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Biomedical subjects

J Jespersen

Publications and source records attributed to J Jespersen.

At least 163 records · Page 9Linked to original sources
PubMed1989

Circadian variation of fibrinolytic activity among Eskimos in Greenland.

Recent studies on circadian variation of blood fibrinolytic activity have suggested a relation between a depressed morning fibrinolytic activity and the frequent onset of myocardial infarction at that time in Caucasians. We have obtained blood samples from 10 Eskimos with an interval of 4 h during 24 h and studied the extrinsic tissue-type plasminogen activator-related fibrinolysis. We observed a significant change in the activity of tissue-type plasminogen activator (t-PA; p less than 0.01) and in the activity of plasminogen activator inhibitor (PAI; p less than 0.001) during 24 h. The activity of t-PA increased more rapidly and the activity of PAI decreased more rapidly during the morning hours in Eskimos compared to reported patterns in Caucasians. A significant negative correlation between PAI and t-PA (r = -0.79, p less than 0.0001) suggested that PAI contributes to the regulation of t-PA activity in the blood. Whether the observations are of importance for the low prevalence of myocardial infarction in Eskimos remains to be further studied. However, our observations demonstrate that it is of utmost importance to standardize the collection of blood samples in order to obtain reliable information on the fibrinolytic system in Eskimos.

Circadian Rhythm↗
PubMed1989

Increased concentrations of heparin cofactor II in diabetic patients, and possible effects on thrombin inhibition assay of antithrombin III.

We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. We suggest that the high concentrations of heparin cofactor II, 117 (SD 17)%, might have caused an overestimation of AT III in this group of patients with diabetes Type I, and should not be overlooked in other clinical situations.

Antithrombin III↗
PubMed1988

Effects of an oral antidiabetic drug on the fibrinolytic system of blood in insulin-treated diabetic patients.

Selected variables of the fibrinolytic system were assessed in 23 men with insulin-treated diabetes with no measurable pancreatic beta-cell function. Gliclazide, a second-generation sulphonylurea drug, was administered to the patients over a period of 6 months in daily doses of 160 mg or 240 mg, and blood samples were obtained before, during, and after treatment. Determined by global assays, the drug did not significantly change plasminogen activator activities in euglobulins. Measurements of specific components of the system of fibrinolysis showed a marginal increase during administration of gliclazide of tissue-type plasminogen-activator antigen and prekallikrein activity in plasma, whereas the activities in euglobulins of the intrinsic plasminogen proactivators remained nearly the same during the study. Levels in plasma and euglobulin of C1-inactivator antigen and in plasma of factor XII antigen and t-PA inhibition capacity remained constant throughout the study. There were no changes of the increase in concentration of t-PA activity and t-PA antigen following venous occlusion. The metabolic state remained the same during the whole study. It is concluded that gliclazide induces small, but significant, non-insulin-dependent extrametabolic effects on the extrinsic (t-PA) and intrinsic (prekallikrein) system of fibrinolysis. Whether these changes are of physiological importance remains to be demonstrated.

Administration, Oral↗
PubMed1988

Venous thrombosis after abdominal surgery. A comparison between subcutaneous heparin and antithrombotic stockings, or both.

In an open controlled study, 248 consecutive patients (age more than 40 yrs) admitted for major abdominal surgery were randomized to one of three prophylactic antithrombotic treatments. Eighty-five patients received subcutaneous heparin, 74 patients had graduated compression stockings to the knee (TED stockings), and 89 patients had both subcutaneous heparin and stockings. Treatment began on the evening before operation and continued to complete mobilization, or for not less than five days postoperatively. On the fourth or fifth postoperative day, the patients underwent a 99mTc-plasmin test of the lower limbs as a test for deep vein thrombosis. There were 29.7% positive tests in the stocking group, 29.4% in the group with heparin prophylaxis, and 25.8% in the combined group. Differences between treatments were not statistically significant.

Abdomen↗
PubMed1988

Pathophysiology and clinical aspects of fibrinolysis and inhibition of coagulation. Experimental and clinical studies with special reference to women on oral contraceptives and selected groups of thrombosis prone patients.

The primary aim of the haemostatic mechanism is to protect the vascular system and to keep it intact after injury in order to secure the function of tissues and organs. A second aim is to provide a matrix in wound healing and tissue repair. The regulation of this physiological mechanism is effected by a dynamic haemostatic balance comprising interactions between endothelial cells, thrombocytes, coagulation, and fibrinolysis. This balance determines the amount of fibrin layed down at a site of injury thereby influencing the progress of the reparative processes. Clinical experience has, as described, shown that the concept of a dynamic haemostatic balance, and the increase in knowledge about the mechanisms involved in its regulation, can be applied with success in the elucidation and treatment of cases of impaired haemostasis, or when during a disease instances of thrombosis or embolism arise, which otherwise would have been difficult to explain or to subject to rational treatment. The results obtained and the experiences gained have therefore substantiated the existence of such a balance. Disturbances in the regulation of the balance may cause the formation and deposition of too little fibrin at a site of injury resulting in impaired haemostasis, ultimately manifesting itself as a haemorrhagic disorder. Or, an enhanced formation or delayed resolution of fibrin may cause thrombosis. Therefore, in the acute clinical cases the balance may adequately be described as a thrombohaemorrhagic balance. These observations have in particular underscored the role of an impaired fibrinolysis or decreased inhibition of coagulation in the pathogenesis of thromboembolic disease. They suggest the existence of an antithrombotic potential, which might be reduced due to a decreased inhibition of coagulation and/or a decreased fibrinolysis. The major stages in the mechanisms of blood coagulation and fibrin resolution are now well elucidated. This has increased our understanding of the interplay between the activating and regulating factors by which the organism keeps the formation of fibrin under control. Effects of disturbances in the balance are illustrated by description of cases of haemorrhagic disorders or thrombosis, and the pathophysiological aspects are surveyed. The regulation of coagulation and fibrinolysis follows in both systems the same pattern. The active enzymes (thrombin and plasmin, respectively) are formed by activation of circulating proenzymes, and inhibitors (circulating or localized) exert their modifying influences at various stages of the total process.(ABSTRACT TRUNCATED AT 400 WORDS)

Antithrombin III Deficiency↗
PubMed1987

Depression of tissue plasminogen activator (t-PA) activity and rise of t-PA inhibition and acute phase reactants in blood of patients with acute myocardial infarction (AMI).

We determined during the acute stage of myocardial infarction selected fibrinolysis variables (tissue-type plasminogen activator, intrinsic plasminogen activators, tissue-type plasminogen activator inhibition, C1-inactivator) and related the observed changes to changes in two acute phase reactants (C-reactive protein, fibrinogen). Acute myocardial injury induce significant increases in blood of tissue-type plasminogen activator inhibition (day one, p less than 0.05), C-reactive protein (day three, p less than 0.01), fibrinogen (day six, p less than 0.01), and C1-inactivator (day eight, p less than 0.01). Tissue-type plasminogen activator activity measured as C1-inactivator resistant fibrinolytic activity showed a minimum day two after the acute attack (p less than 0.01), whereas plasminogen activator activities arising from the intrinsic system of fibrinolysis remained constant. The observed changes did not parallel the occurrence of deep vein thrombosis indicated by a positive Tc-plasmin test (41% of the patients).

Acute-Phase Proteins↗
PubMed1987

A selective depression of tissue plasminogen activator (t-PA) activity in euglobulins characterises a risk group among survivors of acute myocardial infarction.

Among 29 patients recovering from a first-time acute myocardial infarction (AMI) 9 patients suffered reinfarction during a four year follow-up period. The 9 reinfarction patients were found to belong to a subgroup of 17 patients with a selective depression to near zero of euglobulin t-PA activity. None of the group of 12 patients with marked t-PA activity suffered a relapse. Euglobulin fibrinolytic activity as usually assayed did not distinguish between groups with or without relapse.

Aged↗
PubMed1987

On the usefulness of fibrinolysis variables in the characterization of a risk group for myocardial reinfarction.

In a prospective study selected fibrinolysis variables were assessed in plasma samples from 29 consecutive patients recovering a first instance of acute myocardial infarction and the results were correlated with reinfarction during the next four years. Nine patients suffered a reinfarction leaving a group of 20 patients without evidence of relapse. The reinfarction group was characterized by lower tissue plasminogen activator activities in plasma euglobulins (p less than 0.05), significantly higher plasma concentrations of tissue plasminogen activator antigen (p less than 0.002) and a tendency to a higher plasma level of plasminogen activator inhibition capacity. There were no significant differences between the groups in plasma concentrations of plasminogen, histidine-rich glycoprotein, plasminogen kringle-4-binding-protein, and alpha 2-antiplasmin.

Fibrinolysis↗
PubMed1987

Characterization of plasminogen activators in unstimulated and stimulated human whole saliva.

The fibrinolytic activity of saliva from healthy males was studied on plasminogen-free and plasminogen-rich fibrin plates. A cell-bound plasminogen activator in human unstimulated and stimulated whole saliva was demonstrated. The assessed fibrinolytic activities could always be quenched by incorporation into the fibrin plates of IgG antibodies raised against human two-chain tissue-plasminogen activator (t-PA), while additional experiments indicated the absence in normal human saliva of urokinase-like and factor XII-dependent plasminogen activators as well as the absence of inhibitors of fibrinolysis. Thus, t-PA is the only type of plasminogen activator in normal human saliva. The present findings seem to support our recent clinical observations of a decrease in the incidence of bleeding complications and need for replacement therapy in hemophiliacs undergoing oral surgery during local antifibrinolytic therapy with tranexamic acid. Whether the findings might also be of importance in other pathological conditions of the oral cavity, such as impaired wound healing, remains to be elucidated.

Factor XII↗
PubMed1986

The diurnal increase in euglobulin fibrinolytic activity in women using oral contraceptives and in normal women, and the generation of intrinsic fibrinolytic activity.

The diurnal fluctuations in plasma euglobulin fibrinolytic activity in women on oral contraceptives and in normal women showed similar patterns of increase. Following inactivation of inhibitors by flufenamate the individual increases and the evening levels did not differ. The diurnal increase was related to an increase in extrinsic (tissue-type) plasminogen activator (t-PA) activity, which contributes little to the total activity of the euglobulin fraction but induces an activation of the intrinsic system.

Adult↗
PubMed1986

Inhibition of tissue-type plasminogen activator in plasma of women using oral contraceptives and in normal women during a menstrual cycle.

Tissue-type plasminogen activator (t-PA) inhibition in plasma was assessed in 15 normal women and in 10 women using oral contraceptives (OC) containing 30 micrograms ethinyl oestradiol and 150 micrograms levo-norgestrel. The levels of t-PA inhibition were significantly lower in the OC group with marked fluctuations related to the hormone cycle. Normal women had only minor fluctuations.

Adult↗
PubMed1986

A delaying influence of cryoglobulins in the assessment of euglobulin fibrinolytic activity.

The presence of cryoglobulin in plasma was found to interfere with the assessment of euglobulin fibrinolytic activity. Cryoglobulins co-precipitate with the isoelectrically precipitated euglobulins thereby giving rise to erroneous determinations of components of the extrinsic and intrinsic fibrinolytic systems. Cold-promoted activation of the F XII-dependent part of the intrinsic proactivator system was related to the presence of cryoglobulins. Strictly optimized procedures for the preparation of euglobulin solutions are essential in the accurate determination of euglobulin fibrinolytic activity. Resuspended euglobulins should be kept for at least 30 min at 0 degree C followed by at least 2 min at 37 degrees C in order to secure conditions yielding accurate and reproducible assays of activity in samples of patient plasma.

Chemical Precipitation↗