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Biomedical subjects

E Thaulow

Publications and source records attributed to E Thaulow.

At least 109 records · Page 6Linked to original sources
PubMed1986

Heat stroke in endurance exercise.

Six athletes were examined immediately after collapsing from heat stroke during exercise, and then followed for several weeks. At the time of collapse most of the patients were sweating profusely, their rectal temperatures being more than 42 degrees C. All recovered within a few hours. The renal function was not disturbed more than expected during heavy exercise, serum levels of liver enzymes were, however, increased for several weeks. Electrolyte homeostasis was undisturbed but for a transient hypercalcemia that can not be fully explained. The marked increments in plasma levels of catecholamines, vasopressin and renin were as expected after heavy exercise. We conclude that as heat stroke presents as a continuum of clinical pictures, biochemical evidence of liver cell injury is a sensitive and important parameter for the diagnosis.

Adolescent↗
PubMed1984

Effects of a selective thromboxane synthetase inhibitor, dazoxiben, and of acetylsalicylic acid on myocardial ischemia in patients with coronary artery disease.

Thromboxane A2 (TxA2) may aggravate myocardial ischemia by inducing vasoconstriction and platelet aggregation in small coronary vessels, whereas prostacyclin (PGI2) counteracts these effects. Acetylsalicylic acid (ASA) inhibits the formation of TxA2 as well as PGI2, whereas dazoxiben, a thromboxane synthetase inhibitor, reduces TxA2 formation selectively. In 25 patients with coronary artery disease, 2 identical atrial pacing stress tests were performed: before and after the administration of dazoxiben (200 mg) in 15 patients and before and after ASA (250 mg) in 10. The ischemic response, quantified by coronary sinus and aortic lactate levels and by ST depression, was significantly reduced after administration of dazoxiben (p less than 0.02) but not after ASA. Heart rate at rest, myocardial extraction of free fatty acids and the arteriovenous oxygen difference was unaffected by medication. Both drugs reduced TxB2 levels to the same extent, whereas collagen-induced aggregation was more reduced after ASA than after dazoxiben. The effect of dazoxiben on ischemia was probably a result of inhibited TxA2 and preserved PGI2 production, which increased blood flow to ischemic regions.

Aspirin↗
PubMed1984

Platelet function in blood sampled through heart catheters.

Platelet function was studied in blood sampled from the caval vein of 56 patients through various heart catheters. Reduced platelet retention was the most consistent finding while aggregation was not influenced by the sampling procedure. Polyurethane (Cordis and Positrol) catheters affected platelets less than catheters of woven dacron (Sones and Zucker). Sones catheters increased plasma beta-thromboglobulin levels slightly, and some platelets were trapped in the Zucker catheters. Much the same reduction in retention was induced by heparinized as by other catheters. Platelet retention values had a poorer reproducibility than the other platelet function parameters in samples collected at intervals of 45 min, while an acceptable correlation existed between parallel samples. The influence on platelets of blood sampled via polyurethane catheters was very moderate, and should allow the detection of alterations in platelet functions that occur in the circulation.

Blood Platelets↗
PubMed1984

Effects of timolol on platelets in coronary sinus blood and on myocardial ischemia during pacing-induced angina.

The effect of timolol on blood platelet function was studied in coronary sinus and caval vein blood at rest and during pacing-induced angina in 20 patients with coronary heart disease. During pacing-induced angina, lactate measurements confirmed that coronary sinus blood was sampled from ischemic regions in 13 men. The ischemia did not influence platelet function. In blood from non-ischemic myocardium, platelet activation was found during pacing: the ADP-induced aggregation, platelet retention and plasma beta-thromboglobulin levels increased moderately but significantly. Timolol administration prevented this platelet activation, possibly by inhibiting catecholamine release from the myocardium, and reduced the ischemic response during pacing as judged from lactate measurements and ST depressions. It is concluded that timolol reduced platelet activation induced in non-ischemic regions of the heart during tachycardia stress as well as myocardial ischemia.

Adult↗
PubMed1983

Platelet function in blood from the coronary sinus in patients with arteriosclerotic heart disease.

Blood sampled from the coronary sinus was compared with blood collected simultaneously from the superior caval vein in 50 men with angiographically proven coronary heart disease. Primary, ADP-induced aggregation in coronary sinus blood was reduced by 14 per cent, collagen-induced aggregation by 10 and platelet retention by 16 to 30 per cent as compared with blood from the caval vein. The plasma levels of beta-thromboglobulin, platelet counts and number of circulating platelet aggregates were similar in parallel samples. The reduced platelet function in coronary sinus blood hardly reflects refractoriness after previous platelet stimulation, since no release or irreversible aggregation was induced. A reduced function might be the effect of direct depression induced in the coronary circulation. Most surprisingly, a selective thromboxane synthetase inhibitor (Dazoxiben) and acetylsalicylic acid normalized platelet aggregation but did not affect the low platelet retention response in coronary sinus blood. Thus, the reduced platelet function in coronary sinus blood is not only mediated via prostaglandins.

Adenosine Diphosphate↗
PubMed1983

The effect of a thromboxane synthetase inhibitor, dazoxiben, and acetylsalicylic acid on platelet function and prostaglandin metabolism.

Twenty-four men received either placebo, 0.1 g of the thromboxane synthetase inhibitor dazoxiben, 0.25 or 1.0 g of acetylsalicylic acid (ASA). Dazoxiben reduced the maximal rate of collagen-induced platelet aggregation, but less than did ASA. ASA abolished secondary, ADP-induced aggregation, dazoxiben not. Both drugs prolonged the bleeding-time. Plasma thromboxane B2 (TxB2) levels did not change significantly after dazoxiben, whereas the prostacyclin metabolite 6-keto-PGF1 alpha rose. The larger dose of ASA reduced both TxB2 and 6-keto-PGF1 alpha in plasma. Whole blood was allowed to clot in order to estimate prostaglandin metabolism. Both drugs prevented thromboxane production effectively. Formation of 6-keto-PGF1 alpha decreased by 95 per cent after ASA but was more than doubled after dazoxiben. Dazoxiben is a selective and effective thromboxane synthetase inhibitor, but has a weaker effect on platelet reactivity than ASA, possibly because endoperoxide formation is not prevented.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Effects induced on blood platelets in ischemic and nonischemic myocardium.

The function of blood platelets sampled from the coronary sinus and the superior vena cava was studied in 50 men with coronary artery disease at rest and during pacing-induced angina. At rest, a lower platelet aggregation and retention response was found in coronary sinus compared with vena caval blood. This may be due to refractoriness after previous platelet stimulation or to release of platelet inhibitors in the coronary circulation. During pacing-induced angina, lactate levels indicated that blood was sampled from ischemic myocardium in only 27 of the patients. Pacing-induced angina influenced platelet function differently in blood from ischemic and nonischemic regions. Adenosine diphosphate- and collagen-induced aggregation, platelet retention and plasma beta-thromboglobulin levels remained unchanged in blood from ischemic myocardium during pacing, but increased in blood from nonischemic regions. Thus, factors other than ischemia activated platelets in the coronary circulation during tachycardia-induced stress.

Adenosine Diphosphate↗
PubMed1983

Myocardial lactate metabolism during pacing induced angina pectoris.

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.

Angina Pectoris↗
PubMed1982

PR interval in middle-aged men with overt and latent coronary heart disease compared to PR in angionegative and normal men of similar age.

PR was measured prospectively in 2014 apparently healthy men ranging in age from 40 to 59 years (P subjects), and retrospectively in 652 hospitalized men with a diagnosis of coronary heart disease (CHD) (R subjects). A cardiovascular survey examination suggested CHD in 115 of the 2014 P subjects, coronary angiography of 105 of these confirmed this suspicion in 69. The following observations concerning PR were made: (1) the shortest PR was found in angiopositive P subjects, intermediate PR in 1832 normal P subjects, and PR was longest in 36 angionegative subjects. (2) PR was shortest in angiopositive P subjects with triple-vessel disease, and longest in P subjects with single-vessel disease, (3) PR increased with age, and an inverse association was found between PR and resting heart rate in P-subjects. (4) In 98 of 1832 normal P subjects, all without signs or symptoms of heart disease, PR was greater than or equal to 0.22 s. (5) Prolonged PR was no more frequent among the 652 R subjects than among P subjects, despite significant CHD in 595, and a frequent use of drugs known to delay atrioventricular conduction. It is suggested that advanced stable clinical CHD only rarely gives rise to prolonged PR at rest, and that PR in subjects with latent CHD may have somewhat shorter PR than age counterparts without symptoms or signs of CHD. Conflicting data in the literature are probably related to differences in material and methods.

Adult↗
PubMed1982

Coronary artery disease with and without angina--two different entities?

Coronary heart disease (CHD), previously neither diagnosed nor suspected, was strongly suspected in 115 of 2014 men aged 40-59 years during a cardiovascular survey examination. Sixty-nine of 105 men who underwent diagnostic coronary angiography had pathologic angiograms. Twenty-six of these 69 had angina pectoris (AP) with and without pathologic exercise ECGs and 43 had pathologic exercise ECG as the only indicator of CHD. The extent of coronary artery changes was similar in the two groups. The men without AP were in almost all respects similar to 1832 men labelled as normals. The men with AP differed in several respects from their non-AP angiographic counterparts and from their non-AP angiographic counterparts and from the normals: they had more dyspepsia, a higher stress score, higher serum cholesterol and triglycerides, lower antithrombin III levels in the blood and lower blood platelet retention values. These results indicate that coronary artery disease with and without AP may represent somewhat different pathogenetic entities.

Adult↗
PubMed1982

Effects of red rest and prazosin in congestive heart failure.

Twelve patients with congestive heart failure were monitored with invasive and noninvasive techniques to evaluate the effect of vasodilator treatment. During the 18 hours of strict bed rest before administration of prazosin, the hemodynamics improved substantially while only small and transient heModynamic changes were observed after introduction of prazosin. At 6 weeks' control the effect of vasodilator treatment with prazosin, 3 mg x 4, was lost. The beneficial results often credited to vasodilators in studies on congestive heart failure might in part be due to the concomitant bed rest introduced during the monitoring of the patients.

Adult↗
PubMed1982

Comparison of beta-adrenoceptor blockers under maximal exercise (pindolol v metoprolol v atenolol).

1 The time-related, comparative beta-adrenoceptor blocking effect of metoprolol 150 mg twice daily, atenolol 100 mg once daily and pindolol 7.5 mg twice daily on heart rate, blood pressure, work performance, blood lactate, free fatty acids and plasma catecholamines was studied in ten males aged 19--25 years by means of repeated maximal bicycle exercise tests. 2 At steady state several differences in effects were noted among the drugs. These could be explained by differences in beta 1-selectivity, potency of the chosen drug-doses and intrinsic sympathomimetic activity (ISA). 3 This study emphasizes the importance of including strong sympathetic stimuli in any model used for comparing beta-adrenoceptor blockers with and without ISA in order not to underrate the effects of beta-adrenoceptor blockers with ISA. 4 In the chosen doses pindolol was more effective, and atenolol less effective than metoprolol in suppressing heart rate and blood pressure responses to maximal exercise.

Adrenergic beta-Antagonists↗
PubMed1982

Detection of coronary artery disease with gated cardiac blood-pool scintigraphy: comparison of cold pressor test and dynamic exercise.

Forty-six subjects (11 normals with no cardiac disease, 13 persons with a 'false' positive exercise ECG test, and 22 patients with coronary artery disease) were investigated with ECG-gated cardiac blood-pool imaging at rest, during cold pressor stimulation, and during supine bicycle exercise. Changes in left ventricular ejection fraction and intervention induced regional wall motion abnormalities were measured. Cold pressure stimulation did not induce anginal pain in any person, but were generally found more unpleasant than dynamic exercise. Dynamic exercise detected significantly more coronary artery disease patients (20/22, 91%) than did cold stimulation (13/22, 59%) (P less than 0.02). Specificity of dynamic exercise and cold stimulation was not significantly different. It is concluded that cold stimulation is less sensitive than dynamic exercise in the detection of patients with ischaemic heart disease with gated cardiac blood-pool imaging.

Cold Temperature↗
PubMed1982

Platelet function related to the development and presenting symptoms in coronary artery disease. An epidemiological study in apparently healthy men.

Among 2014 apparently healthy men aged 40-59 years platelet function was studied with Hellem's retention method in 488 men. In 55 of these 488 men coronary heart disease (CHD) was strongly suspected and coronary angiography confirmed the diagnosis in 34 of 51 angiographied men. Platelet responsiveness was significantly lower among those who had angina pectoris than among their CHD-suspect counterparts without angina, regardless of coronary angiographic findings. Since angiopositive men without angina and 408 "normals" had similar retention values, it seems as if presenting symptoms, but not the development of CHD are linked to platelet function. During a near maximal bicycle exercise test significantly higher peak exercise blood pressure was found among men with very low retention values than among men with retention values in the middle and upper range. This could not be explained by differences in maximal heart rate or work performance. This indicates that blood pressure regulation during exercise may in part be linked to platelet function related mechanisms.

Adult↗
PubMed1982

Haemodynamic effects of nifedipine and propranolol in patients with hypertrophic obstructive cardiomyopathy.

The haemodynamic effects of nifedipine, propranolol, and the combined administration of the two drugs were studied in 12 patients with hypertrophic obstructive cardiomyopathy. The combined administration of nifedipine and propranolol appeared to be superior to that of nifedipine alone. The spontaneous heart rate was reduced in most cases after nifedipine plus propranolol, and at atrial pacing the following results were obtained: left ventricular peak systolic pressure was reduced from 200 +/- 39 to 157 +/- 30 mmHg; a positive correlation was found between the pre-drug left ventricular end-diastolic pressure and the magnitude of reduction in left ventricular end-diastolic pressure; systolic blood pressure was reduced from 125 +/- 31 to 111 +/- 27 mmHg, and total peripheral resistance was reduced from 1403 +/- 307 to 1160 +/- 209 dyne s-1 cm-5. The combined administration reduced the resting left ventricular outflow gradient from 76 +/- 19 to 45 +/- 26 mmHg, while cardiac index was left unchanged. The effects on mean pulmonary arteriolar resistance and mean pulmonary arteriolar resistance and mean pulmonary capillary venous pressure were in most cases slight and insignificant. The results indicate an improved haemodynamic condition in patients with hypertrophic obstructive cardiomyopathy after the combined administration of nifedipine and propranolol: a treatment that might provide a new and useful alternative to already existing medication.

Adult↗