Biomedical subjects

J W Depenbusch

Publications and source records attributed to J W Depenbusch.

7 recordsLinked to original sources

PubMed1987

Acute regional vascular effects of intravenous captopril in a rat model of myocardial infarction and failure.

The effects of i.v. captopril on regional blood flow (radioactive microspheres, 15 +/- 5 micron), hemodynamics and maximal oxygen consumption were evaluated in conscious rats with congestive heart failure due to large myocardial infarction (n = 9, infarct size 39.5 +/- 2% of left ventricle) and compared to data obtained from rats subjected to sham surgical procedures (n = 8). In both groups data were obtained at rest and during submaximal treadmill exercise during alternate infusion of captopril and saline. In the congestive heart failure group captopril reduced systemic vascular resistance, mean arterial pressure and left ventricular systolic pressure (P less than .05 each). Blood flow to the renal, gastrointestinal and coronary circulations was reduced in the heart failure group treated with saline vehicle. Flow to the renal and gastrointestinal beds of heart failure animals was enhanced to values similar to those observed in sham animals during captopril treatment. Left ventricular coronary flow was also increased significantly by captopril in both sham and heart failure animals. The most prominent effects of captopril occurred in the renal circulation of the heart failure group in which blood flow increased by 55%. Blood flow to skeletal muscle and skin was unchanged by captopril both in sham and heart failure animals at rest and during exercise. Maximal oxygen consumption was not affected by captopril treatment. Thus, captopril induced a differential pattern of vasodilation with the greatest effect in the renal bed and a less intensive effect in the gastrointestinal and coronary beds. The unchanged flow to skeletal muscle may explain the failure of captopril to improve exercise capacity after short-term administration.

Animals↗

PubMed1985

Accuracy and reproducibility of a four-hour method for anaerobe identification.

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.

Bacteria, Anaerobic↗

PubMed1985

Effects of diltiazem on cardiac function and regional blood flow at rest and during exercise in a conscious rat preparation of chronic heart failure (myocardial infarction).

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 less than .05), reduced heart rate (p less than .05), and improved cardiac output during exercise (p less than .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.

Animals↗

PubMed1984

Computed tomographic findings in akinetic mutism.

Brain-injured children who progress from coma to a sleeplike state of akinetic mutism are often misinterpreted by their parents as having improved. In children with akinetic mutism caused by extensive destruction of the cerebral gray matter, the computed tomographic scan may demonstrate the irreversible nature of the pathologic changes.

Akinetic Mutism↗

PubMed1983

The relationship between tegumental disruption and muscle contraction in Schistosoma mansoni exposed to various compounds.

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.

Animals↗

PubMed1983

Tegumental disruption with Triton X-100 and its effects on longitudinal muscle function in male Schistosoma mansoni.

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.

Animals↗

PubMed1982

Effect of Triton X-100 on tegument and muscle in Schistosoma mansoni.

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.

Animals↗