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Biomedical subjects

K Gjesdal

Publications and source records attributed to K Gjesdal.

At least 19 recordsLinked to original sources
PubMed1992

[Cooperation between regional and central hospitals--how to achieve the best results?].

The authors reviews a recent governmental analysis of cooperation between third-line university clinics and local and central hospitals. The hospitals are owned by the government (mainly by the counties), and the various Acts and regulation permit the central authorities to make decisions on all aspects of highly specialized medicine. The analysis concludes that a limited number of problems should be solved by decision of the central government, but only those where national concerns are involved. The counties within a health region should cooperate within a Regional Health Policy Board, to create plans for flow of patients through the health care system, specified for each field of medicine. When such plans have been approved by the Regional Health Policy Board, each county should be willing to accept them. In the event of local disagreement, the central government should decide.

Health Policy↗
PubMed1992

[Highly specialized medicine. How to assign the tasks?].

Norway has four million inhabitants and five university hospitals, each serving one health region. The authors describe the work of a governmental medical committee, whose mandate is to advise on where to locate the various highly specialized medical services. Important questions have been the relationship between experience and quality, and the desire of each university clinic to be able to provide treatment within its own region for most health problems. Their reasons are concern about research and specialist training, and the preference of patients for treatment near to home. A list of proposed national and over-regional centers for certain treatments has been prepared on the basis of the experts' report and comments from all university clinics. These recommendations have provided a medical basis for later economic and political analyses prior to final decision by the Government. Norwegian legislation permits strong governmental regulation of the highly specialized health services.

Health Planning↗
PubMed1992

The effect of transdermal nitroglycerin on exercise tolerance in relation to patch application time--a meta-analysis.

Disagreeing results have been reported in the many studies on continuous treatment with nitroglycerin patches. The effects on exercise tolerance are partly studied at the end of a 24-hour application period, and partly examined only a few hours after patch renewal. The present meta-analysis estimates the overall efficacy of nitroglycerin patches in trials with and without concomitant antianginal therapy, and investigates if the treatment effect depends on the patch application time. A computed search (MEDLINE) identified 110 publications, of which 17 trials on nitrate patch monotherapy and six trials on combined therapy satisfied the inclusion criteria. Data on "exercise duration" and "ST-segment depression" were converted to a standardized treatment effect size d, and pooled to an overall treatment effect size d+. In tests 2-5 hours after patch renewal, moderate but significant effects of nitrate monotherapy were observed; d+ was 1.20 with regard to "ST-segment depression" and 0.39 with regard to "exercise duration" (both p < 0.0001). In contrast, 24 hours after patch application, the values for d+ were 0.09 (not significant) and 0.36 (p < 0.01), respectively. When adding the results from the six trials on combined therapy, d+ with regard to "exercise duration" was reduced to 0.28 (p < 0.0001) 2-5 hours after renewal and to 0.17 (p = 0.04) after 24 hours. Thus, the efficacy of continuous nitroglycerin patch treatment is moderate but evident during exercise tests 2-5 hours after patch renewal; however, it is reduced after 24 hours of patch application.

Administration, Cutaneous↗
PubMed1992

Heating and cooling of the nitroglycerin patch application area modify the plasma level of nitroglycerin.

19 healthy volunteers wore a nitroglycerin patch releasing 10 mg per 24 h for 2 h. Subsequently, the skin area surrounding the patch was exposed to 15 min of local heating with an infrared bulb (Group A, n = 10), or local cooling with an ice-pack (Group B, n = 9). The patch was protected by an insulating shield (Styrofoam). After 10 min of heating, the median (Walsh) plasma nitroglycerin level increased from 3.1 to 7.6 nmol.l-1. Body temperature remained constant. After 15 min of cooling the median plasma level had dropped from 2.1 to 1.4 nmol.l-1. The results demonstrate that changes in skin temperature may cause extensive short-term changes in the bioavailability of nitroglycerin. Presumably, a subcutaneous or cutaneous reservoir builds up during transdermal treatment, and changes in regional cutaneous blood flow affect the rate of drainage from the reservoir into the systemic circulation.

Administration, Cutaneous↗
PubMed1992

The sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension.

The association between blood pressure and coronary artery disease may be caused by a concurrence of atherogenic biochemical abnormalities in hypertensive patients, i.e., the metabolic cardiovascular syndrome (increased total cholesterol, triglycerides, and insulin; decreased high-density lipoprotein (HDL) cholesterol; and insulin resistance, glucose intolerance, and blood platelet dysfunction). There are numerous reports of sympathetic nervous system overactivity in hypertensive subjects that could be of importance for the pathophysiology of the high blood pressure. Plasma catecholamines have metabolic hormonal effects at concentrations slightly above low normal resting levels. Even transiently and certainly chronically raised plasma catecholamine levels may cause biochemical abnormalities. Catecholamines may raise total cholesterol, triglycerides, and insulin, decrease HDL cholesterol, and cause insulin resistance and glucose intolerance, and recent evidence supports an in vivo influence of epinephrine on blood platelets, causing dysfunction in hypertensive subjects. Thus, the sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. Hypertensive subjects may respond to environmental stimuli with larger sympathoadrenal responses than normal subjects. Furthermore, emotional stress has been associated with coronary artery disease. Thus, the metabolic hormonal effects of catecholamines, by causing the metabolic cardiovascular syndrome, may be the crucial link between "stress" and cardiovascular disease.

Blood Platelets↗
PubMed1991

The epinephrine-blood platelet connection with special reference to essential hypertension.

About three decades ago it was shown by an aggregometer that epinephrine activated blood platelets, and it was proposed that platelets could be the link between stress and cardiovascular disease. During the past 10 years this hypothesis has been tested in clinical studies. It has been found that subjects with hypertension consistently have raised plasma catecholamine levels and in particular elevated epinephrine levels. Arterial but not venous epinephrine concentrations correlated with plasma concentrations of the platelet-release reaction marker beta-thromboglobulin (BTG). Plasma BTG is elevated in hypertensive patients, and psychological stress (i.e., hypertension labeling) stimulates plasma epinephrine and BTG. When a physiologic dose of epinephrine is infused into essential hypertensive patients, platelet counts, platelet size, and plasma BTG concentrations increase more than in normotensive subjects. Data suggest that there is a connection between psychological stress, plasma epinephrine levels, and platelet function, especially in patients with essential hypertension.

Adult↗
PubMed1991

Transdermal nitrate therapy: bioavailability during exercise increases transiently after the daily change of patch.

Ten volunteers carried a 10 mg 24 h -1 transdermal glyceryl trinitrate (GTN) patch for 24 h before moderate exercise. Plasma GTN-concentration increased significantly (P less than 0.05) by 19% to peak value at 15 min. Two hours after patch renewal repeat exercise increased GTN concentration by 56% (P less than 0.001). The two nitrate-concentration curves differed significantly (P less than 0.0001). Thus, change of patch augmented nitrate availability during exercise.

Administration, Cutaneous↗
PubMed1990

[Ischemic left ventricular failure. Main stem coronary stenosis treated with angioplasty].

We describe a patient with stenosis on the left main stem and severe impairment of the left ventricular function. Because of reversible myocardial ischaemia in a patient whose clinical situation prohibited surgery, angioplasty on the left main stem was performed, leading to considerable improvement of the ventricular function. Improvement was slow, however, probably due to "stunning" of the myocardium. We underline the importance of early angiography in patients when it is suspected that a larger part of the myocardium is affected by severe, reversible ischaemia.

Angina Pectoris↗
PubMed1990

[Drug therapy of acute myocardial infarction and unstable coronary syndrome].

Questionnaires were sent to 61 Norwegian hospitals treating acute coronary syndromes, and 90% replied. Thrombolytic drug treatment is now the routine when the history of chest pain is short and ischemia appears in ECG. Use of glyceryl trinitrate and beta blocking drugs varies considerably, as does the use of oral anticoagulants and platelet inhibitors. Practice also varies in unstable angina. However, a combination of aspirin, intravenous nitrate, and betablockers is common. Several treatment regimens have an uncertain scientific foundation. The varying practice reflects international scientific debate.

Adrenergic beta-Antagonists↗
PubMed1990

Awareness of high blood pressure stimulates platelet release reaction.

The present study aimed at testing the hypothesis of a link between mental stress and blood platelet function. Twenty-nine 19-year-old men were recruited from the 98th percentile of mean blood pressure (116 mmHg) at a routine medical screening. They were not informed about their elevated blood pressures at the time of the screening. One year later they were randomized into two groups. Group 1 (n = 16) was exposed to mental stress by a letter informing them about their high blood pressure, while group 2 (n = 13) was sent a neutral letter. At an examination 2 weeks later, heart rate (p less than 0.05) and plasma adrenaline (p less than 0.05) responses to a cold pressor test were exaggerated in the informed group. The plasma beta-thromboglobulin (beta TG) concentration was elevated in the informed group (p less than 0.05) as was mean blood pressure (p less than 0.05). beta TG correlated positively with hematocrit (r = 0.59, p less than 0.005) and mean blood pressure (r = 0.43, p less than 0.05), and negatively with plasma HDL (r = -0.61, p = 0.001). The study shows that awareness of hypertension induces a hyperadrenergic state which is associated with the platelet release reaction. Under these circumstances platelet release seems to be correlated to established coronary heart disease risk factors.

Adult↗
PubMed1990

Increased arterial adrenaline is related to pain in uncomplicated myocardial infarction.

Plasma levels of catecholamines, beta-thromboglobulin (BTG) and arginine vasopressin (AVP), and degree of pain were examined in 22 patients with suspected uncomplicated myocardial infarction within 24 h following onset of chest pain. Sixteen patients developed infarction with peak creatine phosphokinase at 1280 Ul-1 (range 293-3770 Ul-1). Fifteen healthy men served as controls (C). Arterial adrenaline levels were significantly higher in patients with pain (1.15 +/- 0.23 nmol l-1, n = 8, mean value +/- SEM) than in those without pain (0.60 +/- 0.10 nmol l-1, n = 14, P less than 0.05). Plasma catecholamines were moderately but significantly elevated in myocardial infarction; the concentration of arterial adrenaline was 0.83 +/- 0.14 nmol l-1 and that of arterial noradrenaline was 2.70 +/- 0.28 nmol l-1 compared with 0.44 +/- 0.04 nmol l-1 (P less than 0.025) and 1.47 +/- 0.05 nmol l-1 (P less than 0.0005), respectively, in C. One week later, plasma catecholamines had returned to baseline levels. Plasma BTG showed borderline elevation (1.0 +/- 0.1 pmol l-1) compared with C (0.6 +/- 0.1 pmol l-1, P = 0.04), and remained unchanged 1 week later. Plasma AVP was at baseline level. Uncomplicated myocardial infarction, regardless of size, was associated with only moderately increased sympathetic tone. Plasma adrenaline was related more to the degree of pain than to the presence of acute myocardial infarction. Arterial adrenaline may be a sensitive marker of sympatho-adrenal activity related to pain.

Arginine Vasopressin↗
PubMed1985

Effects of adrenaline infusion on platelet number, volume and release reaction.

At the end of a diagnostic right heart catheterization ten patients received an intravenous infusion of l-adrenaline which gradually increased the arterial plasma adrenaline concentration from resting physiological values to high values as seen during myocardial infarction, pheochromocytoma and hypoglycemia. Blood was sampled from the brachial artery, femoral vein and hepatic vein. During the adrenaline infusion venous beta-thromboglobulin concentrations increased 23% from 61 +/- 5 to 80 +/- 7 micrograms/l (mean +/- SE), arterial platelet counts 20% from 212 +/- 17 to 253 +/- 25 X 10(9)/l and arterial platelet volume 4% from 7.25 +/- 0.20 to 7.56 +/- 0.21 femtoliter. All changes were significant at the 5% level. Thus, acute increments of arterial plasma adrenaline significantly stimulated the blood platelet parameters studied.

Adult↗