Biomedical subjects
Publications and source records attributed to H M Redetzki.
The Vaughan Williams system of classification of antiarrhythmic drugs provides valuable information concerning their electrophysiologic effects and mechanism of action. Despite its limitations in predicting the clinical effectiveness for treatment of specific arrhythmias, this classification is helpful in allowing many correlations between different drugs and their expected actions and adverse effects.
Diminished gastric motility and lack of bowel sounds have been observed in astronauts aboard the Space Shuttle (4). In this study subjects were given scopolamine 0.6 mg with d-amphetamine 5 mg with and without neostigmine 15 mg. Neostigmine 15 mg alone was also compared with placebo for effect on gastric emptying time. In an additional test, subjects performed head movements in a rotating chair to an end-point of motion sickness short of vomiting. Ten ounces of isotonic saline containing 1 mCl of Tc 99mDPTA was ingested 2 h after the medications and immediately after rotation. The counts from stomach contents were monitored with a Picker small field of view gamma camera every 30 s for 1 h. Gastric motility was inhibited by scopolamine and amphetamine with 14% residual count at the end of 1 h. When neostigmine was added to this combination the results were in the placebo range. Motion sickness produced a profound inhibition of gastric emptying with a 47% residual count. The results indicate that the gastric stasis encountered in space is due mainly to motion sickness with a minimal contribution from the antimotion sickness drugs.
UNLABELLED: Eight subjects, male and female, were rotated using the step method to progressively increase the speed of rotation (+2 rpm) after every 40 head movements to a maximum of 35 rpm. The end-point for motion sickness was the Graybiel Malaise III total of symptoms short of frank nausea. The drug treatments were placebo, scopolamine 0.6 mg and 1 mg, scopolamine 0.6 mg/d-amphetamine 10 mg, scopolamine 1 mg/d-amphetamine 10 mg and amphetamine 10 mg. RESULTS: Scopolamine increased tolerated head movements over placebo level by +81, scopolamine 1 mg + 183, d-amphetamine + 118, scopolamine 0.6/d-amphetamine + 165, and scopolamine 1 mg/d-amphetamine 10 mg + 201. DISCUSSION: The drugs effective in preventing motion sickness are divided into those with central acetylcholine blocking activity and those which enhance norepinephrine activity. A combination of both of these actions produces the most effective antimotion sickness medications. CONCLUSIONS: The balance between the acetylcholine and norepinephrine activity in the CNS appears to be responsible for motion sickness.
Acute ethanol ingestion by human alcoholic subjects produces a marked decrease in serum folate levels within 16 hr. A similar decrease occurs in rats and can be explained by a marked increase in urinary folate excretion following ethanol treatment. To assess the effects of acute ethanol ingestion on urinary folate excretion in healthy human volunteers, two studies were carried out at initial ethanol dose levels of 0.8 g/kg and 1.0 g/kg, respectively. Blood ethanol levels peaked at 70 mg/dl in the first study, but in the second study were 100 +/- 20 mg/dl through 6 hr. Only in the second study were urinary folate levels significantly increased by ethanol administration, and this 8 hr after ingestion. This increase was accompanied by a decrease in urine volume so that in neither study was the total amount of urinary folate excreted from 0-12 hr increased by ethanol ingestion. Studies with various dose levels of ethanol in rats showed that there was a linear dose-response relationship between the total urinary folate excretion and the dose of ethanol. Peak urinary ethanol levels also correlated with urinary folate excretion. These results suggest that doses of ethanol larger than 1.0 g/kg produce increases in urinary folate excretion and that the inability to observe large increases in studies in human subjects is probably related to the limited doses of ethanol chosen.
This project has employed a computerized pursuit meter which has a high correlation with operational performance (2) to test the principal antimotion sickness drugs. Proficiency scores on the pursuit meter task were improved over placebo scores in subjects with d-amphetamine 10 mg and 5 mg, the combination of promethazine 25 mg plus scopolamine 0.4 mg with d-amphetamine 10 mg, and the combination of scopolamine 1 mg with d-amphetamine 10 mg. Scores were not significantly different from placebo scores in tests with scopolamine 0.25 mg, 0.5 mg, or 0.6 mg; marezine 50 mg; meclizine 50 mg; or dimenhydrinate 50 mg. This was also true for the combination of scopolamine 1 mg with d-amphetamine 5 mg, and that of promethazine 25 mg with d-amphetamine 10 mg. A statistically significant decrement of performance scores was seen with scopolamine 1 mg or 0.8 mg, and with promethazine 25 mg oral or 25 mg I.M. The combination of promethazine 25 mg with scopolamein 0.4 mg, and that of promethazine 25 mg oral plus 25 mg I.M. with d-amphetamine 10 mg, also gave significant decrements from placebo scores. These results indicate that selected doses and combinations of antimotion sickness drugs can be used without loss of operational proficiency.
On April 25, 1983, 1,780 lbs of lead monoxide were dumped from a truck on a 1.5 mile stretch of highway. Cooperation between local and state police, health agencies and the Poison Control Center in Shreveport resulted in the evacuation of 120 residents, rapid cleanup by flushing and sweeping of the highway with subsequent scooping of surface soil from both sides of the highway, and setting up of an area lead screening clinic. Initial tests on about 114 residents and cleanup workers included blood lead and FEP analysis from capillary blood (fingerstick). Five of these were elevated, however, retesting with venous blood gave normal blood lead values. Complaints of exposed individuals centered on gastrointestinal upsets (nausea, vomiting, cramping) and upper respiratory irritation. The differences between clinical manifestations of acute and chronic lead poisoning will be emphasized.
The possible influence on operational proficiency of the side effects of the anti-motion sickness drugs was investigated using a computerized pursuit meter as the test device. The medications and doses tested were scopolamine (Hyoscine) 0.25 mg and 0.50 mg oral doses, promethazine (Phenergan) 25 mg oral and 25 mg I.M. doses. Combinations of promethazine 25 mg with 10 mg d-amphetamine (Dexadrine) oral were also used, as was a combination of promethazine 25 mg oral with promethazine 25 mg I.M. and 10 mg of oral d-amphetamine. The proficiency on the pursuit meter task was not significantly altered by 0.25 mg or 0.50 mg doses of scopolamine. The combination of promethazine 25 mg oral with 10 mg d-amphetamine did not produce a significant decrement of performance. When promethazine 25 mg was given as an oral or I.M. dose without amphetamine the decrement of performance was significant and was approximately equivalent to an alcohol blood level of 25-50 mg% (one-two drinks). When a combination of promethazine 25 mg oral plus promethazine 25 mg I.M. with 10 mg d-amphetamine was tested, the error scores were significantly lower than with the oral or I.M. dose of promethazine. This combination also produced an error score significantly higher than placebo level. Promethazine by the I.M. route was slowly absorbed and 6 of the 10 subjects reported drowsiness at 6 h post injection.
Injection of mice with a single ip dose of 2g/kg of ethanol leads to time dependent increases of lactic dehydrogenase plasma isoenzymes indicative of myocardial damage. Electron microscopic analysis of the myocardium shows changes in mitochondrial structure, endoplasmic reticulum and myofibrils. Pretreatment of the animals with 86 units of alpha tocopherol partially prevented the changes in isoenzyme patterns and reduced the electron microscopic evidence of myocardial damage. The study supports previous findings that some of the toxic effects of alcohol might be mediated through free radical mechanisms leading to lipid peroxidation and that the ameliorating effect of alpha tocopherol could relate to its function as antioxidant and free radical scavenger.
Whether vitamin E treatment might have a protective effect in paraquat poisoning was examined in male rats which received single ip paraquat injections in the LD50 dose range (14.8 mg cation/kg body weight). Vitamin E (d, alpha-tocopherol acetate in soybean oil) was administered either 30 minutes after paraquat (923 IU/kg ip) followed by a second injection 24 hours later (462 IU/kg im), or 2 hours before paraquat (1,000 IU/kg im) followed by a second injection 26 hours later (500 IU/kg im). In neither experimental arrangement did the vitamin E therapy alter the acute (7 day) mortality nor reduce the characteristic pathological lung changes observed at death or in 30-day survivors examined by light microscopy when compared with an equal number of non-treated control animals.
We compared results obtained with four commercially available kits for the enzymatic (alcohol dehydrogenase) determination of ethanol in blood, in a practical test in which standardized blood samples were used. Each of the kits yielded reliable results with acceptable reproducibility. A tendency to record slightly lower values in the intermediate and high alcohol range is most likely related to incomplete (inhomogeneous) deproteinization. Blood samples containing ethanol plus various concentrations of methanol and isopropanol were analyzed to evaluate the specificity of assays. Highly toxic blood concentrations of methanol (1.5 g/liter) increased apparent ethanol values only insignificantly, but even small concentrations of isopropanol (0.5 g/liter) interfered in all kits to different but substantial extents. The specific technical characteristics of the kits, their advantages and disadvantages are discussed. Costs are compared for analysis of small numbers of samples.
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Previous studies with rats showed that acute treatment with ethanol (4 g/kg) produce a marked increase in urinary folate levels, followed by a decrease in plasma folate levels. Analogous studies with human volunteer subjects using a lower dose of ethanol showed that there were small, but statistically significant increases in urinary folate levels after four hours. The initial ethanol dose was 1.0 g/kg with a single supplement of 0.1-0.2 g/kg to maintain ethanol blood levels at about 100 mg/dl for six hours. Further studies with rats were designed to test the cumulative effects of repeated daily doses of ethanol. Male Sprague-Dawley rats were treated for 1, 2, 3, or 4 days either with ethanol orally in 4 doses of 1 g/kg each at 0, 1, 2, and 3 hours or with glucose orally in 4 isocaloric doses. Urine was collected at timed intervals up to 12 hours after each daily dose. The pattern of the increase in urinary folate levels was similar in all groups, whether treated for 1, 2, 3 or 4 days. These results suggest that repeated ethanol treatment can lead to a marked cumulative folate loss via increased urinary excretion and that increased urinary folate excretion may contribute to the development of folate deficiency in humans.