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Biomedical subjects

I Hjermann

Publications and source records attributed to I Hjermann.

At least 91 records · Page 5Linked to original sources
PubMed1987

A 24-week multicenter double-blind study of doxazosin and hydrochlorothiazide in patients with mild to moderate essential hypertension.

The new alpha1-adrenoceptor antagonist, doxazosin (DOX), was compared with hydrochlorothiazide (HCTZ), both drugs administered once daily, in a randomized double-blind study including 115 patients. The mean final daily doses used were DOX, 10.8 mg; HCTZ, 89.1 mg. There were no statistically significant differences between treatment groups for blood pressure (BP) changes except that HCTZ produced a significantly greater fall (p = 0.04) in supine systolic BP than DOX. The statistically significant mean differences in changes in lipid parameters (total cholesterol and total triglycerides) were in favour of DOX. The number of patients reporting side-effects were DOX, 27/57; HCTZ, 29/53, with two DOX- and five HCTZ-treated patients withdrawn due to side-effects. In the HCTZ-treated group, laboratory serum tests indicated 11 patients with abnormally low potassium and seven with abnormally high uric acid concentrations. The overall results suggest a benefit-to-risk ratio in favour of DOX.

Adult↗
PubMed1987

Aging and urinary vasopressin excretion in healthy men.

The influence of age on urinary excretion of arginine vasopressin (antidiuretic hormone) was examined in three groups of healthy men, 25 +/- 1 (n = 12), 40 (n = 44) and 50 years of age (n = 28) respectively. Despite increasing plasma vasopressin with progressive age (2.5 +/- 0.6 vs. 3.5 +/- 0.4 vs. 7.4 +/- 1.0 ng/l, respectively) (means +/- SE), urinary excretion of vasopressin turned out similar (6.7 +/- 1.0 vs. 6.8 +/- 0.8 vs. 6.9 +/- 0.6 ng/h). No differences in sodium excretion, serum osmolality and creatinine clearance appeared that could explain these findings. The present results suggest that age-related impairment of renal concentrating capacity is compensated for by increasing circulating plasma vasopressin. Furthermore, differences in tubular handling of the hormone with age may explain the present findings, and may be another compensatory mechanism for decreased urinary concentrating ability.

Adult↗
PubMed1987

Increased platelet size and release reaction in essential hypertension.

Basal platelet function was measured in 35 40-year-old men with untreated mild essential hypertension and compared with 44 age-matched normotensive men. The groups differed significantly with respect to platelet size in venous blood (hypertensive, 7.46 +/- 0.10 X 10(-15) l versus normotensive, 7.11 +/- 0.09 X 10(-15) l; P = 0.01) and arterial concentration of the platelet-specific protein beta-thromboglobulin (hypertensive, 1.11 +/- 0.23 nmol/l versus normotensive, 0.59 +/- 0.04 nmol/l; P = 0.02). The normotensive subjects had significantly higher beta-thromboglobulin (BTG) in venous than in arterial blood (P less than 0.01). The hypertensive men showed no such difference. In contrast to the normotensive subjects, the hypertensive group had reduced arterial compared with venous platelet count (P less than 0.01). This may reflect an increased liability in the hypertensive subjects to lose platelets through adherence to the cannula during arterial blood sampling. The above findings point to increased platelet activity in essential hypertension, particularly in arterial blood.

Adult↗
PubMed1987

Endocrine and haemodynamic responses to graded dopamine infusion in essential hypertension.

Hormonal, mean arterial blood pressure, forearm blood flow and heart rate responses to graded dopamine infusion (0.5-2.0 micrograms/kg/min) were examined in 10 men with untreated essential hypertension WHO group I (147 +/- 4/100 +/- 1 mmHg, means +/- SE), and in 10 normotensive men (129 +/- 2/85 +/- 1 mmHg), all 40 years old. Another 12 normotensive men (126 +/- 3/80 +/- 2 mmHg) were given only saline infusion. Dopamine increased heart rate significantly in the hypertensive group (8 +/- 2 beats/min, p less than 0.001), but the heart rate remained unchanged in the normotensive group (1 +/- 1 beats/min, NS). Although dopamine infusion tended to decrease mean blood pressure, the changes were not significantly different from those observed in the control group. No change in forearm blood flow was observed in either group. In the groups given dopamine, prolactin levels decreased only slightly compared to the control group given saline, the decrement tending to be more pronounced in the hypertensive group. Plasma vasopressin remained unchanged in both groups during dopamine infusion. These results indicate that hypertensive patients exhibit increased sensitivity to the cardiovascular effects of dopamine.

Adult↗
PubMed1986

Oslo Study Diet and Antismoking Trial. Results after 102 months.

The five year (60-month) results from the Oslo Study Diet and Antismoking Trial were published in the Lancet in December 1981. The trial involved 1,232 healthy men, aged 40 to 49 years, at high risk for coronary heart disease, with serum cholesterol values in the range of 7.5 to 9.8 mmol/liter (enzymatic method: 6.9 to 9.0, mean value 7.8 mmol/liter). Eighty percent of the men were daily cigarette smokers at the start of the study, and all participants were normotensive, i.e., systolic blood pressure was less than 150 mm Hg. Subjects were randomly assigned to either a control or intervention group. Follow-up visits were scheduled every six months for the intervention group and yearly for the control group. Once the trial was completed, the regular six-month follow-up visits were discontinued, but eight to nine years (96 to 108 months) after the start of the trial, participants were called for a new follow-up. Risk factors were recorded, and clinical events were diagnosed according to the same procedure as during the trial. The mean serum cholesterol levels in the intervention group remained unchanged three years after the end of the trial, but the cholesterol levels in the control group declined. Daily cigarette smoking increased in the intervention group but remained stable in the control group. At the new follow-up, the difference in incidence of fatal and nonfatal myocardial infarction and sudden coronary death was the same as at the end of the trial three years earlier, yielding significant differences between the two groups for sudden death, total coronary death, and total coronary events. Although the study was not designed to show differences in total mortality, this difference became marginally significant, with 19 deaths in the intervention group and 31 in the control group. It is concluded that although net differences in risk factors between the two groups had been reduced during the three years after the regular intervention period, the significant difference in coronary events and sudden death was maintained.

Adult↗
PubMed1986

Central dopaminergic control of prolactin in essential hypertension.

An exaggerated, early prolactin response (p less than 0.01) was observed in ten patients with untreated essential hypertension (148 +/- 4/97 +/- 1 mmHg, means +/- SE) compared with ten healthy normotensive men of the same age (124 +/- 3/78 +/- 2 mmHg) after administration of metoclopramide, a competitive dopamine antagonist. The normotensive peak value of prolactin never exceeded that of the hypertensive (p less than 0.05). Since prolactin is considered an indicator of central dopaminergic activity, these findings suggest an altered central dopaminergic activity in mild essential hypertension.

Adult↗
PubMed1986

Serum phosphate and sympathetic tone in mild essential hypertension.

Forty-year old, normocalcaemic men with mild essential hypertension (n = 35) had decreased serum phosphate (p less than 0.001) concomitant with elevated plasma adrenaline (p less than 0.03) and heart rate (p less than 0.001). All had unchanged serum immunoreactive parathyroid hormone concentrations compared to age-matched normotensive control men (n = 44). Serum phosphate levels correlated negatively with plasma adrenaline (p less than 0.05), plasma noradrenaline (p less than 0.05), mean blood pressure (p less than 0.001) and heart rate (p less than 0.05). Serum phosphate was significantly lowered by infusion of small amounts of adrenaline at all four infusion rates in a hypertensive group (n = 12) while a similar effect was obtained only at the two highest infusion rates in a normotensive group (n = 10). No change in serum calcium was observed in either group. Thus, hypophosphataemia appears to be inversely related to sympathetic tone in essential hypertension.

Adult↗
PubMed1986

Platelet volume, platelet release reaction and platelet response to infused adrenaline are increased in essential hypertension.

Hypertensive men aged 42 (n = 35) were compared to normotensive men of similar age (n = 44). Platelet numbers were similar in the two groups, but hypertensive men had larger venous platelets than the normotensive (7.46 versus 7.12 femtoliter, p = 0.01). Plasma concentration of beta-thromboglobulin (BTG), a marker of platelet release reaction, was increased in arterial blood in hypertension (40 versus 21 micrograms/l, p = 0.02). The normotensive subjects had markedly higher BTG concentration in venous compared to arterial blood (p less than 0.01), but this arterio-venous difference was not present in the hypertensive group. Twelve normotensive subjects received infused saline, which did not induce changes in platelet variables. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects, with dose gradually increasing to 0.04 microgram/kg/min. Platelet count increased in both groups, but significantly more in the hypertensive group. Platelet volume and BTG both increased markedly in the hypertensive group, but not in the normotensive men. Thus, young men with hypertension have increased platelet activity and increased sensitivity to exogenous adrenaline.

Adult↗
PubMed1986

Increased plasma vasopressin in low renin essential hypertension.

Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 +/- 2.2 [SE] vs 7.5 +/- 1.0 pg/ml; p less than 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 +/- 0.04 vs 0.46 +/- 0.06 Goldblatt units X 10(-4)/ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 +/- 12 vs 68 +/- 6 pg/ml; p less than 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 +/- 0.8 vs 3.5 +/- 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective beta-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 +/- 6.4 to 13.5 +/- 4.2 pg/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1985

Coronary risk factors and their pathway of action through coronary raised lesions, coronary stenoses and coronary death. Multivariate statistical analysis of an autopsy series: the Oslo Study.

From 1972 to 1973, 16,202 Oslo men, aged 40 to 49 years, were examined for cardiovascular disease and coronary heart disease (CHD) risk factors. This report describes the results of autopsy examinations from 204 of 471 men who died in this cohort with regard to associations between selected risk factors and (1) raised coronary atherosclerotic lesions (RL), (2) coronary artery stenosis, and (3) CHD death. Total serum cholesterol and blood pressure levels were positively associated with all 3 measures of coronary atherosclerosis and its complications, both in univariate and multivariate analyses, whereas high-density lipoprotein (HDL) cholesterol was highly and inversely related. Triglyceride levels, cigarette smoking, social class and physical activity at work and at leisure were not significantly associated with either of the 3 measures. When RL was added to the model with stenosis as the dependent variable, the risk factors no longer appeared as independent; this is consistent with the hypothesis that these factors, when significant, work through the development of RL to produce stenosis. HDL cholesterol was the only risk factor independently and significantly associated with CHD death when RL or stenosis or both were put into the model for CHD. This points to the possibility of HDL cholesterol also working through mechanisms other than the prevention of RL and stenosis toward CHD death.

Adult↗
PubMed1985

Multiple risk factor intervention in coronary heart disease.

Intervention studies have shown that the primary prevention of coronary heart disease (CHD), or at least its postponement, is possible in a large proportion of individuals. In the Diet-Antismoking Trial of the Oslo Study, it was concluded that in healthy middle-aged men at high risk of CHD (serum cholesterol, 7.5-9.8 mmol/l, and 80% were smokers), the incidence of myocardial infarction and sudden coronary death was reduced by 47% in the intervention group compared to the controls. This study did not have the power to single out the separate effect of cessation of smoking on the incidence of CHD. A significant positive effect of antihypertensive treatment on cerebrovascular events has been shown in many studies, but unfortunately no significant preventive effect on the first event of CHD has been demonstrated. In the Oslo Study a significant positive correlation was found between total serum cholesterol concentration and blood pressure. It is suggested that both risk factors might be treatable or preventable to some extent by the same measures. In health education, both the population mass strategy for prevention and the high risk strategy for individual intervention are important. The frequent coexistence of two or more risk factors should be kept in mind. For CHD prevention, non-pharmacological intervention seems at the moment to be the safest and very often probably the most effective approach.

Adult↗
PubMed1985

The Oslo Study: diet and antismoking advice. Additional results from a 5-year primary preventive trial in middle-aged men.

In this randomized, primary prevention trial of 1,232 high-risk, middle-aged Oslo men, advice during 5 years about diet and smoking brought about a significant reduction (47%) in incidence of first major coronary heart disease (CHD) events in the intervention group compared with controls. Data are presented indicating that the net difference of 10% in serum cholesterol between groups was the main cause for this achievement and that the antismoking factor, due to a rather small net difference in quit rates (17 and 24% in control and intervention groups, respectively), contributed to a lesser degree. Analysis of social class reveals that the favorable results in the intervention group were present in all social strata, despite the unexpected finding that lower class men experienced a lower CHD incidence than men of higher socioeconomic status. Antismoking advice was especially effective in lower class intervention group men. Among cigarette quitters, lower social class men reduced their serum cholesterol more than higher social class men. However, for the total intervention group, higher status men had at least as great a reduction in serum cholesterol as did lower status men. With endpoint follow-up extended to 8.5-10 years, additional cases of CHD (nonfatal and fatal myocardial infarction and sudden death) numbered 7 and 10 in the intervention and control groups, respectively; CHD cases throughout the trial totaled 25 and 45 (P approximately equal to 0.02). Total deaths numbered 19 and 31, respectively (P approximately equal to 0.05).

Body Weight↗