Biomedical subjects
Publications and source records attributed to S L Rasmussen.
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In a group of 37 patients with definite acute myocardial infarction (AMI) allocated to treatment with either alprenolol (n = 20) or placebo (n = 17) serial determinations of concentrations in serum of myoglobin (S-Mb), creatine kinase (S-CK), aspartate aminotransferase (S-ASAT) and lactate dehydrogenase (S-LDH) were performed. The median peak levels of S-Mb, S-CK and S-LDH were significantly (P less than 0.05) lower among patients treated with alprenolol. The median of the estimated infarct size based on S-CK curves was also significantly (P less than 0.01) lower in the alprenolol group. There was no significant difference between the estimated infarct size based on S-Mb values in the two groups. It is concluded that the present study provides indirect evidence for the assumption that early beta-blockade in AMI can reduce infarct size.
Because of the associations between Alzheimer's disease and Down's syndrome, advanced maternal and paternal age, which are risk factors for Down's syndrome, have been proposed as risk factors for Alzheimer's disease. Parental age data were obtained from a group of patients with Alzheimer's disease and compared with comparable data for a group of nondemented subjects matched for age and socioeconomic level. As a way of detecting a familial causative factor in Alzheimer's disease, life-span data were also collected for parents of patients and control subjects. The results indicated that patients with Alzheimer's disease and nondemented control subjects did not differ in the mean ages of their parents at the time of the patients' or subjects' births, nor did parental age correlate significantly with age at onset of disease. Moreover, the parents of patients with Alzheimer's disease did not differ in mean age at death from the parents of nondemented control subjects.
The effect of long-term treatment with alprenolol on left ventricular function was investigated in a controlled double-blind study of 15 patients with ischaemic heart disease (alprenolol 6, placebo 9), by measurement of systolic time intervals (STI). Significant prolongation of QS2I was observed in patients treated with alprenolol (p less than 0.05), while changes in PEPI, LVETI and PEP/LVET were all insignificant. The heart rate x systolic blood pressure product (RPP) was significantly reduced in the alprenolol group (p less than 0.05). The data suggest that long-term treatment with alprenolol did not impair left ventricular function as evaluated by STI, and that myocardial oxygen demand, assessed by RPP, was reduced during the treatment.
Doxorubicin (Adriamycin) was administered by continuous infusion to reduce peak plasma levels and thus lessen cardiac toxicity. Cardiotoxicity was monitored by noninvasive methods, and endomyocardial biopsy specimens were studied by electronmicroscopy. Cardiotoxicity was compared in 21 patients receiving doxorubicin intravenously over 48 or 96 hours and in 30 control patients treated by standard intravenous injection. Both groups were studied prospectively and were well matched by risk factors for doxorubicin cardiotoxicity. The median cumulative dose for those receiving continuous infusion was 600 mg/m2 body surface area (range, 360 to 1500 mg/m2) compared with 465 mg/m2 (range 290 to 680 mg/m2) in the control group (p = 0.002). Fourteen of the 30 patients in the control group showed severe morphologic changes in the biopsy specimens, precluding further doxorubicin administration, as compared with two of 21 patients receiving the drug by continuous infusion (p less than 0.02). The mean pathologic score for the infusion group, 0.9, was lower than the mean for the control group, 1.6 (p = 0.004). Antitumor activity was not compromised. Decreasing peak plasma levels of doxorubicin by continuous infusion reduces cardiotoxicity.
Thirty-eight patients with advanced breast cancer, multiple myeloma, and malignant lymphoma were treated with partially purified (about 0.1%) leukocyte interferon. Patients were treated with a remission-induction schedule of 3 million to 9 million antiviral units daily intramuscularly for 4 to 26 weeks. Responding patients were maintained on a schedule of 3 million U three times weekly. Tumor regression was observed in seven of 17 patients with breast cancer. Six of 10 patients with multiple myeloma responded with a decrease of at least 50% in serum myeloma protein levels or Bence Jones protein excretion. Six of the 11 lymphoma patients achieved tumor regression. Complete remissions occurred in two patients. Of the 19 responding patients, five remain on study for 52 to 63 weeks. Toxicity included low-grade fever, fatigue, anorexia, and partial alopecia. Myelosuppression (lowest median leukocyte count, 2500/mm3; granulocytes, 1300/mm3) occurred in most patients. On the basis of this pilot study, we conclude that leukocyte interferon can induce tumor regression in patients with advanced cancer.
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A double-blind study of alprenolol versus placebo was done in patients with definite or suspected myocardial infarction to show the effect of the drug on mortality-rate after a year of treatment in patients aged less than or equal to 65 and to study the tolerance of the drug by patients greater than 65 years of age. The dose given was 5--10 mg intravenously, followed by 200 mg twice a day, orally. Patients in whom beta-blockade was contraindicated were excluded. All deaths, side-effects, and dropouts were recorded. Of the 480 patients in the study, 238 patients received alprenolol and 242 placebo. During the year of follow-up 108 patients dropped out from the study. Mortality was not reduced in patients greater than 65 years of age. In those less than or equal to 65 years alprenolol significantly reduced mortality-rate (20% mortality in placebo group vs 9% in treated group). There was also a significant reduction in mortality-rate among those with definite infarction (28% in the placebo vs 15% in the treated group).
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Nitric oxide (NO) is an inhibitory neurotransmitter released by non-adrenergic and non-cholinergic neurons that innervate the smooth muscles of the gastrointestinal tract. We examined whether NO, derived from a sustained-release preparation of isosorbide dinitrate, influenced gastric emptying and gastroduodenal motility after a meal. Eleven healthy volunteers participated in a double-blind, placebo-controlled, cross-over study. Each subject ingested 40 mg isosorbide dinitrate orally as a sustained-release formulation or oral placebo, in random order. Gastric emptying and gastroduodenal motility were measured using scintigraphic and manometric techniques. Isosorbide dinitrate did not change the area under the curve of gastric retention versus time, and did not influence the frequency of antral contractions as assessed at 15-min intervals or the integrated duodenal motility index, as recorded over consecutive 15-min periods. A 40 mg single dose of sustained-released isosorbide dinitrate does not seem to alter gastric emptying or gastroduodenal motility after a meal.