[Can readmissions be prevented? 1-year data from a medical ward in Oslo].
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Biomedical subjects
Publications and source records attributed to E Lorentsen.
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The calcium-blocking agent nifedipine, which possesses vasodilating potency, was tested in 8 patients with peripheral arterial insufficiency. 10 mg sublingually significantly decreased systolic arm and ankle blood pressure. Neither blood flow nor local peripheral resistance in the calf and the forefoot at rest and the calf during postischemic reactive hyperemia changed significantly. During postischemic hyperemia in the forefoot, the drug significantly reduced peak blood flow and increased local peripheral resistance. The drug-induced reduction in forefoot peak blood flow was correlated to the fall in systolic arm and ankle blood pressure. It is suggested that nifedipine may shorten the claudication distance in patients with peripheral arterial insufficiency.
A prospective, randomised, double-blind study was performed to compare the effects of propranolol and placebo on sudden cardiac death in a high-risk group of patients who survived acute myocardial infarction. Altogether 4929 patients with definite acute myocardial infarction were screened for inclusion: 574 (11.6%) died before randomisation, and 3795 (77%) were excluded. Five hundred and sixty patients aged 35 to 70 years were stratified into two risk groups and randomly assigned treatment with propranolol 40 mg four times a day or placebo. Treatment started four to six days after the infarction. By one year there had been 11 sudden deaths in the propranolol group and 23 in the placebo group (p less than 0.038, two-tailed test analysed according to the "intention-to-treat" principle). Altogether there were 25 deaths in the propranolol group and 37 in the placebo group (P less than 0.12), with 16 and 21 non-fatal reinfarctions respectively. A quarter of the patients were withdrawn from each group. Withdrawal because of heart failure during the first two weeks of treatment was significantly more common among propranolol-treated patients than among the controls, but thereafter the withdrawal rate was the same. The significant reduction in sudden death was comparable with that after alprenolol, practolol, and timolol, which suggests that the mechanism of prevention is beta-blockade rather than any other pharmacological property of the individual drugs.
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The calf blood flow and the ankle blood pressure at rest and during post-ischemic reactive hyperemia were measured by an airfilled rubber segment plethysmograph in 5 patients with hyperviscosity of the blood. The patients had no signs of peripheral arterial disease. A normal flow and pressure pattern was obtained. It is concluded that hyperviscosity does not contribute significantly to the peripheral resistance during reactive hyperemia in the patients studied. The importance of hyperviscosity for peripheral resistance in patients with atherosclerosis obliterans is discussed.
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The venous blood pressure response to static muscular exercise was studied in seven young normal subjects by the occluded-limb technique. A slight pressure increase was obtained during the first seconds of the contraction period. Then the pressure response subsided, and the control level was reached after 1/2-1 1/2 min despite sustained contraction. The response was of the same type as that elicited by a voluntary deep breath, but usually of lesser magnitude. It seems to differ from the response to dynamic muscular exercise, suggesting that a continuous stiffening of the capacitance vessels, to maintain a high venous response, is not needed to the same extent during static muscular exercise. In previous studies a similar pressure increase has been obtained during short-lasting static muscular exercise. The present study shows that this pressure increase is confined to the initial part of the contraction period. Observations made after administration of phenoxybenzamine and atropine indicate that the venomotor response is mediated through sympathetic adrenergic nerves.