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Biomedical subjects

L R Jordan

Publications and source records attributed to L R Jordan.

At least 19 recordsLinked to original sources

Direct comparison of the task-dependent discharge of M1 in hand space and muscle space.

Since its introduction in the early 1980s, the concept of a "preferred direction" for neuronal discharge has proven to be a powerful means of studying motor areas of the brain. In the current paper, we introduce the concept of a "muscle-space"-preferred direction (PD(M)) that is analogous to the familiar hand-space-preferred direction (PD(H)). PD(M) reflects the similarity between the discharge of a given neuron and the activity of each muscle in much the way that PD(H) reflects the similarity of discharge with motion along each of the three Cartesian coordinate axes. We used PD(M) to analyze the data recorded from neurons in the primary motor cortex (M1) of three different monkeys. The monkeys performed center-out movements within two different cubical workspaces centered either to the left or right of the monkey's shoulder while we simultaneously recorded neuronal discharge, muscle activity, and limb orientation. We calculated preferred directions in both hand space and muscle space, and computed the angles between these vectors under a variety of conditions. PDs for different neurons were broadly distributed throughout both hand space and muscle space, but the muscle-space vectors appeared to form clusters of functionally similar neurons. In general, repeated estimates of PD(M) were more stable over time than were similar estimates of PD(H). Likewise, there was less change in PD(M) than in PD(H) for data recorded from the two different workspaces. However, although a majority of neurons had this muscle-like property, a significant minority was more stable in Cartesian hand space, reflecting a heterogeneity of function within M1.

Algorithms↗

Changes in the hippocampus induced by glucose in thiamin deficient rats detected by MRI.

Using T2-weighted Magnetic Resonance Imaging (MRI) in a pyrithiamin-treated, thiamin deficient (TD) rat model of Wernicke's encephalopathy (WE), we have observed hyperintensity in the thalamus, hypothalamus, collicular bodies and hippocampus which was enhanced 40 min after a glucose load. Hyperintensity was not evident in these structures in thiamin replete rats receiving glucose nor was it enhanced in TD rats administered 2-deoxyglucose. Residual hyperintensity was still evident in the hippocampus as long as 30 days after thiamin administration and was increased by repeat glucose challenge at that time. These data indicate that the hippocampus is as vulnerable as the thalamus to some persistent pathological change when glucose is metabolised in a state of thiamin deficiency.

Analysis of Variance↗

Survivorship analysis of cementless meniscal bearing total knee arthroplasty.

Four hundred seventy-three consecutive cementless cruciate retaining meniscal bearing primary total knee replacements were done on 375 patients from May 1985 to February 1991. These were observed for a 10-year period (average, 5 years). Seventeen (3.6%) required change of components because of mechanical failure. There were 12 polyethylene fractures or dislocations. There were 5 tibial subluxations secondary to ligamentous instability occurring at an average of 21 months postoperatively. There were 2 component loosenings secondary to bone graft resorption (1 femoral, 1 tibial). There were 5 infections (4 Staphylococcus aureus, 1 Pseudomonas). Significantly, with the exception of the 2 knees with bone graft resorption, there was no component (femoral, tibial, or patellar) loosening. Kaplan-Meier survival estimates, using as an endpoint of revision surgery for any mechanical reason (polyethylene breakage, polyethylene dislocation, or ligamentous instability), showed a survivorship of 94.6% at the 8-year interval. Survivorship related to mechanical loosening of fixation of any component at the 8-year interval was 99%.

Adult↗

A biphasic response to adenosine in the coronary vasculature of the K(+)-arrested perfused rat heart.

Biphasic vasodilatory responses to adenosine and 5'-N-ethylcarboxamidoadenosine (NECA) were observed in the coronary vasculature of K(+)-arrested perfused rat hearts. Dose-response data for both agonists were best represented by two-site models. For adenosine, two sites with negative log ED50 (pED50) values of 8.1 +/- 0.1 (mean +/- S.E.M) and 5.2 +/- 0.1 were obtained, mediating 31 +/- 2% and 69 +/- 2% of the total response. In the presence of 8-phenyltheophylline, the vasodilatory response to adenosine remained best fitted to a two-site model with pED50 values of 7.0 +/- 0.2 and 5.4 +/- 0.2. The relative contribution of each site to the total response remained unchanged. For NECA, pED50 values of 9.6 +/- 0.1 and 6.8 +/- 0.2 were obtained, representing 48 +/- 3% and 52 +/- 3% of the sites, respectively. In contrast, ATP produced a monophasic response with a pED50 value of 8.8 +/- 0.1. These results provide evidence of adenosine receptor and response heterogeneity in the in situ coronary vasculature.

Adenosine↗

A method to evaluate the response of the coronary circulation of perfused rat heart to adenosine.

Exogenous adenosine causes a monophasic dilation of the coronary vessels in paced, perfused rat heart preparations. Because levels of endogenous adenosine in paced hearts may mask the presence of high potency adenosine receptors, we have developed a method to measure coronary vascular responses in a potassium-arrested heart. Hearts from adult male, Wistar rats were perfused at a constant flow rate of 10 mL/min in the nonrecirculating, Langendorff mode, using Krebs-Henseleit buffer. After 30 min, coronary perfusion pressure was 44 +/- 1 mmHg (mean +/- SEM). Hearts were then perfused with a modified Krebs-Henseleit buffer containing 35 mM potassium. Coronary perfusion pressure increased by 84 +/- 3 mmHg. Adenosine-induced reductions in coronary perfusion pressure were expressed as a percentage of the maximal increase in pressure produced by modified Krebs-Henseleit buffer from the equilibration level. A concentration-response curve for adenosine (n = 6) was biphasic and best described by the presence of two adenosine receptors, with negative log EC50 values of 8.8 +/- 0.3 and 4.3 +/- 0.1, representing 29 +/- 3 and 71 +/- 3%, respectively, of the observed response. Interstitial adenosine sampled by microdialysis during potassium arrest was 25% of the concentration found in paced hearts. Endogenous adenosine in nonarrested hearts may obscure the biphasic response of the coronary vessels to adenosine.

Adenosine↗

Low-density lipoproteins inhibit histamine and NaNO2 relaxations of the coronary vasculature and reduce contractile function in isolated rat hearts.

In the present study we examined the action of native and oxidized low-density lipoproteins (LDL) on coronary vascular and cardiac function and ultrastructure in rat hearts perfused isovolumically in the Langendorff mode. Responses of the coronary resistance vessels to the endothelium-dependent vasodilator, histamine, and the endothelium-independent vasodilator, NaNO2, were measured together with contractile function (rate-pressure product) before and after perfusion for 20 min with native - or oxidized-LDL at a concentration of 100 mu g protein/ml. Ultrastructural damage was assessed via electron microscopy of perfusion-fixed heart specimens. When compared to findings in untreated, control hearts, both native and oxidized LDL significantly reduced the responsiveness of the coronary resistance vessels to histamine and NaNO2, by about 50%. The rate-pressure product was decreased more by oxidized-LDL (41%) than by native-LDL (26%). Electron microscopy showed no ultrastructural abnormalities in the vasculature or myocytes of control hearts. The administration of both native- and oxidized-LDL caused distortion of endothelial cells, increased levels of pinocytotic vesicles in both endothelial and smooth muscle cells, detachment of blood vessels from surrounding tissue, and some regions of myocyte injury with evidence of mitochondrial injury and fluid accumulation. Our results show that both native- and oxidized-LDL are toxic to the isolated heart preparation. They inhibit coronary vascular responsiveness to vasodilators, reduce contractile function, and produce damage to cardiac ultrastructure.

Animals↗

Early flexion routine. An alternative method of continuous passive motion.

One hundred knees that underwent primary total knee arthroplasties were divided into 2 groups: the first 50 consecutive knees were assigned retrospectively to Group I (control), and the following 50 knees were assigned prospectively to Group II (early flexion). All procedures were cementless meniscal-bearing total knee arthroplasties and were performed by the same surgeon. Maximum early flexion (Group II) resulted in decreased length of stay, decreased hospital costs, and increased range of motion at 1 year. In light of current government interest in hospital cost reduction, this method should be considered as an attractive alternative to continuous passive motion.

Aged↗

Deleterious effects of hydrogen peroxide on the function and ultrastructure of cardiac muscle and the coronary vasculature of perfused rat hearts.

OBJECTIVE: To examine the effect of hydrogen peroxide on the function and ultrastructure of cardiac muscle and the coronary vasculature in an isovolumic rat heart preparation perfused at constant flow. DESIGN: Ventricular function was monitored via a balloon placed in the left ventricle and the response of the coronary vessels to vasodilators was assessed in hearts arrested with 35 mM potassium and treated with 5 microM phenylephrine to contract the coronary resistance vessels. Changes in coronary perfusion pressure reflect changes in resistance vessel tone. SETTING/ANIMALS: This experimental study consisted of 14 heart preparations, six control and eight treated hearts. INTERVENTIONS: Hydrogen peroxide was included in the perfusate at a final concentration of 250 microM for 20 mins. MAIN RESULTS: Hydrogen peroxide reduced rate-pressure product by 42%, caused a fivefold increase in end-diastolic pressure and increased coronary perfusion pressure by 33%. Also, the response of the coronary vasculature to the endothelium-dependent vasodilator, histamine, and endothelium-independent vasodilator, sodium nitrite, was decreased by 55% and 53%, respectively. Electron microscopy of hydrogen peroxide-treated hearts showed damage to both capillaries and arterioles. Endothelial cells were distorted and contained pinocytotic vesicles, endothelial cell junctions were disrupted and blood vessels were detached from surrounding tissue. A comparatively small amount of injury was seen in the myocyte population. CONCLUSIONS: The greater amount of ultrastructural damage seen in blood vessels compared with cardiac muscle suggests that the smooth muscle and endothelial cells of the vasculature are more susceptible to oxidant injury than the myocytes.

Animals↗

Intraoperative glove perforation. A comparative analysis.

A prospective study was conducted to determine the rate of puncture of the inner glove when various double-gloving protocols were used for elective total joint procedures. Group 1 consisted of 22 cases in which two pairs of regular latex gloves were used. Group 2 consisted of 25 cases in which outer "orthopaedic" gloves were used over regular latex gloves. Group 3 consisted of 24 cases in which Repel gloves were used between two regular latex gloves. The patients were randomly assigned to one of the three groups. All gloves, both inner and outer, were tested for holes at the end of the procedure. All gloves that were changed for presumed intraoperative holes were also tested. The type and duration of the procedure was also documented. Of the inner holes, there were significant differences between each group. Group 1 (double latex) and Group 2 (outer orthopaedic/inner regular) had significantly more holes than Group 3 (Repel between two regular gloves). There were no holes in Group 3, and Group 2 offered significant protection over Group 1.

Gloves, Surgical↗

Cardiovascular effects of parathyroid hormone in conscious sheep.

The cardiovascular effects of the synthetic amino terminal fragment of parathyroid hormone, PTH(1-34), were studied in intact conscious sheep. Physiological doses of bovine (b) PTH(1-34), 0.188, 0.376, 0.56 and 0.75 micrograms kg-1 h-1 were infused in random order into conscious sheep for periods of 1 h each. Isotonic saline was infused as a control. Mean arterial blood pressure (MABP) decreased from 99.2 +/- 1.2 mmHg during the control infusion to 88.9 +/- 1.4 mmHg during infusion of the highest dose of PTH. Heart rate (HR) increased from 81.6 +/- 7.3 beats min-1 during the control infusion to 142.3 +/- 14.0 beats min-1 at the highest PTH dose and plasma renin activity (PRA) increased from 0.33 +/- 0.15 ng ml-1 h-1 to 1.54 +/- 0.46 ng ml-1 h-1. Cardiac output (CO), calculated by an indirect method, increased to 176 +/- 28% of the control values. The changes in all four parameters were dose dependent. Renal blood flow (RBF) increased during the PTH infusion period.

Animals↗

Bound inorganic phosphate and early contractile failure in global ischaemia.

Inorganic phosphate (Pi) accumulates extremely rapidly in ischaemic heart muscle and intracellular binding of this metabolite may account for the precipitous loss of function seen at the onset of severe ischaemia. We have used 31P-NMR spectroscopy to measure the free cytosolic [Pi] and chemical assay techniques to measure total tissue Pi at 0, 1, 2, 3, 4, 5, and 12 min of complete global ischaemia in the isolated isovolumic rat heart. At zero time, the Pi assayed chemically was 30.77 +/- 5.52 mumol/g dry wt (mean +/- SD, n = 7) whilst Pi assayed by NMR was 3.39 +/- 1.21 mumol/g dry wt (n = 15). Thus, 27.38 mumol/g dry wt of Pi was bound at a cytosolic [Pi] of 0.82 mM. After 12 min of ischaemia, 49.88 mumol/g dry wt of Pi was bound at a cytosolic [Pi] of 4.11 mM. When all data were fitted, using a non-linear, least squares fit (p < 0.05), to the binding isotherm: Bound Pi = Bmax'. [Pi]/Kd'+[Pi], the apparent binding parameters Kd' and Bmax' were estimated to be 1.1 +/- 0.6 mM and 64.0 +/- 10.2 mumol/g dry wt respectively. During the first minute of global ischaemia when the rate-pressure product had decreased by 79% of its pre-ischaemic value, bound Pi had increased by 58% and free cytosolic [Pi] by 162%. When functional and metabolite changes were expressed as a fraction of the total change which occurred during the 12-min ischaemic period, bound Pi had the profile most similar to the rate-pressure product. Both the amount of bound Pi and free cytosolic [Pi] correlated with loss of contractile function as the ischaemic period progressed. The results show that during ischaemia, Pi is bound progressively as free cytosolic [Pi] is increased as the result of high energy phosphate hydrolysis. While these results are consistent with the possibility that Pi binding may contribute to ischaemic contractile failure, no molecular explanation for the possible effect of bound Pi on contraction has been proposed.

Animals↗

No evidence of malonyldialdehyde formation during reoxygenation injury in vitamin E-deficient rat heart.

Vitamin E is an endogenous antioxidant and is known to afford protection against lipid peroxidation. If lipid peroxidation was an important factor in the pathogenesis of reoxygenation injury in heart, then both the extent of lipid peroxidation and cell injury would be expected to be exacerbated in vitamin E-deficient hearts. To study reoxygenation injury in the present experiments, rat hearts were perfused in the Langendorff mode with a modified Krebs-Henseleit buffer under anoxic conditions for 60 min before resuming normoxic perfusion for 20 min. Creatine phosphokinase (CPK) activity and malonyldialdehyde (MDA), a product of lipid peroxidation, were assayed in the perfusate effluent from hearts during reoxygenation injury. Also, myocardial MDA and vitamin E contents were measured in extracts of freeze-clamped heart tissue obtained immediately before and 2 min after reoxygenation. Experiments were performed on hearts from groups of weanling rats fed either a vitamin E-deficient or vitamin E-supplemented diet (50 I.U. vitamin E/kg) for 5 to 6 weeks. After 5 weeks, the myocardial vitamin-E content was 103.8 +/- 5.3 (n = 5) and 11.5 +/- 1.6 (n = 4) ng/mg protein (mean +/- SEM) in the vitamin E-supplemented and vitamin E-deficient groups respectively. Perfused hearts from both dietary groups showed a peak of enzyme release 2 to 3 min after the reintroduction of oxygen, and enzyme release from vitamin E-deficient hearts was two-fold greater than enzyme release from vitamin E-supplemented hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗