changes and no symptoms were seen after the operation. We found it important to suspect coronary spasm when ECG showed PVC-like abnormal waves with ST elevation. We consider that continuous administration of nitroglycerin at a rate of 0.5 microgram. kg-1. min-1 was effective for the treatment of coronary spasm in this case.
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PMID:[Coronary spasm during laryngoplasty]. 230 59

Although not unanimously accepted, high-dose fentanyl anesthesia has been associated with hemodynamic stability and little derangement of myocardial oxygen balance. This apparent inconsistency inspired us to investigate the effects on cardiac function and myocardial metabolism of stepwise increasing doses of fentanyl, accumulating to 15, 30, and 50 micrograms.kg-1, with the least possible interference from other drugs. Subjects were unpremedicated patients with ischemic cardiac disease scheduled for coronary artery bypass grafting or major vascular surgery. In an initial study employing succinylcholine for muscle relaxation, we found that heart rate (HR), coronary sinus blood flow (CSF) and coronary vascular resistance (CVR) remained unchanged, while systemic arterial pressure (SBP), rate-pressure product (RPP), coronary perfusion pressure (CPP) and left ventricular work (LVW) decreased. Myocardial uptake of oxygen (MVO2) and free fatty acids (FFA) both decreased in a dose-dependent manner. Arterial lactate concentration and myocardial lactate uptake both increased. These findings opposed the postinduction myocardial ischemia noted by some other investigators. In most of these studies pancuronium bromide had been used for muscle relaxation. Since the latter agent has been claimed to increase cardiac work, a second group of correspondingly diseased patients was studied in which succinylcholine was replaced by pancuronium bromide. In this group HR, RPP, CSF and MVO2 all increased at the lowest dose of fentanyl and HR additionally also at 30 micrograms.kg-1. The cardiac index was higher in the pancuronium group at the lowest and middle dose steps of fentanyl. Lactate uptake decreased with higher doses of fentanyl and relative myocardial lactate extraction declined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscle relaxants change myocardial metabolism in patients with ischemic heart disease during high-dose fentanyl anesthesia. 230 42

At present, phosphodiesterase III inhibitors are commonly used for the treatment of low cardiac output states. Despite their positive inotropic and lusitropic effects, these drugs are still under discussion because of certain adverse effects like thrombopaenia, elevation of transaminases, abdominal disregulation, and excessive peripheral vasodilatation. As a consequence, more cardioselective phosphodiesterase inhibitors were developed with the aim of reducing these adverse effects. One of them, enoximone (Marion Merrell Dow, Fig. 1), an imidazole derivative, has nearly no influence on platelets and abdominal organ function. In addition, in many studies vasodilatation was found to be absent. Recently a new substance, R80122 (Janssen, Belgium, Fig. 1), was developed. First experimental studies showed high cardioselectivity of this substance. The aim of this study was to compare the haemodynamic effects of enoximone and R80122 in patients with ischaemic heart disease. METHODS. This study was thoroughly discussed and approved by the local Ethics Committee; all patients gave written informed consent. Twenty male patients (Table 1) with normal left ventricular function who were about to undergo elective coronary artery bypass surgery were randomly allocated to receive a bolus of either 1.0 mg/kg enoximone or 0.3 mg/kg R80122 after induction of anaesthesia. Premedication consisted of 2 mg flunitrazepam orally the evening before and in the morning 1 h before operation. Anaesthesia was induced with 0.007 mg/kg fentanyl, 0.2 mg/kg etomidate, and 0.1 mg/kg pancuronium bromide and maintained by a continuous infusion of 0.02 mg/min fentanyl and 0.3 mg/min midazolam. After induction of anaesthesia haemodynamic measurements were performed and blood gas samples were taken preoperatively under steady-state conditions before and 5, 30, and 60 min after drug administration. RESULTS. The results of both groups are shown in Table 2 as mean values with standard deviations. Individual changes of cardiac index (CI), mean arterial pressure (MAP), and systemic vascular resistance (SVR) are depicted in Fig. 2. Peak percentage changes of the haemodynamic parameters are shown in Fig. 3. Both substances improved cardiac function; 5 min after drug administration CI increased by 31% and 26%, respectively. This was accompanied by increases in stroke volume (13% and 14%, respectively) and heart rate (15% and 10%, respectively). At the same time, there were declines in SVR (38% and 36%, respectively) and MAP (19% and 21%, respectively). Although mean values of pulmonary arterial and wedge pressure decreased after drug administration, these changes were inconsistent and not of clinical relevance. There were no statistically significant differences between the haemodynamic effects of both substances at any time in this study. CONCLUSIONS. Both enoximone and R80122 showed the expected inotropic effects. Nevertheless, both substances have a distinct vasodilative effect, which leads to a decline in MAP. R80122 does not have higher cardioselectivity than enoximone.
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PMID:[Hemodynamic effects of new phosphodiesterase inhibitors in patients with coronary heart disease. A comparison between enoximone and R80122]. 765 92

Selective beta 2-agonist aerosols may produce significant cardiovascular effects. In the present study we used Holter monitoring to compare the arrhythmogenic effects of inhaled terbutaline (TE), a beta 2-agonist, with that of ipratropium bromide (IB), a nonabsorbable cholinergic drug. Fourteen patients with concomitant obstructive lung disease, ischemic heart disease, and complaints of postinhalation palpitations were studied in a random, double-blind, cross-over fashion. Both drugs significantly improved vital capacity and FEV1. Heart rate and the frequency of premature beats were not significantly affected by the bronchodilators. We conclude that no clear connection between inhaled bronchodilators and arrhythmias could be demonstrated.
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PMID:Cardiac arrhythmias after inhaled bronchodilators in patients with COPD and ischemic heart disease. 840 68

The reaction of the methyl ester of (R)-norcarnitine with 1-bromo-2-heptadecanone produces (+)-6-[(methoxycarbonyl)methyl]-2-pentadecyl-4,4-dimethylmorpholinium bromide, 3, which hydrolyzes to (+)-6-(carboxylatomethyl)-2-pentadecyl-4,4-dimethylmorpholinium (hemipalmitoylcarnitinium, HPC) upon treatment with aqueous sodium hydroxide. Single-crystal X-ray analyses have confirmed the structures of (+)-HPC and 3. (+)-HPC inhibits carnitine palmitoyltransferase (CPT-I) activity for the forward reaction (palmitoyl-CoA + carnitine-->) in intact mitochondria from rat heart and rat liver. (+)-HPC competitively (versus carnitine) inhibits CPT-I activity in both rat heart and liver mitochondria with Ki = 2.8 +/- 0.5 and 4.2 +/- 0.7 microM, respectively. As one of the strongest specific inhibitors of CPT-I, HPC is a potential therapeutic agent in myocardial ischemia and Type II diabetes.
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PMID:(+)-Hemipalmitoylcarnitinium strongly inhibits carnitine palmitoyltransferase-I in intact mitochondria. 842 95

Mental stress may induce myocardial ischemia and ventricular arrhythmia in patients with coronary artery disease, and cholinergic stimulation is a potential protective mechanism. The purpose of this study was to determine the effect of pyridostigmine bromide (PYR), a reversible cholinesterase inhibitor, on the cardiac responses to a mental stress challenge. Twelve healthy young volunteers were submitted to a mental stress test (arithmetic test) 2 hours after the oral administration of either placebo or PYR (45 mg) on two separate days, following a randomized crossover double-blind protocol. Heart rate was reduced after both placebo and PYR (p < 0.05), but the cardiac responses to the mental stress were lower with PYR (p < 0.05): mean RR interval (mean +/- SE)-placebo: 730 +/- 19 msec; PYR: 769 +/- 21 msec; Peak systolic pressure-placebo: 129 +/- 4 mmHg; PYR: 124 +/- 3 mmHg; Peak diastolic pressure-placebo: 92 +/- 3 mmHg; PYR: 89 +/- 4 mmHg; Mean rate-pressure product-placebo: 10,496 +/- 412 bpm x mmHg; PYR: 9,746 +/- 383 bpm x mmHg. In conclusion, 45 mg of pyridostigmine blunted the pressor and chronotropic responses to mental stress in healthy young subjects.
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PMID:Cholinergic stimulation with pyridostigmine blunts the cardiac responses to mental stress. 1021 43

The purpose of the present work was to verify the effect of pyridostigmine bromide, a reversible cholinesterase inhibitor, on the increases in cardiac work and myocardial oxygen demand produced by central sympathetic stimulation in pentobarbital-anesthetized Wistar rats. The pharmacological stimulation of the central nervous system with L-glutamate (1 mg/kg, intracerebroventricular) elicited marked increases in arterial pressure, dP/dt(max), rate-pressure product, and triple product, reproducing the cardiovascular alterations observed during physical effort and stressful situations. The oral administration of pyridostigmine bromide (5, 10 and 20 mg/kg) 2 hours before central stimulation blunted the increases in mean arterial pressure, dP/dt(max), and triple product elicited by glutamate (29, 28 and 57% for 5 mg/kg; 26, 23 and 46% for 10 mg/kg and 19, 17 and 37% for 20 mg/kg, respectively) when compared to the control group (41, 49 and 106%, respectively; p < 0.05). Our results also showed that the activity of plasmatic cholinesterase was effectively inhibited by pyridostigmine bromide. In conclusion, the increases in endogenous acetylcholine induced by cholinesterase inhibition blunted the centrally-evoked increases in myocardial oxygen demand in anesthetized rats. This effect could represent a cardioprotective action in a situation of ischemic heart disease.
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PMID:Pyridostigmine blunts the increases in myocardial oxygen demand elicited by the stimulation of the central nervous system in anesthetized rats. 1022 12

We investigated the function of estrogen receptor-alpha in global myocardial ischemia and reperfusion injury in male estrogen receptor-alpha knockout (ERKO) and wild-type mice. Mouse hearts were subjected to 45 min of global ischemia followed by 180 min of reperfusion. The hearts were excised, cannulated, and maintained in a chilled (4 degrees C) cardioplegia solution until warm (37 degrees C) oxygenated Krebs-Henseleit bicarbonate buffer was perfused through the coronary arteries. ERKO hearts started beating later and had a higher incidence of ventricular fibrillation and/or tachycardia than control hearts. Coronary flow rate was significantly lower in ERKO hearts during the 90- and 120-min periods of reperfusion. Ca(2+) accumulation was significantly greater following 30, 90, 120, 150, and 180 min of reperfusion in ERKO hearts. Nitrite production was significantly less in ERKO hearts following 90, 120, and 150 min of reperfusion. Myocardial reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was significantly lower in experimental ERKO hearts. Marked interstitial edema and contraction bands were seen in hematoxylin-eosin-stained sections of ischemia-reperfused ERKO hearts but not in control tissues. Hematoxylin-basic fuchsin-picric acid-stained sections from experimental ERKO hearts had fewer viable myocytes compared with controls. Transmission electron microscopy revealed swollen and fragmented mitochondria with amorphous and granular bodies, loss of matrix, and rupture of cristae in experimental ERKO hearts. This is the first demonstration that estrogen receptor-alpha plays a cardioprotective role in ischemia-reperfusion injury in males.
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PMID:Myocardial ischemia-reperfusion injury in estrogen receptor-alpha knockout and wild-type mice. 1077 44


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