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Biomedical subjects

D K Anderson

Publications and source records attributed to D K Anderson.

At least 91 records · Page 5Linked to original sources
PubMed1983

Susceptibility of feline spinal cord energy metabolism to severe incomplete ischemia.

Feline spinal cords were subjected to 10 to 30 minutes of severe incomplete ischemia (average reduction in blood flow of 92%) with and without 90 minutes of recirculation, and the L-2 segment was analyzed for high-energy phosphates and certain glycolytic metabolites. Spinal cord tissue lactic acid levels were stepwise elevated, and adenosine triphosphate (ATP), phosphocreatine (P-creatine), and glucose were progressively consumed by increasing durations of ischemia. However, upon restoration of blood flow, there was extensive recovery of energy metabolites and normalized lactic acid, demonstrating resumption of mitochondrial oxidative metabolism. These data indicate that the spinal cord can tolerate at least 30 minutes of severely reduced blood flow before recovery of energy metabolism is significantly impaired upon restitution of blood flow.

Adenosine Triphosphate↗
PubMed1982

Microvascular perfusion and metabolism in injured spinal cord after methylprednisolone treatment.

The purpose of this study was to determine the effect of treatment with the synthetic glucocorticoid, methylprednisolone, on the microvasulature and metabolism of the traumatized spinal cord. Spinal cords of cats were compressed with a 170-gm weight for 5 minutes and were treated with either high-dose methylprednisolone (HDMP, 15 mg/kg/24 hrs) or megadose methylprednisolone (MDMP,60 mg/kg/24 hrs). Animals were sacrificed at 2, 8, or 24 hours following injury. Treatment with HDMP resulted in substantial preservation of injured spinal cord microvascular perfusion at 8 hours as compared with injured untreated cats. Compression trauma caused a partial derangement of energy metabolism and a shift toward anaerobic glycolysis in both treated and untreated groups for the entire 24-hour postinjury period. Tissue levels of adenosine triphosphate, phosphocreatine, and total adenylates in the HDMP-treated cats sacrificed at 8 hours after trauma were significantly elevated over untreated controls, but those in the 2- and 24-hour groups were not. Concentration of energy intermediates in MDMP-treated cat were either equal to or below those of injured untreated animals al all three postinjury time period. The postinjury metabolite pattern and concentrations seen in this study possibly result from differing levels of blood flow and neuronal activity in the injured untreated, HDMP-, and MDMP-treated spinal cords. Better tissue perfusion in the HDMP-treated cats might be expected to result in an improved tissue energy state in these animals. However, intensive high-dose glucocorticoid treatment has been demonstrated to augment spinal cord monosynaptic and polysynaptic reflex transmission and primary afferent excitability. Furthermore, acute single intravenous dose studies have shown this direct neuronal action to be dose-related. Thus, additional high-energy phosphate molecules that may be reformed as a result of HDMP treatment were perhaps used as the energy source for any increased neuronal activity caused by steroid administration. The beneficial effects of glucocorticoid treatment in experimental spinal cord trauma might derive from preserved cellular structural integrity. This could result in increased levels of neuronal activity, energy utilization, and production in treated as compared with untreated tissue.

Animals↗
PubMed1981

Flow through collapsible tubes at high Reynolds numbers.

The pressure-flow relationships of collapsible tubes were studied utilizing the Starling resistor model. Reynolds numbers much higher than previously reported were used to simulate high cardiac output states. Alterations which occur in vivo, including longitudinal tension, stretch, tubing diameter, length, and outflow resistance were also simulated and systematically investigated. The pressure-flow curves showed an initial rising phase, a plateau phase, as well as a late-rising phase which has not been reported previously. Self-induced oscillations occurred during the plateau phase and persisted throughout the late-rising phase. These perturbations were markedly increased by longitudinal tension and stretch, but were attenuated by increased diameter, length, and outflow pressure. These instabilities may prove to be an explanation for the "venous hum."

Animals↗
PubMed1981

Effect of methylprednisolone in compression trauma to the feline spinal cord.

The purpose of this study was to determine the effect of methylprednisolone sodium succinate on clincal recovery and tissue preservation following compression trauma of feline spinal cord. Cats were anesthetized with pentobarbital and injured by placing a 170-gm weight on the spinal cord for 5 minutes. One hour after injury, the animals were given intravenous steroid (15 mg/kg/day) for 2 days in three devided doses, 15 mg/kg/day for 1 day intramuscularly, 7.5 mg/kg/day intramuscularly for 3 days, and 3.75 mg/kg/day intramuscularly for 3 days, for a total of 9 days. In a control group, the animals were injured but untreated. At 60 days after injury, the animals were sacrifieced by perfusion fixation with 10% formalin. The spinal cord was removed and evaluated for a number of morphometric parameters, including percentage of spinal cord cross-sectional area containing the cavity (%area) and percentage of spinal cord volume occupied by the cavity (%volume). A clinical recovery score (recovery index) was devised to evaluate neurological recovery. Steroid-treated cats showed significantly greater recovery than the untreated controls (p less than 0.001). Moreover, the spinal cord of treated cats displayed greater tissue preservation as measured by %area (p leass than 0.005) and %volume (p less than 0.004). Correlation coefficients comparing the recovery index with morphometric parameters revealed a negative correlation between cavity size and recovery. These data provide evidence for a beneficial effect of methylprednisolone in promoting recovery and preserving spinal cord tissue following blunt injury to the feline spinal cord.

Animals↗
PubMed1980

Spinal cord energy metabolism in normal and postlaminectomy cats.

The purpose of this study was to determine 1) normal concentrations of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), phosphocreatine (P-creatine), glucose, lactate, and pyruvate in upper (L-2) and lower (L-5) feline lumbar spinal cord, and 2) whether previously reported laminectomy-induced reduction in spinal cord blood flow (SCBF) resulted in disturbance of spinal cord energy metabolism. Concentrations of ATP, P-creatine, pyruvate, and glucose were significantly higher at L-5 than at L-2, probably as the result of larger amounts of gray matter at L-5 than L-2. Significant increases in ADP and AMP levels were the only metabolite changes noted 15 minutes following laminectomy. The authors speculate that the increase in ADP and AMP is due to a laminectomy-induced stimulation of ATP utilization. However, lack of change in other metabolites implies an efficient energy homeostasis. These results indicate that although laminectomy can reduce SCBF, the degree of this reduction is insufficient to adversely affect spinal cord energy metabolism. Thus, tissue from beneath or near the laminectomy site is viable and essentially normal.

Adenosine Diphosphate↗
PubMed1980

Spinal cord energy metabolism following compression trauma to the feline spinal cord.

The purpose of this study was to determine the spinal cord metabolic state for 24 hours after compression trauma to the feline spinal cord. Cats were anesthetized with pentobarbital and injured by placing a 190-gm weight on the spinal cord for 5 minutes. Biochemical analysis of the injured segment revealed a significant depletion in the levels of adenosine triphosphate (ATP), phosphocreatine (P-creatine), and total adenylates for the entire 24-hour recovery period. Glucose levels initially declined, but by 1 hour had normalized, and at 8 and 24 hours were significantly supranormal. The lactate/pyruvate ratio and tissue lactate concentrations increased four and five and half times, respectively, for the first 4 hours after injury. Between 8 and 24 hours, lactate levels remained elevated, whereas the lactate/pyruvate ratio declined to contol levels as the result of a significant rise in the tissue pyruvate concentration. This sequence of metabolic changes suggested that metabolism was probably not homogeneous throughout the injured segment, and that tissue metabolic rate was depressed for the initial 4 hours after trauma then increased in metabolically active tissue for the remainder of the 24-hour recovery period. This model of spinal cord trauma results in a severe, prolonged ischemia and metabolic injury to the affected tissue. Whether these metabolic changes results from or cause the tissue damage and irreversible paraplegia associated with this type of spinal cord injury remains to be determined.

Adenosine Monophosphate↗
PubMed1979

An agar--gel immunodiffusion test for detection of Brucella antibodies in human serum.

A comparison was made of results obtained with a Brucella agar--gel immunodiffusion (AGID) test and the standard tube-agglutination test on 612 human sera. Agreement between the tests was 97% when the titer was 1:160 or higher. Of 448 sera that showed no agglutination titer, 447 were negative with the AGID test. Results of the AGID test were also compared to those obtained with the 2-mercaptoethanol (2-ME) agglutination test on 148 sera that demonstrated a standard tube-agglutination titer of 1:20 or higher. All sera with a 2-ME-agglutination titer of 1:40 or higher were positive with the AGID test. Of 123 sera that showed no 2-ME-agglutination titer, 21 were positive with the AGID test. Two of these 21 sera were obtained from patients with bacteriologically proven brucellosis, and eight were from abattoir employees with suspected but not bacteriologically proven brucellosis.

Agglutination Tests↗
PubMed1978

Pilot scale purification of alpha-galactosidase A from Cohn fraction IV-1 of human plasma.

Human plasma alpha-galactosidase A (alpha-D-galactoside galactohydrolase, EC 3.2.1.22) was purified 7000-fold over plasma levels from Cohn Fraction IV-1. The yield per kg starting material averaged 11 000 units (nmol galactose liberated per h) and the specific activity was about 600 units per mg protein with 4-methylumbelliferyl-alpha-D-galactoside. The ratio of 4-methylumbelliferyl-alpha-galactosidase to ceramide trihexosidase activities was 6.2. Both activities were heat labile and exhibited the same relative mobilities on polyacrylamide gel electrophoresis. Enzymatic activity was stable for at least 4 months at 4 and -20 degrees C. The endotoxin concentration of this preparation averaged 0.26 mg per mg protein.

Galactosidases↗
PubMed1978

Effects of laminectomy on spinal cord blood flow.

The effect of a one-segment (L-2) laminectomy on spinal cord blood flow (SCBF) was determined by the reference sample method using isotope-labeled microspheres. The SCBF was measured before laminectomy (control) and at 15 minutes postlaminectomy with the dura exposed (Series 1), 1 hour postlaminectomy with the laminectomy site closed (Series 2), 24 hours postlaminectomy with the laminectomy site closed (Series 3), and 24 hours postlaminectomy with the dura exposed (Series 4). With the laminectomy site open, SCBF was significantly depressed (22% to 45%) along the entire length of the spinal cord at 15 minutes postlaminectomy. At 1 hour postlaminectomy (with the laminectomy site closed), SCBF approached control values, although areas with significantly lowered flow were still observed in all portions of the spinal cord. By 24 hours postlaminectomy, SCBF had returned to prelaminectomy levels. However, if within 1 hour preceding the 24-hour SCBF measurement, the laminectomy site was reopened, SCBF tended to fall at and caudad to the laminectomy site. These data indicate that laminectomy can cause a significant decline in SCBF. At the present time, the mechanism(s) for this laminectomy-induced depression of SCBF are unknown, although a temperature-induced vasoconstriction is suspected.

Animals↗
PubMed1978

Microvascular perfusion experimental spinal cord injury.

Microperfusion of the spinal cords in cats was studied using a colloidal carbon perfusion technique following compression injury at 1/2 hour, 2 hours, 4 hours, 8 hours, 24 hours, and 51 days. Quantitative estimates of vascular filling were determined at these post-compression intervals. Microperfusion diminished in both the gray and white matter at 1/2 hour following injury and severe lack of perfusion was evident at 8 and 24 hours. Diminished filling of the vessels of gray and white matter seemed to parallel the degree of hemorrhagic necrosis of the gray matter. An increased number of vessels were evident in the spinal cords of long term survivals. The observation that microperfusion in the white matter of the spinal cord was diminished at 24 hours is at variance with some previous investigations. The hypoperfusion of the white matter found in this study suggests that ischemia plays a role in paraplegia resulting from experimental compression injury of the spinal cord.

Animals↗
PubMed1977

The lymphatics in experimental flaps.

The lymphatics dilate greatly after a flap delay procedure. After they return to normal in two weeks, they do not undergo further dilatation after a second delay; this suggests that alternate pathways are opened, possibly lymphaticovenous communications, for the egress of lymph. When hexamethonium is given before a primary delay, the delay is not followed by lymphatic dilatation in, or gross edema of,the flap.

Animals↗
PubMed1976

Cell potential and the sodium-potassium pump in vascular smooth muscle.

An electrogenic sodium-potassium pump appears to contribute materially to the steady-state potential and to certain of the transient potential responses of vascular smooth muscle. Since changes in cell potential in turn can lead to changes in contractile state, the pump is implicated in some of the constriction-dilation responses of blood vessels. The vasodilator action of potassium is explainable, for instance, through an effect on cell potential if (and only if) an electrogenic pump is assumed to be extruding sodium at a faster rate than it takes up potassium. This is supported by the observation that ouabain, an inhibitor of Na,K-ATPase activity, will eliminate or reverse the vascular effect of potassium. Furthermore, when the in vivo and in vitro effects on vascular smooth muscle of altered extracellular potassium concentration are compared to calculated cell potentials based on a model that includes an electrogenic pump, the experimental findings are shown to be logical and predictable.

Adenosine Triphosphatases↗
PubMed1976

Autoregulation of cerebral blood flow and its relation to cerebrospinal fluid pH.

Internal carotid artery blood flow (IFBF) was determined in each of nine Macaca mulatta by means of a flow transducer implanted around an internal carotid artery. The monkeys were lightly anesthetized, intubated, and paralyzed. Normoxia and normocarbia were maintained stable throughout the experiment. ICBF was monitored while mean arterial blood pressure (MABP) was lowered by withdrawal of blood. MABP was kept within the known limits of autoregulation in order not to compromise CBF. Cerebrospinal fluid (CSF) from the cisterna magna was analyzed for pH PCO2, and PO2 before and after a 30-min hypotensive period in which MABP was lowered from 116 +/- 4 to 70 +/- 2 mmHg (mean +/- SE). Corresponding HCO3- concentrations were calculated. The decrease in MABP did not result in a significant reduction in ICBF but elicited a 37% reduction in calculated cerebrovascular resistance, indicating normal autoregulation. Mena CSF pH was not significantly decreased (P less than 0.05); it changed from 7.320 +/- 0.010 to 7.317 +/- 0.010 after the induced hypotensive period. Thus CSF pH does not appear to have a significant role in cerebral blood flow autoregulation.

Animals↗
PubMed1976

Cerebrospinal fluid lactate and electrolyte levels following experimental spinal cord injury.

Cerebrospinal fluid (CSF) lactate, sodium (Na+), potassium (K+), calcium (Ca++), magnesium (Mg++), and chloride (C1-) levels were determined for 17 to 21 days following experimental spinal cord compression in cats. Laminectomies were performed at L-2 under general anesthesia with aseptic techniques. Paraplegia was produced by applying a 170-gm weight transdurally for 5 minutes. Significant increases in CSF lactate levels were observed on the first through ninth days post injury with peak levels (50% above normal) occurring at Day 5. The only significant postinjury CSF electrolyte changes were elevation in Ca++ concentration on Days 3, 9, 11, 13, and 15, elevation in K+ concentration on Days 9 and 11 and decline in C1- levels on the first day. The CSF K+ increase probably reflected cellular loss of K+ from damaged tissue whereas the Ca++ rise may have resulted from increased CSF protein levels. The prolonged elevation of CSF lactate indicates that tissue hypoxia plays a role in spinal cord compression paralysis, and that there is a continuing hypoxia of metabolically active spinal cord tissue for several days post injury.

Animals↗