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Biomedical subjects

G Olsson

Publications and source records attributed to G Olsson.

At least 55 records · Page 3Linked to original sources
PubMed1995

Effects of injury on apoB kinetics and concentration in rabbit aorta.

Endothelial injury or dysfunction and deposition of lipoproteins and cholesterol are key events during the development of atherosclerosis. We have studied the lipoprotein kinetics in arterial tissue in relation to endothelial injury and re-endothelialization. Endothelial injury was induced in rabbits by use of a balloon catheter. With a specific immunoradiometric assay, apoB levels in arterial tissue were measured at different time points for up to 10 weeks after injury. Forty-five minutes before being killed, the rabbits were injected with 125I-LDL, and influx of LDL was calculated from the accumulation of radioactivity in the arterial tissue. The concentration of apoB in the injured arterial tissue was four times higher than that in control arterial tissue (P < .0001). Within the lesion the concentration was as high in nonendothelialized as in re-endothelialized regions. The tissue pool of apoB was divided into a loosely bound fraction and a tightly bound fraction. The increase of apoB in the injured areas was primarily due to an increase in the tightly bound fraction. The influx of apoB was severalfold higher in nonendothelialized tissue than in re-endothelialized tissue or control areas (P < .005). When retention time was calculated, this was found to dramatically increase (by seven times) the tightly bound pool of apoB in the re-endothelialized areas. In addition to the large increase of a tightly bound apoB pool in injured areas, we found a prolonged retention time of apoB in the lesions, but only in the re-endothelialized areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The rationale for nitrates in angina pectoris.

Organic nitrates are among the oldest drugs used in the management of patients with ischemic heart disease. The most frequently used nitrates are nitroglycerin, isosorbide dinitrate and isosorbide-5-mononitrate. Their duration of action can be influenced by choice of substance, frequency of administration, formulation (eg, extended release) and route of administration. As well as providing effective treatment of acute angina, nitrates produce a long term prophylactic effect. Stable plasma nitroglycerin levels lasting longer than 10 to 12 h are not desirable due to the rapid development of tolerance. Simple, well-designed dosing schedules can avoid tolerance and rebound phenomena and can improve patient compliance.

Angina Pectoris↗
PubMed1993

Early intravenous beta blockade and thrombolytics in acute myocardial infarction.

This article discusses therapy with beta blockade and thrombolytic agents in acute myocardial infarction. In large and well-controlled studies both treatment strategies have been shown to increase survival. Both therapies have also been demonstrated to be safe in acute myocardial infarction. Historically, the 2 different treatment strategies have been tested during different time periods, resulting in few studies with the main objective to study the combined effects of the 2 agents. From the data that are presently available, however, there is a clear suggestion of additive beneficial effect and the 2 treatments given in combination are well tolerated.

Adrenergic beta-Antagonists↗
PubMed1993

Periparturient concentrations of insulin glucagon and ketone bodies in dairy cows fed two different levels of nutrition and varying concentrate/roughage ratios.

High producing multiparous dairy cows were fed either diets differing in energy content or diets with identical energy and protein content but differing in roughage content at the end of the dry period and beginning of lactation. Basal insulin and ketone bodies were analysed every week from 3 weeks before to 7 weeks after calving. Pancreatic glucagon was estimated 3 weeks before, 1-3 days after, and 3 weeks after calving. Before calving the feeding regimen had a very strong influence on the basal insulin level. High amounts of concentrate increased basal insulin levels until one week before calving and caused an interruption in the physiological decreasing course. After calving the insulin levels were low in all groups of cows. Before calving there were small variations in the glucagon levels, and no influence of feeding was observed. After calving there was a strong increase, especially in the cows fed the highest amounts of concentrate. Feeding high amounts of concentrate resulted in varying and in many cases increased levels of ketone bodies in plasma. Hyperketonemic cows had lower insulin and higher glucagon levels than normal cows. The influence of non-structural carbohydrates in the feed on pancreatic hormones is a cause of ketogenesis is discussed.

Animal Feed↗
PubMed1992

Metoprolol does not reduce platelet aggregability during sympatho-adrenal stimulation.

The possibility that beta-adrenoceptor blockers, especially beta 1-selective agents might inhibit platelet function is of considerable interest, as this might be of pathophysiological importance in cardiovascular diseases. Platelet function, however, is difficult to assess and in vivo related data are scarce. The effect of one week of treatment with metoprolol 200 mg/day on platelet aggregability during mental stress (colour word conflict test; CWT) and low and high dose adrenaline infusions has been evaluated in a double-blind, placebo-controlled, cross-over study in 10 healthy male volunteers. Platelet function in vivo was assessed using ex vivo filtragometry, and the urinary excretions of beta-thromboglobulin (HMW beta-TG) and 11-dehydro-TxB2 (a thromboxane metabolite). Conventional in vitro aggregometry and the urinary levels of 2,3-dinor-6-keto-PGF1 alpha (a prostacyclin metabolite) were also studied. During the interventions there was increased platelet aggregability in vivo, as filtragometry readings were shortened by 41 +/- 11% during high dose adrenaline infusion, urinary HMW beta-TG levels increased and urinary 11-dehydro-TxB2 tended to increase. In contrast, platelet sensitivity to ADP in vitro was reduced. The urinary 2,3-dinor-6-keto-PGF1 alpha levels were increased during the interventions. Despite the cardiovascular and biochemical signs of beta-adrenoceptor blockade at rest and during the interventions, metoprolol failed to influence platelet function in vivo, as measured by ex vivo filtragometry, or urinary HMW beta-TG or 11-dehydro-TxB2 levels. It tended rather to enhance the stress response measured by ex vivo filtragometry. Platelet aggregability in vitro and urinary 2,3-dinor-6-keto-PGF1 alpha levels were not altered by metoprolol.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Minimum heart rate and coronary atherosclerosis: independent relations to global severity and rate of progression of angiographic lesions in men with myocardial infarction at a young age.

The relations of hemodynamic factors, plasma fibrinogen concentration, serum lipoprotein levels, and clinical risk indicators to coronary atherosclerosis were studied in 56 men who had survived a first myocardial infarction before the age of 45 years and who subsequently underwent two coronary angiographies with an intervening time interval of 4 to 7 years. Presence, severity, and rate of progression of both diffuse lesions and distinct stenoses were determined by means of separate classification systems in 15 proximal coronary arterial segments. High minimum heart rate measured during a 24-hour period in connection with the reangiography was associated with progression of both diffuse lesions and distinct stenoses. High minimum heart rate also correlated positively with angiographic scores of global severity of diffuse atherosclerosis and stenoses. Progression of disease was predicted independently by minimum heart rate and low-density lipoprotein/high-density lipoprotein ratio, whereas lipoprotein A, fibrinogen levels, hypertension, smoking, and beta-adrenergic receptor blockade treatment did not discriminate between patients with and without progression.

Adult↗
PubMed1992

Metoprolol-induced reduction in postinfarction mortality: pooled results from five double-blind randomized trials.

Several postinfarction trials have evaluated the effect of secondary prophylaxis with different beta-blockers. Although so called meta-analysis of the results from all the trials have shown a beneficial effect of postinfarction beta-blockade, many of the individual studies have shown inconclusive results, mainly due to low statistical power. In order to obtain an evaluation of the merits of postinfarction therapy with metoprolol, data from the five available studies with metoprolol have been pooled into one database. In the total material 5474 patients (4353 men, 1121 women) have been studied during double-blind therapy with metoprolol 100 mg twice daily or matching placebo. The follow-up ranges from 3 months to 3 years. In total 4732 patient years of observation have been obtained. In total there were 223 deaths in the placebo-treated patients as compared to 188 deaths in the metoprolol-treated patients (P = 0.036), which corresponds to mortality rates of 97.0 and 78.3 per 1000 patient years, respectively. The mortality reduction was found both in men and women. As has been reported from individual postinfarction beta-blocker trials, the pooled results showed a marked reduction in sudden deaths (104 in the placebo group, 62 in the metoprolol group, P = 0.002). In a Cox regression model the influence of sex, age and smoking habits on the effect of metoprolol was evaluated. None of these factors influenced the metoprolol effect significantly. It is concluded that metoprolol therapy after acute myocardial infarction reduces the total number of deaths, and especially sudden cardiac deaths. The mortality reduction was independent of gender, age and smoking habits. Available data support a continuous beneficial effect.

Double-Blind Method↗
PubMed1992

Absence of pre-dose rebound phenomena with once daily 5-ISMN in a controlled-release formulation.

To avoid the development of nitrate tolerance secondary to relatively constant elevated plasma nitrate concentrations, intermittent nitrate dosing has been advocated. However, a nitrate-free interval may induce a rebound increase in myocardial ischaemia, and thus increase anginal symptoms during the latter portion of the dosing interval. This was suggested by the results of recent studies in which nitroglycerin patches were administered intermittently with a 12 h nitrate-free interval. The present investigation was carried out to determine whether a controlled-release formulation of 60 mg isosorbide-5-mononitrate (5-ISMN) would produce such a rebound phenomenon. Seventy-nine patients, who had participated in four crossover, placebo-controlled studies in which the treatment arms lasted for between 1 and 2 weeks, were reviewed. These studies had assessed the efficacy of this nitrate preparation by exercise testing and each had included exercise testing at the end of each treatment phase, 24 h after the last medication had been administered. There were no differences noted in the time to onset of angina, the time to onset of 1 mm ST segment depression or the total exercise duration between the two treatment phases, indicating an absence of rebound phenomena at the end of the dosing interval. The reason for the absence of a detectable pre-dose rebound is unclear, but the plasma concentration profile of 5-ISMN produced by the presently used preparation, resulting in a nitrate-low instead of nitrate-free interval, may have contributed.

Adult↗
PubMed1992

Prophylactic nitrate therapy in angina pectoris--is there an optimal treatment regimen?

1. Nitrates have a place in the prophylactic treatment of patients with angina pectoris. Their efficacy is not in doubt. 2. However, there may be some practical problems associated with their use, such as unreliable absorption, short duration of action, treatment-induced headache, development of nitrate tolerance and a suggested rebound phenomenon observed during intermittent dosing. Furthermore, patient convenience with treatment schedule and patient compliance have to be considered during prophylactic treatment. The present article discusses how many of these problems may be solved by selection of formulation as well as nitrate compound. 3. The development of controlled-release formulations producing sufficiently high nitrate plasma concentration during part of the day followed by nitrate-poor rather than nitrate-free interval, have the potential to prevent both nitrate tolerance and rebound phenomenon, and produce a sufficiently long duration of action with a convenient once daily regimen.

Angina Pectoris↗
PubMed1992

A comparative study of arterial and venous blood acetate concentration in cows fed different diets close to parturition.

Blood samples were collected from the coccygeal artery and a jugular vein two weeks before expected calving, one to five days after calving and three weeks after calving of cows which were fed either a high roughage or a low roughage diet from four weeks before to 14 weeks after calving. The mean venous acetate concentration ranged from about half to three-quarters of the arterial concentration. No differences were observed at any time between concentrations of acetate in either the arterial or venous blood of the cows on the different diets.

Acetates↗
PubMed1991

Evaluation of the antianginal effect of nifedipine: influence of formulation dependent pharmacokinetics.

Nifedipine capsules t.d.s. and an extended release formulation of nifedipine, nifedipine-ER tablets, given once daily in corresponding daily doses, have been compared with placebo in a double-blind, three-way cross-over study in 24 patients with stable angina pectoris. The objective was to study the influence on the antianginal effect of the different pharmacokinetics of several preparations of nifedipine. All patients received concomitant treatment with beta-adrenoceptor blockers. Antianginal efficacy was assessed by a dynamic exercise test at the end of the dosage intervals, i.e. 8 and 24 h after nifedipine capsules and nifedipine-ER, respectively, as well as 6 h after dosing. Six h after dosing the time of onset of chest pain and total exercise time were longer and total work was significantly higher during both nifedipine-ER (plasma concentration 260 nmol/l) and placebo treatment than after nifedipine capsules (plasma concentration 78 nmol/l). Time to 1 mm ST depression was longer during nifedipine-ER than during nifedipine capsule treatment. No significant difference was seen between nifedipine-ER and placebo. At the end of the dosage interval (24 and 8 h after nifedipine-ER and nifedipine capsules, respectively), no significant difference was found between nifedipine-ER (plasma concentration 75 nmol/l) and the other two treatments. However, placebo was superior to nifedipine capsules (plasma concentration 58 nmol/l) both in the time to onset of chest pain and total exercise time. The lack of effect at the end of the dosage interval was probably due to the subtherapeutic plasma nifedipine level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Primary prevention of sudden cardiovascular death in hypertensive patients. Mortality results from the MAPHY Study.

In a randomized primary prevention trial including 3,234 men with mild to moderate uncomplicated hypertension, the effect of the beta-blocker metoprolol or a thiazide diuretic as an initial antihypertensive therapy was compared regarding the risk of sudden cardiovascular death during a follow-up ranging from 2.3 to 10.8 years (median of 4.2 years). Only men aged 40 to 64 years were included in the study. The randomization of patients into the metoprolol (n = 1,609) or diuretic group (n = 1,625) was performed after stratification for age, smoking habits, serum cholesterol, and systolic blood pressure. At baseline the two treatment groups were well matched. Metoprolol was given in a mean dose of 174 mg daily and the mean dose of thiazide diuretic was either 46 mg hydrochlorothiazide daily or 4.4 mg bendroflumethiazide daily. Identical blood pressure control was achieved using the fixed therapeutic schedule. Total and cardiovascular mortality were significantly lower for metoprolol than for diuretics, owing to fewer deaths from coronary heart disease and stroke. Of the cardiovascular deaths, 78% were classified as sudden cardiovascular deaths (occurred within 24 h after the onset of symptoms). There were significantly fewer sudden cardiovascular deaths in the metoprolol group compared to the diuretic group (32 v 45, P = .017). The present results suggest that initial antihypertensive therapy with metoprolol is associated with a lesser incidence of sudden cardiovascular deaths than initial diuretic treatment in uncomplicated hypertension.

Adult↗
PubMed1991

Metoprolol versus thiazide diuretics in hypertension. Morbidity results from the MAPHY Study.

The present study in hypertensive men (40-64 years old) with untreated diastolic blood pressure above 100 mm Hg was aimed at investigating whether metoprolol (n = 1,609) given as initial treatment would lower the risk for coronary events (sudden death and myocardial infarction) more effectively than thiazide diuretics (n = 1,625). A substantial part of this study was the metoprolol arm of the Heart Attack Primary Prevention in Hypertension (HAPPHY) study. The HAPPHY study was a pooling of the effect of different beta-blockers, mainly metoprolol and atenolol, in which no favorable effect in relative risk was observed for atenolol as compared with diuretics. In the present study, 255 patients suffered definite coronary events during follow-up; 25% of these events were fatal, 39% were acute myocardial infarctions, and 36% were silent myocardial infarctions. The risk for coronary events was significantly lower in patients on metoprolol than in patients on diuretics (111 versus 144 cases, p = 0.001, corresponding to 14.3 versus 18.8 cases/1,000 patient years and a relative risk of 0.76 at the end of the trial; 95% confidence interval 0.58-0.98). This difference in risk has potentially important implications for clinical practice because of the large number of hypertensive patients who are at increased risk for coronary events. Because a placebo group, for ethical reasons, could not be included, relative risk can only be expressed in relation to diuretics. There was no difference between the two treatment groups in baseline characteristics, blood pressure during follow-up, or stroke rates. Thus, the difference in risk for coronary events is probably mediated via mechanisms other than blood pressure control. However, present data might suggest that different beta-blockers may have different efficacy in preventing coronary events. The reasons for this possibility are as yet unknown.

Adult↗