Gene/Protein Disease Symptom Drug Enzyme Compound
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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of catecholamines, beta-thromboglobulin (BTG) and arginine vasopressin (AVP), and degree of pain were examined in 22 patients with suspected uncomplicated myocardial infarction within 24 h following onset of chest pain. Sixteen patients developed infarction with peak creatine phosphokinase at 1280 Ul-1 (range 293-3770 Ul-1). Fifteen healthy men served as controls (C). Arterial adrenaline levels were significantly higher in patients with pain (1.15 +/- 0.23 nmol l-1, n = 8, mean value +/- SEM) than in those without pain (0.60 +/- 0.10 nmol l-1, n = 14, P less than 0.05). Plasma catecholamines were moderately but significantly elevated in myocardial infarction; the concentration of arterial adrenaline was 0.83 +/- 0.14 nmol l-1 and that of arterial noradrenaline was 2.70 +/- 0.28 nmol l-1 compared with 0.44 +/- 0.04 nmol l-1 (P less than 0.025) and 1.47 +/- 0.05 nmol l-1 (P less than 0.0005), respectively, in C. One week later, plasma catecholamines had returned to baseline levels. Plasma BTG showed borderline elevation (1.0 +/- 0.1 pmol l-1) compared with C (0.6 +/- 0.1 pmol l-1, P = 0.04), and remained unchanged 1 week later. Plasma AVP was at baseline level. Uncomplicated myocardial infarction, regardless of size, was associated with only moderately increased sympathetic tone. Plasma adrenaline was related more to the degree of pain than to the presence of acute myocardial infarction. Arterial adrenaline may be a sensitive marker of sympatho-adrenal activity related to pain.
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PMID:Increased arterial adrenaline is related to pain in uncomplicated myocardial infarction. 214 43

We wanted to examine how adenosine stimulates ventilation in man. Bolus doses of adenosine were given i.v. in an antebrachial vein in multiples of 2.65 mg. The minute ventilation was increased by adenosine 5.3 to 15.9 mg (median values) from control 12.6 +/- 1.9 l min-1 to 42.5 +/- 4.7 l min-1 in a dose-dependent manner. The adenosine receptor antagonist theophylline, 58.3 +/- 3.3 (mean +/- SEM) mumol l-1 plasma, inhibited the response by approximately 25%. Dipyridamole 10 mg, an adenosine uptake blocker, enhanced the effect of adenosine by approximately 60%. The ventilation was not affected by metoprolol, atropine, naloxone or cromolyn sodium but was attenuated by hyperventilation. The respiratory stimulation started before chest pain and cardiovascular effects such as AV-block were encountered. It is concluded that this respiratory stimulation shows characteristics of adenosine receptor mediated responses but the location of such adenosine receptors is uncertain. The findings are compatible with a stimulatory or facilitating effect of adenosine on afferent pathways.
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PMID:Adenosine receptor mediated stimulation of ventilation in man. 249 64

From January 1983-December 1986 a total of 880 patients were received by the 'Flying Squad Team' from Rawalpindi and Islamabad. The average delay between the onset of chest pain and medical aid was considerably less in those patients evacuated by 'Flying Squad' compared to those who came on their own (3.2 + 1.2 SEM hours vs 6.5 + 2.0 SEM hours). Eighteen cases developed cardiac arrest outside hospital of which 14 (77.8%) were successfully resuscitated. Eleven (61.1%) left the hospital alive. Pre-hospital coronary care is an important adjunct to the hospital coronary care which significantly reduces mortality.
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PMID:Pre-hospital coronary care--an important extension of hospital coronary care. 250 57

Plasma concentrations of immunoreactive atrial natriuretic peptide (mean (SEM] were measured in 135 patients admitted to two coronary care units with myocardial infarction, ischaemic chest pain, or non-ischaemic chest pain. Concentrations were significantly higher in patients with acute myocardial infarction not treated with systemic thrombolysis (60.4 (14.3) pg/ml) than in patients with non-ischaemic chest pain (21.1 (4.3) pg/ml). Patients with ischaemic chest pain had intermediate values (39.3 (7.1) pg/ml). Patients with acute myocardial infarction treated with intravenous streptokinase had normal concentrations of plasma atrial natriuretic peptide (20.2 (3.6) pg/mg), which were significantly lower than those in patients with myocardial infarction not given streptokinase. These changes could not be explained by factors such as age, pre-existing hypertension, renal dysfunction, or cardiac failure, nor treatment other than streptokinase. Raised plasma concentrations of atrial natriuretic peptide in acute myocardial infarction may be a homoeostatic response acting to reduce atrial pressures by natriuresis, diuresis, and venodilatation. The lower concentrations of atrial natriuretic peptide in patients with acute myocardial infarction treated with streptokinase may reflect a short term beneficial haemodynamic effect of streptokinase.
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PMID:Plasma atrial natriuretic peptide in patients with acute myocardial infarction: effects of streptokinase. 252 82

In a double blind placebo controlled trial, 434 patients with suspected myocardial infarction were randomised to treatment with nifedipine (n = 217) or placebo (n = 217) within six hours from the onset of chest pain. During the treatment period of 48 hours, a 10 mg capsule containing nifedipine or placebo was given sublingually every four hours for 24 hours, then orally every four hours for the next 24 hours. Acute myocardial infarction was confirmed in 295 patients (146 in the nifedipine group and 149 in the placebo group). The median delay time to intervention with nifedipine in patients with acute myocardial infarction was 111 minutes. Infarct size was assessed by the estimation of release of creatine kinase isoenzyme MB and creatine kinase from blood samples taken every four hours for 48 hours. The total mean (SEM) creatine kinase MB released was 406.4 (27.2) IU/l in the nifedipine group and 345.7 (20.5) IU/l in the placebo group. Total mean (SEM) creatine kinase released was 2749.6 (165.1) IU/l in the nifedipine group and 2698.4 (145.9) IU/l in the placebo group. In hospital mortality was similar for both the nifedipine and placebo groups (6.6% and 5.8% respectively). Treatment with nifedipine in the early phase of acute myocardial infarction seems to have no effect on enzymatically measured infarct size.
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PMID:Effect of nifedipine on enzymatically estimated infarct size in the early phase of acute myocardial infarction. 328 77

The effects of early spontaneous coronary patency on the evolution of myocardial infarction were evaluated in 41 patients. They had coronary arteriography (mean (SEM)) 3.1 (0.2) hours after the onset of chest pain with repeat studies 90 minutes and three days later. In 12 (29%) patients the infarct related coronary artery was patent at the first arteriogram (group 1). A further 10 patients, nine of whom received thrombolytic treatment, showed early recanalisation of the infarct related coronary artery within 90 minutes of treatment (group 2). In the remainder the infarct related coronary artery was persistently occluded (group 3). Baseline values for infarct location, the sum of ST elevation in all leads, QRS scores, and serum creatine kinase activity did not permit discrimination between the groups. Nevertheless, patterns of ST segment change and enzyme release in group 1 were closely similar to those that occurred in response to thrombolysis in group 2. Thus compared with group 3, groups 1 and 2 showed earlier 50% reduction in the sum of peak ST elevation in all leads and earlier peaking of serum creatine kinase activity. Importantly, creatine kinase release was significantly attenuated in group 1, rising to a peak serum activity (mean (SEM)) of only 1242 (415) IU/1. Analysis of angiographic left ventricular ejection fractions at three days indicated limitation of infarct size in groups 1 and 2 compared with group 3. Mean (SEM) ejection fraction, however, was best preserved in group 1 (62(6)%) and in this group the frequency of non-Q wave infarction was higher than in groups 2 and 3. Thus in patients who present with a patent infarct related coronary artery early during infarction: (a) there is a reduction in the pattern of infarct size as reflected by attenuation of release of creatine kinase, preservation of left ventricular ejection fraction, and a relatively high frequency of non-Q wave infarction; (b) patterns of ST segment change and creatine kinase release resemble those that occur after successful thrombolytic treatment, suggesting that early coronary patency is the result of spontaneous recanalisation of a previously occluded artery.
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PMID:The effects of early coronary patency on the evolution of myocardial infarction: a prospective arteriographic study. 331 51

To determine whether endogenous opioids play a role in modulating the appreciation of chest pain in angina pectoris, the specific opioid antagonist, Naloxone, was used. The hypothesis was that the appearance time of ischemic myocardial pain should decrease after Naloxone if centrally mediated pain perception is significantly influenced by the endorphin system in angina pectoris. A randomized double blind clinical trial was conducted in 5 men with effort-induced angina pectoris associated with ST segment changes. Three multi-stage exercise tests, using the Bruce protocol were performed on the same day and time, on three successive weeks. Chest pain was reported 4.3 +/- 0.3 (SEM) minutes after starting exercise on the first or baseline test. On subsequent tests patients received either Naloxone 2 mg IV or a similar volume of saline placebo. Angina pectoris occurred significantly (p. less than 0.05) earlier (1.6 +/- 0.2 minutes) after Naloxone compared to placebo. There were no significant differences in myocardial ischemia indicated by ST segment changes and no significant differences in resting or exercise blood pressure and heart rate between Naloxone and placebo. Thus, these data focus attention on a neglected area of myocardial ischemic pain and suggest that endogenous opioids play a significant role in the recognition of the pain of effort-related angina pectoris.
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PMID:Effect of naloxone on exercise-induced angina pectoris: a randomized double blind crossover trial. 351 46

Placebo-controlled trials are not available to assess the efficacy of smooth muscle relaxants in the treatment of painful esophageal motility disorders. Therefore, we compared the effects of oral nifedipine (10-30 mg t.i.d.) and placebo in 20 patients (mean age 50 yr) with chronic noncardiac chest pain and the nutcracker esophagus in a 14-week double-blind crossover study. Compared to placebo, nifedipine significantly decreased distal esophageal contraction amplitude (mean +/- SEM, 198 +/- 11 mmHg to 123 +/- 9 mmHg; p less than 0.005), as well as duration and lower esophageal sphincter pressure. Nifedipine, however, was no better than placebo in the relief of daily chest pain frequency, severity, or index (frequency X severity) as assessed by patient diaries. Despite these disappointing results, long-term follow-up (mean, 16.6 mo) suggests these patients do improve. Mean daily chest pain index significantly (p less than 0.005) decreased from 10.3 +/- 2.0 at the beginning of the study to 3.2 +/- 0.8 at follow-up. Prescription drug use and physician visits for chest pain also significantly decreased. Distal esophageal contraction pressures significantly fell during the long-term follow-up but there was poor correlation with chest pain improvement. This study suggests that identification of the esophagus as the cause of chest pain coupled with supportive intervention may be more effective than drug therapy in improving these patients' chest pain.
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PMID:Oral nifedipine in the treatment of noncardiac chest pain in patients with the nutcracker esophagus. 358 8

In this single centre prospective, double blind study, 98 patients with suspected acute myocardial infarction (AMI) were randomized, within six hours, to nifedipine 10 mg (46 patients) or placebo (52 patients) both administered sublingually. The delay time from onset of chest pain to treatment was 3.33 +/- 0.2 hours (mean +/- SEM) and 3.28 +/- 0.18 hours for the nifedipine and placebo treated groups, respectively. Treatment was continued orally for 3 days. AMI was confirmed in 28 patients given nifedipine and 23 patients given placebo. Infarct sizing by CK-MB isoenzyme release was possible, for technical reasons, in only 23 patients on nifedipine and 17 patients on placebo. CK-MB isoenzyme release was 710 +/- 104 IU l-1 and 655 +/- 118 IU l-1 for the nifedipine and placebo treated groups respectively (P greater than 0.05). In the acute coronary insufficiency (ACI) group--18 patients given nifedipine and 29 patients given placebo--there was no significant difference in duration of admission, urgent cardiac readmission or progression to AMI within one month. Study withdrawal occurred in 15.3%--8 nifedipine and 7 placebo. Overall, one month mortality was 10.2% with 5 deaths in both the nifedipine and placebo treated groups. Early treatment with nifedipine did not reduce enzymatically determined infarct size or one month mortality in patients with AMI, or reduce one month morbidity or mortality in patients with ACI.
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PMID:Effect of early treatment with nifedipine in suspected acute myocardial infarction. 379 47

To investigate the effect of theophylline on cardiac electrophysiology, electrophysiologic testing was performed before and during aminophylline (theophylline ethylenediamine) infusions in 10 male patients with stable COPD. This produced a mean plasma theophylline concentration of 15.6 +/- 0.9 micrograms/ml (mean +/- SEM) and increases in plasma catecholamine concentrations consistent with activation of the sympathetic nervous system. Plasma epinephrine increased from 40 +/- 6 to 57 +/- 9 pg/ml (p less than 0.05), and plasma norepinephrine increased from 406 +/- 63 to 522 +/- 90 pg/ml (p less than 0.01) during the aminophylline infusion. Significant reductions were seen in the atrioventricular (81.4 +/- 6.8 to 73.0 +/- 5.6 ms, p less than 0.05) and His-Purkinje (40.7 +/- 4.3 to 36.1 +/- 3.8 ms, p less than 0.02) conduction intervals, sinoatrial conduction time (81.3 +/- 10.3 to 65.0 +/- 7.6 ms, p less than 0.05), corrected sinus node recovery time (199.0 +/- 13.4 to 148.2 +/- 22.9 ms, p less than 0.05), shortest atrial pacing interval producing 1:1 atrioventricular conduction (391.0 +/- 25.5 to 325.0 +/- 15.5 ms, p less than 0.001), and atrial effective refractory period (ERP) (224.0 +/- 7.0 to 201.0 +/- 7.2 ms, p less than 0.01), but there was no change in the intraatrial (PA) conduction interval or ventricular ERP. Although no arrhythmias were induced, 5 patients had symptoms (3 presyncope and 2 chest pain) with rapid atrial pacing during but not prior to the aminophylline infusion. These changes could be caused by direct action of theophylline on cardiac conduction tissue or they may be caused at least in part by the associated increase in sympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Theophylline-induced alterations in cardiac electrophysiology in patients with chronic obstructive pulmonary disease. 381 92


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