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Biomedical subjects

J Gormsen

Publications and source records attributed to J Gormsen.

At least 37 records · Page 2Linked to original sources
PubMed1982

Profound sensorineural hearing loss in polyarteritis nodosa. An atypical case of Cogan's syndrome.

Parameters of importance for the development of thrombosis were investigated in a patient with polyarteritis nodosa (PAN) and profound sensorineural hearing loss. During the acute phase, platelet hyperaggregability, shortened platelet survival, and decreased fibrinolytic activity were found. The possibility is discussed that the etiology of the acoustico-vestibular symptoms in this patient could be an inner ear thromboembolic disorder. It is suggested that platelet functions and fibrinolytic activity should be investigated in patients with acoustico-vestibular symptoms and PAN or other systemic diseases. If abnormalities are found, specific platelet inhibitory and/or fibrinolysis-increasing treatment should be considered as an addition to the conventional medical treatment.

Fibrinolysis↗
PubMed1982

Platelet function and fibrinolytic activity following distance running.

6 long distance runners from the Danish marathon elite and 6 non-runners completed test runs of 28 and 12 km, respectively. Distance runners and non-runners showed the same responses in platelet function. We found a significant decrease in ADP induced platelet aggregability, a decreased serotonin release induced by ADP and collagen and an increase in platelet factor 4 immediately following the run. The antithrombin III levels remained constant. Euglobulin lysis time was shortened (by approximately 50%) and the plasminogen levels significantly increased. The last 2 findings indicate an equal increase in fibrinolytic activity during distance running in both groups. While short term, strenuous exercise induces platelet hyperaggregation, long term distance running induces a state of exhaustion of platelet aggregation capacity.

Adenosine Diphosphate↗
PubMed1981

Effect of long-term beta-blockade with alprenolol on platelet function and fibrinolytic activity in patients with coronary heart disease.

In 14 patients with coronary heart disease the effect of long-term treatment (mean 16 months, range 12-33) with alprenolol on platelet function and fibrinolytic activity was studied. While on the beta-blocker and two weeks after gradual withdrawal of it, the patients performed a bicycle-ergometer test and blood samples were obtained before and following exercise. Pre-exercise fibrinolytic activity, assessed by the euglobulin clot lysis time, was 183 +/- 27 min (mean +/- SEM) while on alprenolol as compared to 111 +/- 18 min (p less than 0.01) after its withdrawal. Activation of fibrinolysis following exercise was not significantly influenced by alprenolol. In patients treated with alprenolol, the pre-exercise threshold level of ADP, producing platelet aggregation was 3.3 muM (geometric mean) and 5.1 muM after stopping treatment (p less than or equal to 0.05). In patients receiving the beta-blocker, the ADP- threshold value dropped from 3.3 muM before exercise to 2.3 muM immediately after exercise (not significant). The corresponding values after withdrawal of alprenolol were 5.1 muM and 2.7 muM (p less than or equal to 0.02). Adrenaline - stimulated aggregation was not significantly influenced by alprenolol. Serotonin release from platelets following maximal ADP- and adrenaline stimuli was not significantly changed by exercise in patients on beta-blockade. After stopping treatment, ADP-induced serotonin release was 22 +/- 4.1% before and 15 +/- 4.7% after exercise (p less than 0.02). the corresponding values using the adrenaline stimulus were 29 +/- 5.7% and 17 +/- 4.7% (p less than 0.05). It is suggested that during physical stress alprenolol may protect platelets against aggregatory stimuli.

Adenosine Diphosphate↗
PubMed1981

Impaired platelet aggregation and increased bleeding time during general anaesthesia with halothane.

A significant correlation was found between the inhibition produced by 1% halothane with nitrous oxide and oxygen on platelet aggregation in vitro and the increase in bleeding time during anaesthesia with halothane, nitrous oxide and oxygen in 10 patients. It is suggested that halothane in nitrous oxide with oxygen inhibits platelet aggregation in vivo and in vitro. The inhibition is not seen when platelet aggregation is studied in platelet-rich plasma from anaesthetized patients because the agents evaporate during preparation of platelet-rich plasma and during analysis in the aggregometer.

Anesthesia, Inhalation↗
PubMed1981

Disseminated intravascular coagulation, antithrombin III, and complement in meningococcal infections.

Serial assessments of some blood coagulation factors, antithrombin III (AT III), and complement were made in 18 patients with meningococcal (mgc) infection. All patients displayed laboratory evidence of activation of the blood clotting system. Two patients showed clinical signs of disseminated intravascular coagulation. Only AT III differed significantly between patients with and without complications. There was no correlation between changes in blood clotting, activation of the complement system and the course or duration of the disease. These results do not enable one t identify patients who need specific prophylactic therapy. Controlled clinical trials, including administration of heparin, dextran, aprotinin, and others, are still required to ensure optimal treatment in fulminant mgc infections.

Adolescent↗
PubMed1980

Effects of halothane on platelet function.

Human platelets in platelet rich plasma (PRP) incubated at 37 degrees C with 0.3-2% halothane for 5-10 min lost the ability to aggregate with ADP, epinephrine and collagen. At the same time uptake and release of 14C-serotonin was inhibited. When halothane supply was removed, platelet functions rapidly returned to normal. However, after high concentrations of halothane, the inhibition of platelet aggregation was irreversible or only partially reversible. The results suggest that halothane anaesthesia produces a transient impairment of platelet function.

Adenosine Diphosphate↗
PubMed1980

Changes in platelet functions, coagulation and fibrinolysis in uncomplicated cases of acute myocardial infarction.

Platelet aggregation and serotonin-release in vitro and some coagulation and fibrinolysis parameters were studied closely in 12 patients with non-complicated acute transmural myocardial infarction from the very beginning, for 3 weeks. The aggregability with ADP, epinephrine and collagen and the serotonin-release was significantly reduced the first days. Significantly increased aggregability and serotonin-release developed after a week, with peak activity on days 14-16. Most patients still exhibited increased activity at the discharge on days 21-22. Positive ethanol gelation tests developed after day 1 in most patients with a peak at day 5, contemporary with peak activities of factor VIII and negatively correlated to factor XIII activity, quantitated biologically. These values were normalized on discharge. Antithrombin III (Xa) remained unchanged, normal to slightly elevated. The fibrinolytic activity decreased after day 1 with lowest activity on day 5, contemporary with peak activity of antiplasmin. Around 50% of the patients showed decreased activity on discharge.

Adenosine Diphosphate↗
PubMed1980

Oral levo-norgestrel - testosterone effects on spermatogenesis, hormone levels, coagulation factors and lipoproteins in normal men.

Four healthy men volunteered to be treated for eight to nine months with daily oral levo-norgestrel (250 micrograms) and oral testosterone (200-600 mg) as a possible contraceptive. This was followed by a recovery phase of 5-10 months. The oral steroid combination significantly decreased sperm count in 3 of 4 subjects, and significantly increased abnormal spermatozoa, serum LH was decreased during treatment but serum FSH remained constant, except for one volunteer. Serum testosterone was decreased except for 2 daily peaks associated with the oral testosterone. During the recovery period, sperm counts and morphology, serum testosterone and serum LH returned to normal, whereas serum FSH levels were increased. Platelet aggregability induced by ADP, increased in 3 volunteers during treatment as did fibrinolytic activity and fibrinolytic capacity (2 of 3 subjects). There was a reduction in the hepatic triglyceride lipase activity but no change was seen in serum triglycerides, serum cholesterol, serum LDL, serum HDL, peripheral lipoprotein lipase activity and the intravenous fat tolerance test. No other toxicological side effects were seen.

Adult↗
PubMed1980

Platelet aggregation and fibrinolytic activity in young alcoholics.

Alcoholism has been shown to predispose to cerebrovascular thrombosis in normotensive males under the age of 50. To elucidate this phenomenon platelet aggregation and fibrinolytic activity were studied in 29 alcoholic males under 50 years of age who showed no evidence of acute cerebrovascular disease. Age matched healthy nonalcoholic volunteers made up the control population. Platelet aggregation did not differ significantly (P greater than 0.05) in the two groups. Fibrinolytic activity was significantly reduced in the alcoholics as compared to the controls (P = 0.005). The data suggest that the alcoholics have an increased thrombotic tendency. This may cause alcoholics to be at a greater risk of suffering stroke at an early age.

Adult↗
PubMed1980

Effect of cyproterone acetate on platelet aggregability, fibrinolytic activity and fibrinolytic capacity in normal men.

Nine healthy men were treated with a daily dose of 5 or 10 mg of the anti-androgen cyproterone acetate. Platelet aggregability was increased in 6 of 9 men; fibrinolytic activity decreased in 7 of 7 and the fibrinolytic capacity decreased in 5 of 7 volunteers. We conclude that platelet aggregability, fibrinolytic activity and capacity may be modified by anti-androgen treatment and therefore attention should be paid to the coagulation parameters when cyproterone acetate is used.

Adenosine Diphosphate↗
PubMed1980

The influence of low dose heparin in elective surgery on blood coagulation, fibrinolysis, platelet function, antithrombin III and antiplasmin.

Patients undergoing elective abdominal surgery were randomized into 2 groups, one receiving low dose of heparin (LDH) and one placebo. The code was not opened until all clinical and laboratory tests had been evaluated. LDH had no significant influence on APTT, thrombin time or presence of fibrin monomers except that significantly more patients in the LDH group had prolonged APTT on postoperative day 1, thrombin times greater than 19 sec preoperatively, and fibrin monomers less frequently on postoperative day 5. No significant influence on fibrinogen-related antigens was demonstrable. LDH did not influence the platelet counts or the postoperative increasing aggregability, as illustrated by decreasing threshold concentrations of ADP and adrenalin, increasing frequency of spontaneous platelet aggregation and increase in serotonin release. In contrast the antithrombin III activity against IIa and Xa dropped sigifnicantly more postoperatively in thd LDH group apparently due to increased consumption. The antiplasmin concentration dropped significantly more peroperatively and the fibrinolytic activity increased significantly more in the LDH group immediately postoperatively. The antiplasmin concentrations were significantly in creased later in the postoperative period in both groups, significantly less in the LDH group. These changes induced by LDH favour the inhibition and lysis of thrombus formation.

Abdomen↗
PubMed1979

Fibrinolytic activity in patients with sudden sensorineural hearing loss.

Fibrinolytic activity and capacity were studied in a group of 18 patients with sudden sensorineural hearing loss of unknown etiology. The fibrinolytic activity and capacity were found reduced in 12 patients. No distinct changes in platelet aggregation in vitro could be demonstrated. Further, repeated studies in this category of patients should be performed.

Acute Disease↗