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Biomedical subjects

L Hansson

Publications and source records attributed to L Hansson.

At least 469 records · Page 26Linked to original sources
PubMed1980

Human leucocyte antigens in patients with previous essential malignant hypertension.

1. Human leucocyte ABC antigens were determined by means of a lymphocytotoxicity test in 27 patients with previous essential malignant hypertension and in 500 blood donors. 2. In 18 patients with grade IV retinopathy human leucocyte antigen B15 (HLA B15) was found in 44%, as compared with 23% in the control subjects (P = 0.888). 3. All patients with HLA B15 had a positive family history for hypertension. 4. In 18 patients with grade IV retinopathy HLA B15 was found in eight whereas none of the nine patients with grade III retinopathy had this antigen (P = 0.039). 5. Of the 27 patients, 19 had a positive family history of hypertension and of these eight had HLA B15, whereas none of the eight patients with a negative family history had this antigen (P = 0.068). 6. The findings do not rule out that HLA B15 may be associated with the development of the malignant phase in patients with essential hypertension, but a statistically significant relationship could not be established.

Adolescent↗
PubMed1980

Noise as a contributory factor in the development of elevated arterial pressure. A study of the mechanisms by which noise may raise blood pressure in man.

Arterial pressure and other hemodynamic variables (stroke volume (SV), cardiac output and total peripheral resistance) were studied in 18 healthy males before and during exposure to recorded industrial noise. All measurements took place under strictly standardized conditions in a noise laboratory. the frequency distribution and level of noise used for stimulation were continuously monitored and kept constant within close limits throughout the experiments. SV was measured with impedance cardiography. Indirect blood pressure (BP) in the brachial artery was measured with an automatic device and the derived parameters, cardiac output and total peripheral resistance, were calculated from these measurements. Compared with resting conditions at 40 dBA, stimulation with industrial noise at 95 dBA caused significant increases in diastolic BP, mean arterial pressure and total peripheral resistance. Minor but statistically significant reductions of SV and cardiac output were seen. Heart rate and systolic BP did not change. These alterations of the hemodynamic variables persisted throughout 20 min of noise stimulation and were maintained for 5 min following cessation of noise stimulation. All variables had returned to their initial levels 10 min after discontinuation of noise stimulation. This study suggests that exposure to industrial noise at levels prevailing during several industrial processes may cause acute elevations of arterial BP and peripheral vascular resistance. In animal studies, repeated elevations of BP due to exposure to noise have been shown to cause a permanent elevation of BP. Therefore, we suggest that noise may be one of several external stimuli contributing to the development of arterial hypertension in man.

Adult↗
PubMed1980

Borderline hypertension. Hypertension seminars at Ostra Hospital, Göteberg, Sweden.

Borderline hypertension was the topic of one of the "Hypertension seminars" arranged by the Hypertension Section at the Ostra Hospital, Göteborg, Sweden. On that occasion Professor Stevo Julius, Ann Arbor, Michigan USA, was an invited guest. During the seminar, various aspects of borderline hypertension were discussed, e.g. the natural history, hemodynamics and management of this condition. The present review is based on these discussions.

Adolescent↗
PubMed1979

Hemodynamic and hormonal changes induced by noise.

Eighteen healthy male volunteers with normal hearing were exposed to industrial noise at different sound levels (75, 85 and 95 dB A) in a noise laboratory. Blood pressure, heart rate, stroke volume and cardiac output were recorded with noninvasive techniques. Adrenaline and noradrenaline concentration in venous plasma were analyzed before and during noise exposure. The mean resting blood pressure of the whole group was 120/70 mm Hg. During noise stimulation diastolic blood pressure increased (12.2%, p less than 0.001) as did mean arterial pressure (6.6%, p less than 0.001) and total peripheral resistance (12.7%, p less than 0.001). Stroke volume (7.3%, p less than 0.001) and cardiac output (5.0%, p less than 0.01) were both reduced at 95 dB A. Heart rate and systolic blood pressure did not change significantly. At 75 and 85 dB A there were similar but smaller changes in the hemodynamic parameters. There were no changes in adrenaline and noradrenaline in plasma during maximal noise exposure. The noise induced hemodynamic changes remained 5 minutes after the noise stimulation was stopped but had disappeared after 10 minutes of rest.

Adult↗
PubMed1979

Malignant hypertension--improving prognosis in a rare disease.

A follow-up was made of 69 patients diagnosed as having malignant hypertension during 1969--76, essential in 26, secondary in 39 and unclassified in 4. A clear male dominance was seen (41 men, 28 women), particularly in the group with essential hypertension (18 men, 8 women). The mortality in this series was less than in previously published series. Thus, the 5-year survival rate was 75% in the patients with essential and 72% in those with secondary hypertension. In part this was due to haemodialysis and renal transplantation. The importance of renal function at the time of diagnosis was evident in this study. In most patients with essential hypertension and serum creatinine levels below 300 mumol/l, renal function could be maintained or improved when antihypertensive treatment was instituted, whereas progression of the renal damage was seen in those with serum creatinine levels above 300 mumol/l in spite of antihypertensive treatment with 3 or more drugs. The incidence of new cases of malignant hypertension tended to decrease during the observation period, particularly as regards essential hypertension.

Adolescent↗
PubMed1979

Effect of treatment of hypertension in the primary preventive trial, Göteborg, Sweden.

1 A treatment group comprising 635 hypertensive men (casual SBP greater than 175 or DBP greater than 115 twice) was compared with a reference group (n = 391 men; casual SBP greater than 175 or DBP greater than 115 only at screening). All men belonged to the same population sample of 7,455 men aged 47-54 yr. 2 The two groups did not differ with respect to age, smoking habits or cholesterol values, but screening BPs were higher in the treatment group. 3 During 4.3 years' follow-up there was a significantly lower total death rate in the treatment group compared with reference group. 4 There was also a strong tendency towards lower incidence of non-fatal myocardial infarction (P = 0.06). The pooled incidence of non-fatal myocardial infarction and fatal CHD was lower in the treatment group than in the reference group (P less than 0.03).

Adrenergic beta-Antagonists↗
PubMed1979

Effect of Sar1-ala8-angiotensin II on blood pressure and renin in Bartter's syndrome, before and after treatment with prostaglandin synthetase inhibitors.

Three patients suffering from Bartter's syndrome were studied before and after 5 days of treatment with the prostaglandin synthetase inhibitors, aspirin and indomethacin. Saralasin was given by intravenous infusion in increasing doses from 0.6 to 42 micrograms/min.kg/BW. During saralasin infusion a blood pressure reduction was observed in all patients. Aspirin treatment did not affect this response and nor did it affect other manifestations of the syndrome. Indomethacin treatment changed the blood pressure response to saralasin in such a way that the blood pressure was increased in one patient and was unchanged in the other. Indomethacin also tended to normalize other features of Bartter's syndrome, such as the hyperreninaemia and angiotensin unresponsiveness, but did not affect the hypokalaemia. The saralsin effect on blood pressure is thus evidently inversely related to the prevailing activity of the renin-angiotensin system in this condition also, and the patients obviously depended on the renin-angiotensin system to maintain their blood pressure. Our findings, together with data in the literature, indicate that angiotensin unresponsiveness of the vascular bed is not a primary feature in Bartter's syndrome. Chloride loss is currently thought to be the basic abnormality and this may link the Bartter's syndrome with other diseased states characterized by chloride loss, such as the syndrome of habitual vomiting and chronic treatment with loop diuretics.

Adolescent↗
PubMed1979

Agarose gel electrophoresis of duodenal juice in normal condition and in children with malabsorption.

Agarose gel electrophoresis (at pH 8.6) was used for qualitative determination of pancreatic enzymes in duodenal juice. The various enzymes were identified by staining techniques with specific chromogenic substrates, by quantitative determination of enzymes in eluates of gel slices, and by immunoelectrophoresis. The various protein bands corresponded to the following enzymes (from the anode to the cathode): chymotrypsin, trypsin, carboxypeptidase A, chymotrypsin, amylase (around the slit), lipase, elastase, and trypsin. The method was applied to a study of exocrine pancreatic function in 10 adults and 83 children suspected of having malabsorption. The duodenal juice, also analyzed for trypsin and amylase content, was collected in fasting condition and after a test meal of water. In patients with normal pancreatic function, all the enzyme bands were present and easy to recognize. In 87 patients carboxypeptidase A was present as two bands in 68 (80%), anodal trypsin as two bands in 39 (45%), and cathodal trypsin as two bands in 85 (97%). Electrophoresis of duodenal juice gave as much information from the fasting sample as after the test meal. Six children with pancreatic insufficiency (cystic fibrosis and Shwachmar's syndrome) had no or only faintly stained enzyme bands and a strongly stained albumin-containing band most anodally. The method is simple, rapid, and useful in routine work. The combination of this qualitative test with a quantitative one (e.g. trypsin determination) provides good information about exocrine pancreatic function.

Adolescent↗
PubMed1979

Tienilic acid in mild to moderate hypertension.

Tienilic acid has blood pressure lowering properties alone and in combined treatment with beta-adrenergic blocking agents; 250 mg of tienilic acid seems to correspond to 50 mg of hydrochlorothiazide. Tienilic acid effectively reduces serum urate and has no marked or rapid effect on potassium balance. During short-term treatment, no impairment of glucose tolerance was found.

Adrenergic beta-Antagonists↗
PubMed1979

Blood pressure reduction and vascular adaptation. A study on long-term effects of treatment with mefruside or atenolol.

Systemic BP reduction, calf blood flow and vascular resistance in the calf were determined in forty-two previously untreated patients with mild to moderate essential hypertension (WHO I-WHO II) before and after 6 weeks, 6 months and 18 months of BP-lowering treatment with mefruside (25 mg daily) or atenolol (100--400 mg daily). Blood flow was determined with venous occlusion plethysmography using a mercury-in-rubber strain gauge technique in the supine patient. Auscultatory BP was measured on the right arm simultaneously with the flow determinations and resistance was calculated from the flow and pressure. BP was reduced significantly and to the same extent by the two drugs. In the atenolol group a rise in resting resistance and a corresponding fall in resting blood flow was seen initially. These changes were entirely normalized during continued treatment for 18 months. In the mefruside group no significant haemodynamic changes during treatment were observed at rest apart from the BP fall. None of the drugs reduced resistance at "maximal" vasodilatation, indicating that no regress of the hypertensive structural changes of the calf blood vessels had taken place.

Adult↗
PubMed1979

Blood cadmium and plasma zinc measurements in acute myocardial infarction.

Blood cadmium and plasma zinc were measured in a series of 47 patients admitted for myocardial infarction (MI) and in 37 control subjects divided into 3 groups. Certainly increased blood cadmium values, for the MI patients, were found in 33%. The mean blood cadmium value of the MI series was significantly (P less than 0.001), but not invariably, higher against the control subjects. The difference between the zinc values of the series was studied in 35 MI patients with raised serum enzyme activity. In MI patients, the mean plasma zinc content was significantly (0.001 less than P less than 0.01) lower than in healthy controls. Of the enzymes, the highest positive correlation was found between the ratio of blood cadmium to plasma zinc and the GOT activity. Of the ratio, the MI patients had values in excess of the controls range in 43%, and values within the limits of the healthy controls in 40%. Therefore, the rise in the ratio is of limited value for the diagnosis of myocardial infarction in an individual patient.

Acute Disease↗