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Biomedical subjects

D Shander

Publications and source records attributed to D Shander.

At least 19 recordsLinked to original sources
PubMed1994

Enhanced auscultation with a new graphic display system.

BACKGROUND: To provide an objective method to support and teach auscultation, a new portable system (graphic display system) was evaluated for graphic display and printing of heart sounds. METHODS: Ninety-one patients from three institutions, with a variety of heart sound abnormalities, were studied by two examiners. A graphic recording was made in each and compared with the auscultatory findings. RESULTS: The findings of the graphic system confirmed the auscultatory impressions of both examiners in 77 (85%) of the 91 cases. Brief sound transients, such as split second sounds and ejection sounds, third heart sounds, and prosthetic opening and closing sounds, were all regularly recorded with the graphic system, often allowing resolution when examiners were in disagreement. Graphic recordings commonly were at variance with examiners in detecting fourth sounds, possibly because of examiners' difficulty in distinguishing these from split first sounds as well as limitations of the graphic system itself. High-pitched murmurs of low intensity (< grade 2), as exemplified by those of aortic and mitral regurgitation, were occasionally missed by the graphic system, probably because of baseline interference by background noise. CONCLUSIONS: The graphic display system can often provide more information than can be obtained by standard auscultation alone, especially in the detection of low-frequency and multiple sounds, and in the accurate timing of intervals. It is often unable to detect soft high-frequency murmurs. Permanent records allow for more objective comparison of the auscultatory findings of various examiners at different times. This system provides an excellent means by which auscultation skills may be taught or enhanced, especially since its speed and portability allow immediate feedback for comparison with auditory perceptions.

Computer Graphics↗
PubMed1990

Hypothesis: warfarin administered simultaneously with heparin infusion will prevent heparin-discontinuance associated coronary thrombosis.

Recent studies have evidenced an association between the time of heparin discontinuance and coronary artery reocclusion. Some investigators have concluded that inadequate heparinization was responsible, and further heparin infusion or an increase in dose would have been indicated. However, several investigators (Rao: Thrombosis Research 24:181-186, 1981; Marciniak and Gockerman: Lancet September 17:581-584, 1977; Fisken et al.: Lancet December 10: 1231, 1977; Conard et al.: Thrombosis Research 22:507-511, 1981; Kakkar et al.: Lancet January 12:103-104; Green: Lancet February 16:374, 375; Harborne and Nicolaides: Thrombosis Research 43:657-662, 1986; Bonen et al.: Thrombosis Research 27:123-124, 1982; Blomback et al.: Acta Physiologica Scandinavica 58:306-318, 1963; Holm et al.: Scandinavian Journal of Haematology 35:564-569, 1985; Andersson et al.: Thrombosis Research 34:333-340, 1984) have demonstrated that antithrombin III levels are reduced in patients on intravenous heparin. Both reduced antithrombin III levels and reduced rate of antithrombin inhibition of thrombin at the time of heparin discontinuance may increase the risk of coronary rethrombosis. If this theory is correct, increasing heparin infusion may exacerbate this risk. We propose an investigation that will provide evidence for or against the decreased antithrombin III theory, and in doing so, test an experimental therapy designed to prevent coronary reocclusion upon heparin discontinuance. In a randomized, placebo-controlled double-blinded study, we will determine whether simultaneous administration of warfarin with heparin initiation provides more time to increase antithrombin III levels and prevent coronary reocclusion upon heparin discontinuance, compared to heparin without warfarin therapy.

Antithrombin III↗
PubMed1980

Role of the preoptic brain in the regulation of preovulatory gonadotropin surges in the hamster.

These studies have examined the role of the preoptic-suprachiasmatic area (POA-SC) in brains of cyclic female hamsters in regulating proestrous preovulatory gonadotropin surges. The spontaneous release of LH and FSH which normally occurs on proestrous afternoon was blocked with phenobarbital. Temporal changes in serum LH and FSH were measured in such blocked animals after delivery of direct current (100 muA/60 s) to the POA-SC or that portion of the medial basal hypothalamus (MBH) which includes the arcuate nuclei and the median eminence. Bilateral dc treatment of MBH resulted in a 30-fold increase in serum LH and a 4-fold rise in serum FSH over basal concentrations. Unilateral MBH dc treatment produced a 12-fold increase in serum LH but FSH levels remained basal. In contrast, the delivery of dc to the POA-SC did not evoke any increase in serum LH or FSH. Sham electrode placement in the MBH or POA-SC also did not alter basal LH and FSH serum concentrations. These results suggest that, unlike the rat, passage of dc with concomitant production of an irritative lesion and deposition of ferrous ion does not activate structures responsible for preovulatory gonadotropin surges in hamsters. In a second study, discrete electrochemical lesions were produced in the basal anterior portion of the preoptic brain. These lesions did not involve the medial preoptic area or the suprachiasmatic nuclei. Following such brain destruction, spontaneous ovulation, LH surges, and 4-day vaginal cyclicity ceased. When the suprachiasmatic nuclei or extensive regions of the dorsal medial preoptic area, including the anterior commissure, were destroyed, vaginal cyclicity was disrupted for only 8-12 days. Thereafter, these animals had spontaneous preovulatory gonadotropin surges and ovulated. Seemingly, input from the medial basal anterior preoptic region (anterior to the SC) is essential for preovulatory LH and FSH surges to occur.

Animals↗