Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial lactate metabolism was studied in 20 patients with coronary heart disease during and immediately after slight angina pectoris induced by atrial pacing. Myocardial lactate extraction ratio (MLE) decreased from 0.27 +/- 0.03 (SEM) before angina to 0.01 +/- 0.06 during angina, and further to -0.32 +/- 0.11 at 15 sec after pacing. Lactate production was found to occur in eight patients during pacing and 13 patients after pacing. Cardiac venous flow was measured by thermodilution in eight of these patients. 'Net ischaemic lactate efflux' increased by 23 +/- 4 mumol/min 15 sec after pacing, whereas 'lactate uptake in non-ischaemic regions' diminished by 11 +/- 2 mumol/min. Lactate production 15 min after pacing was revealed in all patients with subtotal stenosis of the left anterior descending coronary artery (LAD), whereas it was less frequently observed in patients with occluded LAD and collaterals to the post-stenotic area. Increased washout of metabolites from the ischaemic myocardium during the early recovery period is the main reason for the rather high sensitivity of ischaemia detection by this procedure. This permits shorter pacing periods and less pain than in earlier studies. Both MLE and electrocardiographic changes were equally reproducible after 20 and 45 min recovery period.
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PMID:Myocardial lactate metabolism during pacing induced angina pectoris. 662 63

To study the effects of acute myocardial infarction on its pharmacokinetics a single oral dose of 400 mg mexiletine HCl was administered to seven patients. The study was performed within 24 h of the onset of pain (Study I) and was repeated 10-14 days later, during the recovery phase (Study II). Mexiletine in plasma and urine was quantified by a GLC method. The peak plasma concentrations of mexiletine were 0.65 +/- 0.05 (SEM) microgram ml and 1.08 +/- 0.11 micrograms/ml (p less than 0.05) in Studies I and II, respectively. The corresponding peak times were 4.68 +/- 2.04 h and 1.46 +/- 0.17 h (N.S.). The lag time averaged 0.48 +/- 0.08 h in Study I and 0.39 +/- 0.05 h in Study II (N.S.). The area under the plasma concentration-time curve remained unchanged. The elimination half-life was 15.03 +/- 0.61 h and 11.75 +/- 0.80 h (p less than 0.01) in Studies I and II, respectively. The recovery of unchanged mexiletine in urine and its renal clearance was also the same in both studies. The plasma protein binding of mexiletine was similar in Studies I and II (61 +/- 2% and 63 +/- 3%; N.S.). Thus, the rate of gastrointestinal absorption of mexiletine was definitely slowed in the acute phase of myocardial infarction, whereas the extent of absorption was not altered. The prolongation of the elimination half-life of mexiletine in the acute phase of myocardial infarction is probably related to an increase in its volume of distribution.
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PMID:Pharmacokinetics of oral mexiletine in patients with acute myocardial infarction. 666 76

The effects on severe arterial ischaemia of infusions of Prostaglandin E1 (PGE1) a vasodilator and inhibitor of platelet aggregation, were studied in 49 patients (aged 17-80). Criteria for patient selection included rest pain and/or digital ulceration and gangrene secondary to predominantly small vessel disease. PGE1 was infused at a low (6 ng/kg/min), intermediate (10 ng/kg/min) or high (14 ng/kg/min) dose rate via a central venous cannula on 52 occasions without serious side effects. Doppler studies, pulse volume recordings and infra red radiometry were used to quantify the clinical effects. Improvements in digital perfusion were demonstrated by increased pulse volume amplitude (7.1 +/- 1.1 to 21.6 +/- 2.7 mm mean +/- SEM) which remained significantly raised at 6 weeks (14.2 +/- 2.9 mm; P = less than 0.001 paired t test). Infra red digital temperatures were also significantly raised 6 weeks post infusion (27.2 +/- 0.6 degrees C to 29.5 +/- 0.6 degrees C; P less than 0.001). The majority of patients reported improvement in pain, and two thirds of 12 superficial ulcers healed in 6 weeks. These results show that PGE1, improves digital perfusion for several weeks in patients with severe arterial ischaemia.
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PMID:Prostaglandin E1 infusion for small vessel arterial ischaemia. 668 32

M-mode echocardiograms were recorded in 12 patients with Prinzmetal's angina during 29 episodes of transient myocardial ischemia at rest (18 spontaneous and 11 ergonovine-induced). At peak ST segment elevation a regional mechanical impairment was observed in the interventricular septum during 23 episodes of angina and in the posterior wall during six episodes. In the 18 spontaneous episodes the left ventricular ischemic wall, when compared to the basal state, was found to have a significant reduction in motion (-76.3 +/- 9.1%) (mean +/- SEM), in diastolic thickness (-11.7 +/- 2.5%), and in percent systolic thickening (-88.0 +/- 5.6%). Increase in left ventricular end-diastolic diameter (+13.1 +/- 2.1%) and decrease in percent fractional shortening (-38.1 +/- 3.7%) were also observed. When ST segment was back to the isoelectric line, a transient overshoot in regional left ventricular function was observed. In induced episodes statistically significant changes could be detected by M-mode echocardiography even before appearance of ST segment elevation and anginal pain. No significant difference was found in type or degree of mechanical impairment between induced and spontaneous episodes. Therefore, in patients with Prinzmetal's angina: (1) M-mode echocardiography allows detection of mechanical changes due to transient myocardial ischemia; and (2) mechanical impairment occurs earlier than clinical (pain) and electrocardiographic (ST segment elevation) signs of transmural ischemia.
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PMID:Transient changes in left ventricular mechanics during attacks of Prinzmetal's angina: an M-mode echocardiographic study. 669 89

A group of 73 patients suffering from painful alcoholic, chronic pancreatitis, hospitalized from 1971 to 1981, has been analyzed retrospectively. The aim was to assess the effects of alcohol withdrawal and pancreatic surgery on the course of pancreatic pain. The mean number of years during which the patients complained of pain was 3.5 +/- 0.5 (m +/- SEM). At the end of follow-up, 70 p. 100 of the patients did no longer suffer, alcohol withdrawal was obtained in 45 p. 100 and surgery had been performed in 41 p. 100. Continued alcohol abuse did not prevent pain relief: 60 p. 100 of patients continuing to drink at the end of follow-up, did not suffer any longer. One year after pancreatic surgery, pain relief was more frequent, if alcohol abstinence had been obtained before surgery (p less than 0.01). Among the 53 patients followed up to 5 years after the start of pain: a) the cumulative actuarial probability of disappearance of pain was 17 p. 100 at 2 years, 52 p. 100 at 5 years, 62 p. 100 at 8 years after the start of pain. Alcohol abstinence and surgery were observed during the first five years of pain; b) the mean number of years of pain was lower among the patients who became abstinent early (less than 4 years after the beginning of pain) than among those who did not (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic alcoholic pancreatitis: relation of pain to withdrawal and pancreatic surgery]. 673 54

We measured lung volumes, forced expirograms, and arterial blood gases in 2 groups of elective pediatric surgical patients (mean age, 11.4 +/- SD 2.8; n = 11, 12 operations) the day prior to surgery (control) and between the first and eighth postoperative days. The patients were Group I: peripheral surgery (n = 6) and Group II: reconstructive surgery for scoliosis (n = 5). The preoperative lung volumes and forced expiratory volume in one second were within the predicted normal range in both groups, except for a reduction in total lung capacity (TLC) and vital capacity (VC) in Group II. The postoperative lung volumes in Group I were not significantly different from the preoperative volumes. In group II, on postoperative Days 2 and 3, the lung volumes as a percent of preoperative volumes (mean +/- SEM) were VC, 44 +/- 11; functional residual capacity (FRC), 81 +/- 6; residual volume, 124 +/- 10; TLC, 61 +/- 10. Although the mean FRC returned to the preoperative volume by postoperative Days 5 and 6, the VC and its components remained reduced on postoperative Days 5, 6, and 8. We conclude that postoperative lung volume abnormalities are related to the site and magnitude of surgery and associated phenomena, such as pain, and preoperative respiratory function abnormalities.
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PMID:Postoperative pulmonary function in children. Comparison of scoliosis with peripheral surgery. 674 10

In a double-blind prospective trial 26 consecutive patients with proved ureteric colic were allocated at random to receive 100 mg pethidine or 0.3 mg buprenorphine by intramuscular injection. Pain relief was assessed by standard linear analogue and ordered categories scales. The mean pain relief on the linear analogue scale was 3.80 +/- SEM 0.64 in patients receiving pethidine and 6.86 +/- 0.40 in those receiving buprenorphine (p less than 0.001). The corresponding values for mean pain relief in the ordered categories scale was 1.78 +/- 0.26 v 2.76 +/- 0.20 (p less than 0.01). These observations suggest that buprenorphine is superior to pethidine as analgesia in ureteric colic.
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PMID:Prospective double-blind comparison of buprenorphine and pethidine in ureteric colic. 680 15

The muscle blood flow (MBF) in m. trapezius was studied in 7 subjects with fibromyotic pain syndrome before and during treatment with ultrasound (1 Watt/cm2) and during placebo treatment, using the local 133Xe-washout technique. MBF in the fibromyotic muscles was significantly reduced during ultrasound treatment (p less than 0.05) compared to the blood flow before the treatment and during placebo treatment 1.57 +/- SEM 0.52 and 2.51 +/- SEM 0.43 ml/100 g/min, respectively. In 6 normal trapezius muscles the mean MBF was 2.30 +/- SEM 0.44 ml/100 g/min before ultrasound treatment and 2.31 +/- SEM 0.41 ml/100 g/min during ultrasound therapy. MBF decreased in a lidocaine blocked fibromyotic muscle during ultrasound treatment while no effect on MBF was detectable during ultrasonic treatment a normal lidocaine pretreated muscle. It is concluded that ultrasound treatment decreases MBF in fibromyotic muscles and that this is paradoxical effect of ultrasound might be due to a direct effect on the vessels or a local release of vasoactive substances in the fibromyotic muscles.
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PMID:Reduced blood flow in fibromyotic muscles during ultrasound therapy. 682 29

Twenty patients undergoing thoracotomy were given 2, 4, or 6 mg morphine epidurally in a double-blind, randomized study for postoperative analgesia. Administration at T12-L1 or L1-L2 resulted in a dose-related analgetic duration (514 +/- 118 min, 778 +/- 207 min, and 938 +/- 155 min; means +/- SEM, respectively, for the groups). For the three groups, peak plasma morphine concentrations (range 19-34 ng/ml) were reached within 15 min. The plasma curves had a similar appearance as after an intramuscular injection and pharmacokinetic calculations showed an elimination half-life (mean +/- SEM) of 173 +/- 24 min, 200 +/- 60 min, and 213 +/- 57 min for the groups, respectively. The morphine concentrations in the CSF were considerably higher compared with plasma (45-100 times the plasma concentration at 1 h, 100-250 times at 3 h, and 125-175 times at 5 h) but the elimination half-life of morphine in the cerebrospinal fluid (CSF) was similar to that in plasma. The lumbar approach was used with similar efficacy as reported for thoracic administration. Side effects were few and nonsignificant. The authors conclude that epidural morphine administration results in a dose-dependent analgesia, as well as concentrations in the CSF that are considerably higher than in plasma. With similar elimination half-lives for morphine in CSF and plasma, the long analgetic duration probably depends on the locally high morphine concentrations achieved. For safety purposes, one may use the lumbar approach to the epidural space even for thoracic pain without reducing the efficacy.
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PMID:Pharmacokinetic aspects of epidural morphine analgesia. 685 84

Although coronary artery disease and gastroesophageal reflux disease are common conditions which, therefore, may coexist, it is unknown whether or not the presence of one affects the other. We performed esophageal acid perfusion tests, with concurrent blood pressure, heart rate, and 12-lead electrocardiographic monitoring, in 37 patients, 25 with angiographically documented coronary disease and 12 with normal coronary arteries. Rate-pressure product, an index of myocardial work load, was calculated. In patients with coronary disease who developed chest pain during acid perfusion, rate-pressure product increased from 10.0 +/- 1.0 x 10(3) (mean +/- SEM) basally to 15.2 +/- 1.5 x 10(3) (p less than 0.001), and 3 of 9 patients showed concomitant electrocardiogram evidence of myocardial ischemia. In addition, in coronary disease, 64% of patients with infrequent or absent reflux symptoms by history had positive acid perfusion tests, and 56% of patients with coronary disease who developed pain during esophageal acid perfusion could not distinguish that pain from their usual angina. We conclude that in coronary disease, acid perfusion (and, presumably, gastroesophageal reflux) resulting in chest pain causes rate-pressure product elevation and can induce myocardial ischemia. The presence of esophageal acid sensitivity is not accurately predicted by clinical history in coronary disease, and pain of esophageal origin is often confused with angina.
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PMID:Esophageal acid perfusion in coronary artery disease. Induction of myocardial ischemia. 686 55


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