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Biomedical subjects

K Winther

Publications and source records attributed to K Winther.

At least 19 recordsLinked to original sources
PubMed1992

Effects on platelet aggregation and fibrinolytic activity during upright posture and exercise in healthy men.

The circadian variation of acute myocardial infarction suggests that daily activities such as assuming the upright posture and performing different daily activities may trigger the onset of coronary thrombosis. Such triggering may result from unfavorable alterations in the balance between the prothrombotic and antithrombotic properties of the blood. The present study compares the effects of 2 common daily activities, assuming the upright posture and exercise, on platelet aggregation and fibrinolytic activity. In healthy male subjects, assuming the upright posture in the morning significantly increased platelet aggregation and produced only a moderate increase in fibrinolytic activity within 10 minutes. These changes were still present after 90 minutes in the upright posture. Supine posture for 45 minutes resulted in levels of fibrinolytic activity and platelet aggregation comparable to that observed before initially assuming the upright posture in the morning. Return to the supine posture for 45 minutes resulted in levels of fibrinolytic activity and platelet aggregation comparable to that observed before the initial assumption of upright posture. The changes recurred when upright posture was taken later in the day. Exercise did not increase platelet aggregation to levels beyond that produced by the upright posture, but was associated with a marked increase in fibrinolytic activity. Thus, exercise and upright posture produce distinctive alterations in the thrombogenic potential of the blood that may influence the timing of clinical vascular events.

Adult↗
PubMed1992

[Preclinical and prenatal diagnosis of familial adenomatous polyposis].

In order to investigate the possibility of preclinical and prenatal genetic diagnosis of familial adenomatous polyposis (FAP) by means of DNA-systems and other markers, blood samples were collected from 246 persons in 29 families, including 90 with the clinical diagnosis FAP and 73 clinically unaffected first degree relatives (persons at risk). The material was studied with up to 4 DNA-marker systems located in the region around the disease gene. Among the first degree relatives eight (11%) had probably inherited the disease gene, while 31 persons (42%) in this risk group had probably not inherited the gene. It was not possible to evaluate the risk in the remaining 34 persons (47%). In 45 (85%) out of 53 persons under 40 years the DNA-systems were informative, so that it would be possible to offer the option of prenatal diagnosis. It is concluded that preclinical and possibly prenatal genetic diagnosis may be offered; but the current practice of prophylactic proctosigmoidoscopic surveillance should be maintained.

Adenomatous Polyposis Coli↗
PubMed1992

Rapidity and duration of platelet suppression by enteric-coated aspirin in healthy young men.

The recent demonstration of aspirin's ability to prevent and reduce the severity of myocardial infarction has led to a marked increase in its use and to a need for information regarding the time-course of onset and offset of its antiplatelet effect. A study of healthy men was conducted to determine (1) the rapidity of onset of inhibition of platelet aggregation in response to adenosine diphosphate, and thromboxane A2 production after chewed enteric-coated aspirin (325 mg, n = 10); and (2) the duration of platelet inhibition after cessation of enteric-coated aspirin (325 mg) every other day for 14 days (n = 10). When chewed, enteric-coated aspirin greatly inhibited platelet aggregation response to adenosine diphosphate and thromboxane A2 production within 15 minutes. Complete recovery of platelet aggregation occurred in half of the subjects by day 3, and in 80% of the subjects by day 4; the platelet response was not affected by exercise. This study demonstrates a rapid onset of aspirin's antiplatelet effect and provides information relevant for optimal timing of initiation of aspirin for acute conditions such as myocardial infarction and unstable angina, and cessation of aspirin before surgery.

Adenosine Diphosphate↗
PubMed1992

Enhanced risk of thromboembolic disease in hypertension from platelet hyperfunction and decreased fibrinolytic activity: has antihypertensive therapy any influence?

Enhanced platelet function and a decrease in fibrinolytic activity have been reported in patients with mild hypertension after treatment with various nonselective beta-blockers. Until now, such changes have not been reported during treatment with beta 1-selective drugs or with agents that have intrinsic sympathomimetic activity. The impact of angiotensin-converting enzyme inhibitors and diuretics on platelet function and fibrinolytic activity has not been fully elucidated. Calcium antagonists of various types, however, are known to decrease platelet release in vivo whereas their effects on platelet aggregation and fibrinolytic activity are less clear. The new dihydropyridine calcium antagonist isradipine, when tested in a group of patients with mild hypertension, resulted in a decrease in platelet aggregation, a shortened euglobulin clot-lysis time, and a dramatic increase in t-PA (tissue-plasminogen activator) activity after 14 days of treatment. These changes remained stable throughout the 1-year study period. The fact that antihypertensive therapy does not always result in the hoped-for prolongation of life, despite satisfactory blood pressure reduction, may be in part due to an unfavorable impact on various components of the blood-clotting system.

Antihypertensive Agents↗
PubMed1991

Platelet aggregation and fatty acid composition of platelets in type 1 diabetes mellitus.

A raised content of arachidonic acid in platelets from diabetic patients with retinopathy was found without differences in platelet aggregation: platelet aggregability was not related to platelet fatty acid composition. In diabetes, platelet aggregation was inversely correlated to non-esterified fatty acids in plasma and may suggest an inhibiting effect. Mean platelet volume was raised in the diabetic patients, but without hyperaggregability. The findings do not exclude a relationship between platelet fatty acids and platelet aggregability, but suggest that variations in levels of non-esterified fatty acids in plasma might interfere with platelet aggregation.

Adult↗
PubMed1991

[LongoVital in the prevention of recurrent aphthous stomatitis. 1].

LongoVital (LV) (DK. reg. no. 5178/75) is a herbal based tablet enriched with recommended doses of vitamins. The present study was undertaken to investigate prevention of recurrent aphthous ulceration (RAU) during daily intake of LV for six months as compared with placebo in a double-blind, randomised clinical, cross-over 1-year study. The population comprised 29 otherwise healthy minor RAU patients (18F, 11M) mean age 36 (18-67), with an estimated average number of recurrences the previous year of 12.8 (3-30). The number of recurrences was significantly reduced on treatment with LV during the latter four of the six months (p less than 0.01) where 31% were totally free of recurrences. Subjective all-over evaluation of treatment period was significantly in favour of LV. LV induced no adverse reactions and is the first harmless systemic treatment which has proved better than placebo in the prevention of RAU.

Adult↗
PubMed1991

[Immunomodulating effect of LongoVital in patients with recurrent aphthous stomatitis. 2].

LongoVital (LV) (DK. reg. no. 5178/75) is a herbal-based tablet enriched with recommended doses of vitamins. Peripheral lymphocyte subsets: T-helper/CD4 (OKT4+) and T-suppressor/cytotoxic/CD8 (OKT8+) were studied quantitatively in 31 otherwise healthy patients with minor recurrent aphthous ulceration (RAU) during six months' daily LV intake in a double-blind, randomised, crossover 1-year study. Fourteen had had LV during the first six months (GrA) and 17 LV during the latter six months (GrB). OKT4+ percentages increased significantly during the LV period in both groups (p less than 0.05). OKT8+ percentages increased in both groups, however, only significantly in GrA (P less than 0.05). It is concluded that LV acts as an immunostimulator in patients with RAU and that the increase in T-lymphocyte subsets may account for the previously reported benefit of LV in RAU prevention.

Adult↗
PubMed1991

Decreased fibrinolytic activity and increased platelet function in hypertension. Possible influence of calcium antagonism.

Twelve patients with mild hypertension were compared, after 14 days of placebo, with an age- and gender-matched group of 12 healthy volunteers for platelet aggregability and fibrinolytic activity. Following this, 10 of the 12 hypertensives were treated with the calcium antagonist isradipine for 12 months. Blood was drawn for determinations of platelet aggregation and fibrinolytic activity after two weeks and 12 months of treatment. Platelet aggregation tended to increase in the hypertensives compared with controls, indicated by a lowering of the adenosine diphosphate (ADP) threshold value for irreversible aggregation. Tissue-plasminogen activator (t-PA) activity was significantly decreased in hypertensives compared to controls (P less than .05). During therapy, platelet aggregation decreased and t-PA activity increased (P less than .05). The present data suggest that fibrinolytic activity is decreased and platelet aggregation increased in mild hypertension. Besides the blood pressure-lowering effect, isradipine may protect against thromboembolic diseases by modifying platelet function and fibrinolytic activity.

Adult↗
PubMed1991

Platelet-associated immunoglobulins in patients with primary Sjögren's syndrome.

Ten patients with primary Sjögren's syndrome (7 females) were examined in order to evaluate whether in vivo-bound platelet-associated immunoglobulins (PAIg) and/or in vitro binding of circulating Ig to normal platelets influences platelet function. With an ELISA technique it was found that 9/10 patients had increased amounts of in vivo PAIgG, 4/10 patients of in vivo PAIgA and 5/10 patients of in vivo PAIgM. There was no correlation between patients platelet aggregability and the presence of in vivo PAIg. Incubation of platelets from a healthy person with plasma from the 10 patients caused in vitro binding of IgG in 7/10 cases, of IgA in 0/10 cases and of IgM in 1/10 cases. Adenosine diphosphate (ADP)-induced aggregability of the normal platelets was impaired in 7/10 incubation experiments (no correlation to in vitro PAIg) and unchanged in 3/10 cases. Epinephrine- and collagen-induced platelet aggregability was unchanged in all cases. It is concluded that increased amounts of in vivo and in vitro PAIg seem to occur frequently in patients with primary Sjögren's syndrome, but do not influence platelet aggregability.

Blood Platelets↗
PubMed1991

Association of wake time and the onset of myocardial infarction. Triggers and mechanisms of myocardial infarction (TRIMM) pilot study. TRIMM Study Group.

A morning increase in onset of acute myocardial infarction (MI) has been documented, but its association with wake time and possible triggering events is unclear. The community-based, ongoing Triggers and Mechanisms of Myocardial Infarction (TRIMM) study was designed to investigate the factors associated with the transition from chronic coronary artery disease to acute MI. During the pilot phase in 1989, 224 consecutive hospitalized MI patients (176 men and 48 women, aged 60.3 +/- 9.2 years) of the prospectively defined Monitoring of Trends and Determinates of Cardiovascular Disease (MONICA) Augsburg MI register were interviewed 16.8 +/- 6.5 days after the event. The frequency of onset of MI was significantly higher (p less than 0.01) during the morning from 6 to 9 AM compared with other times of day. After adjustment for individual wake times, the peak of onset of MI was markedly sharper; the relative risk of MI during the 3-hour peak interval (the 3 hours after awakening) compared with other times of day increased from 1.8 (95% confidence interval, 1.3-2.4) to 2.4 (95% confidence interval, 1.8-3.1). Sixty-seven percent of the patients reported possible acute triggers of MI and/or unusual life events; among those, 52% reported stress or emotional upset. The TRIMM pilot study demonstrated the feasibility of a community-based study of possible triggering events of MI. The circadian variation of MI appears to result primarily from increased onset after awakening. This narrowing of the time frame of increased risk of MI should facilitate study of pathogenic mechanisms and aid in the design of more effective preventive regimens.

Adrenergic beta-Antagonists↗
PubMed1991

Does antihypertensive therapy affect the natural protection against thrombosis?

Fibrinolytic activity was measured in a 14-day placebo-controlled study of propranolol and the calcium antagonist isradipine in 20 mildly hypertensive patients (diastolic blood pressure 95-115 mm Hg) compared with 24 healthy volunteers. The parameters under study included euglobulin clot-lysis time, and tissue-plasminogen activator activity and its inhibitor (PAI). The two drugs exerted equal antihypertensive effects in the patients who had raised blood pressure, but had markedly different actions on the fibrinolytic system. Propranolol substantially reduced the fibrinolytic activity in both the hypertensive and healthy control groups. Isradipine, on the other hand, had no effect on fibrinolytic activity in the controls, but augmented the activity in the hypertensive subjects. The possible mechanisms for the different actions of the two agents may be related to the vascular endothelium.

Adult↗
PubMed1991

Platelet function and fibrinolytic activity in hypertension: differential effects of calcium antagonists and beta-adrenergic receptor blockers.

Platelet function was investigated in healthy volunteers and patients with essential hypertension by measurement of thresholds for ADP and adrenaline-induced aggregation and plasma concentrations of platelet factor 4 (PF-4) and beta-thromboglobulin (beta-TG) after administration of antihypertensive drugs. Fibrinolytic activity was investigated by the euglobulin clot lysis time (ECLT) and tissue plasminogen activator (t-PA) activity. Compared to normotensive controls, patients with essential hypertension showed increased aggregation as evidenced by a decrease in ADP thresholds for ex vivo platelet aggregation. ECLT was significantly prolonged and t-PA significantly lowered, indicating impaired fibrinolytic activity in mild hypertension. In different studies, we have shown that various antihypertensive drug regimens differ in their effects on platelet function and fibrinolytic activity when given to healthy volunteers or patients with mild-to-moderate essential hypertension. In normal volunteers, treatment with the calcium antagonists verapamil, nifedipine, and felodipine lowered plasma concentrations of PF-4 and beta-TG, indicating a reduced platelet activity in vivo. Fibrinolytic activity was not influenced by calcium antagonist treatment in the normal volunteers. Interestingly, however, t-PA increased significantly in the hypertensive group. When compared to placebo or beta 1-selective blockers, propranolol, a non-selective beta-adrenergic blocker without partial agonist activity, reduced ADP and adrenaline threshold values for ex vivo platelet aggregation in hypertensive subjects and impaired fibrinolytic activity in the normal volunteers as well as in the hypertensive groups by increasing ECLT and reducing t-PA. Hypothetically, the effects of antihypertensive drugs on platelet function and fibrinolytic activity could be of importance for their proposed actions on cardiovascular morbidity and mortality.

Adrenergic beta-Antagonists↗
PubMed1991

Beta 1-blockade and acute coronary ischemia. Possible role of platelets.

Although the benefit of beta-adrenergic blocking agents in acute coronary ischemia has been well documented, it is unclear whether the responsible mechanisms include the modification of platelet function. In recent studies, metoprolol appeared to reduce the total number and duration of episodes of silent ischemia in patients with stable coronary artery disease throughout the day. This effect was not associated with a change in baseline or circadian variability of the platelet aggregability. Since the treatment caused significant decreases in heart rate and blood pressure, the drug effect is more likely to be based on reduction of myocardial oxygen demand. Metoprolol, however, prevented a platelet aggregability increase and intracellular cAMP decrease during exercise stress testing in patients with stable angina pectoris. We speculate that this effect of beta 1-adrenergic blockade may be due to hemodynamic and neurohormonal changes, or possibly also to an increase in synthesis or release of platelet inhibiting substances.

Acute Disease↗
PubMed1990

Dose-dependent effects of verapamil and nifedipine on in vivo platelet function in normal volunteers.

The effects of 1 week of treatment with low and moderate doses of verapamil or nifedipine upon platelet function has been studied in 12 healthy volunteers. The ex vivo platelet aggregation threshold for ADP or adrenaline was not altered by verapamil or nifedipine. The plasma concentrations of beta-thromboglobulin and platelet factor 4 were significantly reduced by low but not by moderate doses of verapamil and nifedipine. Low doses of verapamil and nifedipine inhibit in vivo platelet activity in healthy volunteers.

Adenosine Diphosphate↗
PubMed1990

Exercise-induced platelet aggregation in angina and its possible prevention by beta 1-selective blockade.

Moderate exercise increased platelet aggregability of 12 middle-aged men with stable angina pectoris: the mean ADP threshold fell from 4.58 +/- 0.63 to 3.18 +/- 0.41 microM, P less than 0.01. Exercise did not, however, alter platelet aggregability in 12 healthy matched controls. Physical effort approximately doubled the plasma levels of adrenaline and noradrenaline in patients as well as in controls. Under the same conditions the cAMP content of platelets fell in the angina group from 20.86 +/- 1.86 to 17.78 +/- 1.71 pmol 10(-9) platelets, P less than 0.01, while there was no change in control levels. The fall of cAMP could account for the observed increase in platelet aggregability. We speculate that the increased aggregability of platelets in the exercising anginal subjects represents an imbalance between prostacyclin release and haemodynamic changes. The beta 1-selective blocker metoprolol, in usual therapeutic dosages, prevented the observed platelet changes probably by minimizing the haemodynamic disturbances and stimulating release of prostacyclin.

Adrenergic beta-Antagonists↗
PubMed1990

Platelet P1, P4-Di (adenosine-51) tetraphosphate (AP4A) in migraine patients before and during beta-adrenoceptor blockade.

P1,P4-Di(adenosine-51) tetraphosphate (AP4A) is a metabolically inactive nucleotide which can be released from platelet dense granules. This study was designed firstly, to investigate whether platelet content of AP4A was decreased in patients with classical migraine and secondly, whether the content of AP4A was changed by beta-adrenoceptor blockade. No significant difference in platelet dense granule content of AP4A, was observed between 10 migraine patients and 10 normal controls. Both metoprolol, a beta 1-selective blocker and propranolol, a non-selective beta-blocker significantly decreased the migraine attack rate. However, while propranolol significantly reduced the platelet content of AP4A, metoprolol did not. Therefore, the present data suggest that platelet dense granule release, as estimated by the content of AP4A is not of major importance in migraine.

Adenosine Triphosphate↗