The antischistosomal drugs praziquantel and Ro 11-3128, which cause a tetanic contraction of Schistosoma musculature, concurrently produce a disruption of the parasite's tegument. Both phenomena are attenuated by preincubation of the parasites in high Mg2+ containing media before addition of the drugs, and the therapeutically inactive stereoisomers of these drugs cause neither effect. Other antischistosomal drugs tested cause neither muscle contraction nor tegumental disruption. Some unrelated agents which cause muscle contraction (but have no antischistosomal effect) alter the parasite's tegument, while others do not. Cytochalasin B, but not colchicine, causes tegumental disruption without affecting muscle tension. Thus, there is no simple correlation between a drug's antischistosomal activity or ability to contract the parasite's muscle and its ability to damage the parasite's tegument.
In this study, we evaluated the ability of a 4-h enzyme assay kit system, the RapID ANA method (Innovative Diagnostic Systems, Inc., Atlanta, Ga.) to accurately and reproducibly identify a spectrum of clinically significant anaerobic bacteria in two separate institutions. Additional tests were performed as required. Of a total of 188 organisms tested at Hershey Medical Center (HMC), 86.2% were correctly identified to species level without additional tests, 5.9% required extra tests for correct identification, and 8.0% were misidentified. Of 53 strains tested at Johns Hopkins Hospital (JHH), 52.8% were correctly identified without extra tests, 28.3% required extra tests for correct identification, and 18.9% were misidentified. Of 21 organisms tested at both institutions, those tested at JHH required additional tests for correct identification in 38.1% of cases, compared with 9.5% at HMC. Misidentification rates were identical (9.5%) in both centers. Of strains tested at HMC only, 86.8% were correctly identified without extra tests, 5.4% were identified with additional tests, and 7.8% were misidentified: corresponding data for JHH were 53.1, 21.9, and 25.0%, respectively. Of 53 strains tested in triplicate at JHH, 56.7% yielded the same result on each occasion, 37.7% were identical in two of three tests, and 5.7% gave different results on each of three occasions. Discrepancies between identification rates at HMC and JHH may be explained by differences in species tested (more commonly encountered species were tested at HMC) and interpretation of reactions by the two different readers. The RapID ANA method has the potential for rapid identification of clinically isolated anaerobes; however, accuracy and reproducibility may vary as a function of the specific laboratory setting.
The effects of intravenous infusion of diltiazem on regional blood flow (radioactive microspheres), hemodynamics, and maximum rate of oxygen consumption were evaluated in conscious rats with congestive heart failure caused by large myocardial infarction (n = 10, infarct size 41.8% of left ventricle) and compared with data obtained from rats subjected to sham surgical procedures (n = 9). In both groups data were obtained at rest and during submaximal treadmill exercise during alternate infusion of diltiazem and saline. In the group with heart failure, diltiazem increased stroke volume at rest and during exercise (p < .05), reduced heart rate (p < .05), and improved cardiac output during exercise (p < .05) without increasing left ventricular end-diastolic pressure in any of the animals. Blood flow to renal and splanchnic circulations was reduced in the group with heart failure but was increased by diltiazem to values similar to those observed in sham-operated animals. Although skeletal muscle flow during exercise was significantly increased by the drug, maximal rate of oxygen consumption was not, indicating unchanged oxygen availability within working muscle. Thus diltiazem caused redistribution of blood flow to kidney and gut in animals with myocardial infarction and failure, thereby restoring blood flow to circulatory beds known to be impaired in this setting.
Longitudinal muscles in adult male Schistosoma mansoni appear to remain in almost all respects functional after tegumental disruption by Triton X-100. Responses to high K+, ouabain, low temperature, praziquantel and neurotransmitters are still present. Muscle membrane potentials remain near those of control animals and lanthanum nitrate is still excluded from the muscle after the Triton treatment. Although muscle contractility remains after tegumental disruption, sodium and calcium levels, as measured by plasma emission spectroscopy, increase by 20-30% while potassium and magnesium levels decrease by 15%. 45Ca2+ accumulation is double that of control animals. Upon exposure to a bathing medium lacking Ca2+, Triton-treated animals lose responsiveness to high K+, ouabain, low temperature and praziquantel more rapidly than do control animals. D-600, which effectively blocks the high K+ response in control animals, has no measurable effect on the high K+ response in Triton-treated animals, suggesting that voltage-dependent Ca2+ channels are present in the tegument.
Short periods of in vitro incubation of Schistosoma mansoni with low concentrations of the nonionic detergent Triton X-100 caused marked changes in the physiological and morphological status of the parasite. Less than 15 min of exposure to 1 mM Triton at 37 C led to irreversible destruction of the tegument, relaxation and depolarization of the muscle, and loss of response to electrical stimulation, to 60 mM K+-HBS, or to 10(-6) M praziquantel. A 5-min incubation in 100 microM Triton X-100 caused no gross structural damage, changes in tegumental or E2 electrical potential, or decrease in response to praziquantel, but markedly inhibited the ability of 60 mM K+-HBS or electrical stimulation to cause muscle contraction. Radioactive calcium influx measurements indicated that a 5-min exposure to 100 microM Triton X-100 may be uncoupling membrane depolarization from development of muscle tension by interfering pharmacologically with calcium channels. Longer incubations (15 min) in the presence of 100 microM Triton X-100 caused transitional physiological changes suggesting that the mode of action of the detergent was passing from a specific, pharmacological mode to a nonspecific disruptive action.
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