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R Hotchkiss

Publications and source records attributed to R Hotchkiss.

11 recordsLinked to original sources
PubMed1998

Radioulnar load-sharing in the forearm. A study in cadavera.

Custom-designed miniature load-cells were inserted into the distal end of the ulna and the proximal end of the radius in ten fresh-frozen forearms from cadavera. The forces transmitted through the bones at these sites were measured under 134 newtons of constant axial load that was applied through the metacarpals as the forearm was rotated from 60 degrees of supination to 60 degrees of pronation. The simultaneous measurements of these forces allowed the calculation of radioulnar load-sharing at the wrist and the elbow as well as the calculation of the amount of force that was transferred from the radius to the ulna through the interosseous membrane. With the elbow in valgus alignment (that is, with contact between the radial head and the capitellum), the main pathway for load transmission through the forearm was direct axial loading of the radius; measurements from both load-cells were unaffected by the angle of elbow flexion. When the forearm was in neutral rotation, the mean force in the distal end of the ulna averaged 2.8 per cent of the load applied to the wrist and the mean force in the proximal end of the ulna averaged 11.8 per cent; this indicated that only a small amount of tension developed in the interosseous membrane. With the elbow in varus alignment (that is, with no contact between the radial head and the capitellum), load was transmitted through the forearm by a transfer of force from the radius to the ulna through the interosseous membrane. When the forearm was in neutral rotation, the force in the distal end of the ulna averaged 7.0 per cent of the load applied to the wrist and the force in the proximal end of the ulna averaged 93.0 per cent; the force through the interosseous membrane decreased with supination of the forearm. Testing with the elbow in valgus alignment and shortening of the distal end of the radius in two-millimeter increments produced corresponding increases in force in the distal end of the ulna and decreases in force in the radial head. The forces through the interosseous membrane remained low after each amount of radial shortening.

Aged↗
PubMed1997

Quantification of ion transport in perfused rat heart: 133Cs+ as an NMR active K+ analog.

Proper ion balance between intra- and extracellular compartments is necessary for normal physiological function. Conversely, alterations in membrane ion transport occur in numerous pathological states. As a noninvasive, nondestructive spectroscopic technique, nuclear magnetic resonance (NMR) offers a powerful approach to the study of ion balance in intact biological systems. Unfortunately, rare NMR active nuclides that are isotopes of the 100% naturally abundant 23Na+ and 39K+ are not available for tracer kinetic studies of Na1 and K+ transport. However, Cs is a biologically active analog of K+, and the 100% naturally abundant NMR active 133Cs+ nuclide can be employed to examine K+ transport (Davis, D. G., E. Murphy, and R. E. London. Biochemistry 27: 3547-3551, 1988). The distinguishing feature of 133Cs+ is that it naturally gives two separate well-resolved NMR resonances for intra- and extra-cellular 133Cs+, permitting study of the time course changes of either of these compartments independent of the other. In this report, the experimental procedures and compartmental modeling formalism are developed that allow quantitative analysis of Cs+ membrane transport in the perfused rat heart. Intracellular 133Cs+ is shown to be 100% visible by solution-state NMR methods and its influx transport to be markedly inhibited by ouabain, a confirmation of findings previously reported by others. Intracellular 133Cs+ spin-lattice and spin-spin relaxation times at 7 T were determined to be 2.1 +/- 0.3 (SD)s (n = 8) and 0.065 +/- 0.007 (SD) s (n = 8), respectively, for T1 and T2. The rate constant for Na(+)-K(+)-ATPase pump dominated intracellular influx was measured to be 0.25 +/- 0.07 (SD) min-1 (n = 27) and that for efflux 0.005 +/- 0.001 (SD) min-1 (n = 14). The rate constant for 133Cs+ equilibration in the extracellular space at supraphysiological perfusate flow rate (20 ml/min) was found to be 4.6 +/- 0.9 (SD) min-1 (n = 20). Thus extracellular diffusion limitations do not dominate the 133Cs+ transport measurements.

Animals↗
PubMed1997

Inhibition of ion transport in septic rat heart: 133Cs+ as an NMR active K+ analog.

Sepsis, the systemic response to severe infection, and the resulting multiorgan failure it induces are major contributors to intensive care unit morbidity and mortality. A number of abnormalities in ion transport processes and intracellular free Na+ ([Na+]i) and K+ ([K+]i) concentrations have been reported to occur during sepsis/endotoxemia. An effect of sepsis on the NA(+)-K(+)-ATPase may be an important contribution to changes in intracellular ion balance and the resultant pathophysiology of the disorder. The purpose of this study was to examine the effect of sepsis on the Na(+)-K(+)-ATPase in the isolated perfused rat heart using 133Cs+ nuclear magnetic resonance (NMR). Cs+ is a K+ analog, and 133Cs-NMR offers the opportunity to examine Na(+)-K(+)-ATPase activity in the intact organ via tracer kinetics. Sepsis was induced in halothane-anesthetized male Sprague-Dawley rats using the cecal ligation and perforation (CLP) model. Twenty-four to thirty-six hours after surgery, hearts from CLP or sham-operated rats were perfused with Krebs-Henseleit buffer containing 1.25 mM Cs+. The influx rate constant for Cs+ was decreased by 24% in septic rat hearts, i.e., 0.25 +/- 0.08 (SD) min 1 for controls and 0.19 +/- 0.04 (SD) min-1 for septic animals (P = 0.003). There was no difference for Cs+ efflux [0.005 +/- 0.001 (SD) min-1 for controls and 0.005 +/- 0.002 (SD) min-1 for septic animals; P = 0.8]. These results are consistent with an inhibition of the Na(+)-K(+)-ATPase pump during sepsis/endotoxemia. A decrease in the activity of the Na(+)-K(+)-ATPase pump may be responsible for or contribute to the changes in [Na+]i and [K+]i during the disorder.

Animals↗
PubMed1994

Hyperthermia induces IL-1 alpha but does not decrease release of IL-1 alpha or TNF-alpha after endotoxin.

Heat treatments administered prior to the onset of sepsis or endotoxemia markedly increase survival. A potential mechanism for the beneficial effect of heat could be effects on IL-1 alpha and TNF-alpha, important mediators of sepsis and endotoxemia. Administration of IL-1 or TNF prior to development of sepsis and endotoxemia increases survival; thus, prophylactic heat treatments may protect by releasing IL-1 or TNF. Paradoxically, an alternative mechanism of protection of prophylactic heat treatments could be to decrease the amount of IL-1 and TNF released during sepsis or endotoxemia. Cells pretreated with heat do not produce as much IL-1 or TNF in response to endotoxin as cells that have not been pretreated with heat. The purpose of this investigation was to determine if hyperthermia caused release of cytokines and/or blunted the rise in cytokines occurring after endotoxin. Mice were anesthetized with ketamine/xylazine and immersed in a water bath at 37.0 or 42.0 degrees C for sham or heat treatments. At 6-7 h after recovery from anesthesia and immersion, sham and heat-treated mice were injected with Escherichia coli endotoxin. Both heat-treated and sham mice had elevated plasma IL-1 alpha 2 h after anesthesia and immersion but IL-1 alpha was approximately 3-fold greater in the heated mice, 732 +/- 50 vs. 256 +/- 76 pg/ml (p < 0.01). Blood samples obtained after endotoxin revealed no difference in levels of TNF-alpha (5477 +/- 742 vs. 6514 +/- 652 pg/ml) or IL-1 alpha (546 +/- 72 vs. 603 +/- 121 pg/ml) in the sham vs. heated mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Hyperthermia protects mice against the lethal effects of endotoxin.

Recently, investigators have reported that heat shock proteins (HSPs) can protect isolated cells from cytotoxicity induced by two important mediators of sepsis: interleukin-1 and tumor necrosis factor. The present study was undertaken to examine the hypothesis that transient whole body hyperthermia could decrease mortality from subsequent challenge with gram-negative endotoxin. We demonstrate that heat pretreatments improved long-term survival fivefold in a mouse endotoxin model and this was correlated with the production of HSPs. There was a marked difference in individual organ expression of the inducible 72-kDa heat shock protein (HSP72). Heat treatments caused significant HSP72 formation in lung, liver, kidney, and small intestine, but much lesser formation in heart, brain, and abdominal wall muscle. Additional experiments demonstrated that the protective effect of hyperthermic treatments against an endotoxin challenge occurred early, i.e., 1 and 2 h after heating, was maximal at 12 h, and had significantly diminished by 48 h. The formation and decay of HSP72 demonstrated a time course that paralleled the survival curve from endotoxin challenge, thus suggesting a possible role for HSP72 in the protective effect. Surprisingly, and in contrast to studies reported in incubated cells, endotoxin alone did not cause significant formation of HSP72 in vivo.

Anesthesia↗
PubMed1992

Variations in digital nerve anatomy.

One hundred digital nerves from 10 cadaver hands were dissected, and branching patterns were analyzed. Contrary to the traditional belief that the digital nerve predictably trifurcates at the distal interphalangeal crease, much variation exists. Terminal branching occurred distal to the crease in 60% of the thumb digital nerves and in 78% of the digital nerves supplying the other four digits. The number of terminal branches also varied from two to seven in the thumb and from two to five in the other four digits. No significant differences were seen in branching patterns between digits or between radial and ulnar sides. These findings are clinically relevant to the surgeon who is contemplating digital nerve repair.

Cadaver↗
PubMedDate not supplied

The public health response to 2,3,7,8-TCDD environmental contamination in Missouri.

In 1971, waste oil containing 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was sprayed for dust control on a number of residential, recreational, and work areas in Missouri. In several of them, the level and extent of environmental contamination were not known until late 1982 or 1983. Extrapolation from existing toxicological data indicated the potential for substantial adverse health effects in highly exposed populations. As a result, the Missouri Division of Health and the Centers for Disease Control initiated close collaboration with the Environmental Protection Agency (EPA) on review and evaluation of environmental data, the development of health advisories to EPA on the need for remedial or preventive actions at specific contaminated sites, a health education effort for the medical community and general public, establishment of a dermatological screening clinic, establishment of a central listing of potentially exposed persons through administration of a health effects survey questionnaire, and a pilot medical study of a "highest risk" cohort. Strategies for additional interventions will continue to be based on findings derived from this first phase of the investigation.

Animals↗