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Biomedical subjects

R Vink

Publications and source records attributed to R Vink.

87 records · Page 5Linked to original sources
PubMed1987

Decrease in total and free magnesium concentration following traumatic brain injury in rats.

31P magnetic resonance spectroscopy was used to determine the intracellular free Mg2+ concentration prior to and following fluid percussion induced traumatic brain injury in rats. Prior to injury, cerebral intracellular free Mg2+ concentration in the rat was 0.93 +/- 0.19 mM (mean +/- SE; n = 5). Following injury, free Mg2+ in the injured cortex declined by 70% within the first hour, and did not recover over the next 3 hours. Total Mg2+ also declined by 10% over this time period; however, there were no changes in brain Na+ or tissue water content. Because of its primary role in cellular metabolism, the early decline in tissue Mg2+ following brain trauma may be a critical factor in the development of irreversible tissue injury.

Adenosine Triphosphate↗
PubMed1987

Alterations in tissue Mg++, Na+ and spinal cord edema following impact trauma in rats.

Alterations in water content and total tissue Na+ and Mg++ of rat spinal cord tissue were followed over time after a 100 g-cm impact injury to the T-9 spinal cord segment. Rats subjected to laminectomy but not trauma served as controls. In the injured segment there was a progressive increase in water content with increased Na+ and decreased Mg++ at 1 hour and 24 hours after trauma. At seven days, water and Na+ content remained elevated, whereas Mg++ levels had returned to preinjury baseline values. Because of its important role in many metabolic and physiological regulatory processes the early decline in Mg++ concentration after trauma may contribute to the development of secondary tissue damage after spinal cord injury.

Animals↗
PubMed1987

31P magnetic resonance spectroscopy of traumatic spinal cord injury.

31P magnetic resonance spectroscopy (MRS) was applied in vivo to study metabolic changes in spinal cord after experimental traumatic injury. Severe trauma, resulting in spastic paraplegia, caused an early and sustained loss of high energy phosphates with profound intracellular acidosis. Early metabolic changes after traumatic spinal injury may predict irreversible tissue damage.

Animals↗
PubMed1987

Effects of traumatic brain injury on cerebral high-energy phosphates and pH: a 31P magnetic resonance spectroscopy study.

Traumatic injuries to the CNS produce tissue damage both through mechanical disruption and through more delayed autodestructive processes. Delayed events include various biochemical changes whose nature and time course remain to be fully elucidated. Magnetic resonance spectroscopy (MRS) techniques permit repeated, noninvasive measurement of biochemical changes in the same animal. Using phosphorus MRS, we have examined certain biochemical responses of rats over an 8-h period following lateralized brain injury (1.5-2.5 atmospheres) using a standardized fluid-percussion model recently developed in our laboratory. Following injury, the ratio of phosphocreatine to inorganic phosphate (PCr/Pi) showed a biphasic decline: The first decline reached its nadir (4.8 +/- 0.4 to 2.8 +/- 0.7) by 40 min post-trauma with recovery by 100 min, followed by a second decline by 2 h that persisted for the remaining 6-h observation period (mean 2.5 +/- 0.5). The first, but not the second, decrease in PCr/Pi was associated with tissue acidosis (pH 7.10 +/- 0.03 to 6.86 +/- 0.11). No changes in ATP occurred at any time during the injury observation period. Such changes may be indicative of altered mitochondrial energy production following brain injury, which may account for the reduced capacity of the cell to recover from traumatic injury.

Animals↗
PubMed1987

Traumatic brain injury in the rat: alterations in brain lactate and pH as characterized by 1H and 31P nuclear magnetic resonance.

Application of both phosphorus (31P) and proton (1H) magnetic resonance spectroscopy (MRS) to the study of brain metabolism permits the noninvasive measurement of intracellular pH and brain lactate level. We have used water-suppression 1H MRS with novel lactate-editing techniques, together with 31P MRS, to characterize sequential changes in brain lactate level and pH in vivo over an 8-h period following fluid-percussion brain injury of graded severity in the rat. A transient fall in intracellular pH (from 7.09 +/- 0.07 at baseline to 6.88 +/- 0.09 at 40 min postinjury) occurred in animals subjected to moderate- (1.5-2.2 atm) and high- (2.5-3.3 atm) but not low-level (0.1-1.2 atm) injury; intracellular pH returned to baseline by 90 min postinjury. Transient elevations in brain lactate level were observed that temporally paralleled and were significantly correlated with the pH changes for all injury levels (r = 0.93, p less than 0.001). Postinjury alterations in intracellular brain pH and lactate level were identical in magnitude in animals subjected to either moderate or high-level injury. However, animals subjected to moderate injury had a moderate chronic neurological deficit that persisted up to 4 weeks postinjury, whereas animals subjected to a high level of injury showed greater histopathological damage and a more severe chronic neurological deficit. These data suggest that the extent of posttraumatic intracellular cerebral acidosis in our model of experimental head injury is not directly related to the severity of functional neurological deficit.

Animals↗
PubMed1985

Regulation of the glucose phosphotransferase system in Brochothrix thermosphacta by membrane energization.

Uptake of 2-deoxyglucose, alpha-methylglucopyranoside, and glucose into intact cells of Brochothrix thermosphacta (formerly Microbacterium thermosphactum, ATCC 11509) was stimulated by KCN or CCCP. The glucose analogs were recovered almost totally as the sugar phosphates. Membrane vesicles were isolated from protoplasts and shown to be right side out by freeze fracturing and by using ATPase as a marker for the cytoplasmic membrane surface. Uptake of glucose into vesicles was dependent on the presence of phosphoenolpyruvate. NADH oxidation, K+ -diffusion gradients, and externally directed lactate gradients (pH greater than 7 initially) were used to generate transmembrane potentials across membrane vesicles. Above a threshold value of about -50 mV, uptake of glucose into membrane vesicles was reduced. Likewise, the maximum uptake of glucose and its two analogs into cells occurred when the protonmotive force was less than about -50 mV.

Adenosine Triphosphatases↗
PubMed1984

Estimation of H+ to adenosine 5'-triphosphate stoichiometry of Escherichia coli ATP synthase using 31P NMR.

High-field 31P NMR techniques have been used to measure transmembrane delta pH in wild-type, unc A, and hem A mutants of Escherichia coli. delta psi was measured by distribution methods with radioactive tetraphenylphosphonium bromide and 86Rb+ ions as the probes, while intracellular ATP, ADP, and inorganic phosphate concentrations were determined from the 31P NMR spectra. delta G'p and the stoichiometry for ATP synthesis [delta G'p/(F delta p)] were then calculated. The stoichiometry of the ATP synthase was found to vary as a function of the cellular metabolic state. In nongrowing, wild-type cells delta p was 192 +/- 16 mV with succinate as the substrate and saturating oxygen tension. With limiting oxygen (congruent to microM oxygen), delta p was 125 +/- 14 mV. Nucleoside triphosphate synthesis was observed in both cases. The H+/ATP stoichiometry varied from 2.15 +/- 0.35 under aerobic conditions to 3.6 +/- 0.8 at low oxygen tension. delta p for unc A cells was 140 +/- 14 mV with glucose as the substrate (greater than 2.5 microM oxygen) and for hem A mutants was 115 +/- 10 mV. The bulk phase potentials in oxygen-limited, wild-type cells and in respiratory deficient (hem A) cells are comparable, but in the former the ATPase is poised for synthesis while in the latter it generates delta p. The data support a role for localized interactions between the redox and the ATPase sites.

ATP Synthetase Complexes↗
PubMed1983

High-field phosphorus NMR studies of the stoichiometry of the lactate/proton carrier in Streptococcus faecalis.

High-field 31P-NMR studies of whole cells of Streptococcus faecalis have shown that delta pH can be formed by ATP hydrolysis and also by lactate transport. We have used 31P-NMR to measure the pH dependence of the variable stoichiometry of the proton/lactate carrier. At low external pH (pH approximately equal to 6.5) the influx stoichiometry was 1.1 H+/lactate, while at high pH (7.5) the ratio was almost 2; the apparent midpoint pH of this variable stoichiometry is 7. delta psi measurements support the electrogenic nature of lactate transport at high pH; the variable rate of membrane depolarization caused by lactate transport also had a midpoint near pH 7.0. The data is consistent with a symmetrical carrier operating with variable stoichiometry as proposed by Michels et al.

Biological Transport↗
PubMedDate not supplied

Efficacy of competitive vs noncompetitive blockade of the NMDA channel following traumatic brain injury.

N-methyl-D-aspartate (NMDA) receptor antagonists have been demonstrated widely to be neuroprotective in cerebral ischemia, hypoxia, and traumatic brain injury. However, although noncompetitive NMDA antagonists have typically proven efficacious under all of these conditions, competitive antagonists have not been shown to be beneficial following moderate traumatic brain injury. The present study has used phosphorus magnetic resonance spectroscopy ([31P]MRS) to examine the effects of the competitive antagonist cis-4-(phosphonomethyl) piperidine-2-carboxylic acid (CGS-19755) and the noncompetitive antagonist dextromethorphan on biochemical outcome following fluid percussion-induced traumatic brain injury in rats. Five minutes prior to induction of moderate (2.8 +/- 0.2 atm) fluid percussion brain injury, animals received either CGS-19755 (10 mg/kg iv), dextromethorphan (10 mg/kg iv), or equal volume saline vehicle. [31P]MRS spectra were then acquired for 4 h post-trauma and intracellular pH, free magnesium concentration, cytosolic phosphorylation potential, and oxidative capacity determined. Both CGS-19755-treated animals and saline treated controls demonstrated significant and sustained declines in intracellular free magnesium concentration and bioenergetic status following trauma. In contrast, administration of dextromethorphan significantly attenuated free magnesium decline and improved bioenergetic state during the post-traumatic monitoring period. These results suggest that the neuroprotective actions of NMDA antagonists following traumatic brain injury are associated with attenuation of free magnesium decline and that such actions seem to be preferentially mediated by noncompetitive blockers.

Animals↗
PubMedDate not supplied

Paracetamol overdose: pathophysiology and nursing management.

Paracetamol overdose now represents one third of all self-poisoning cases. In contrast to other drugs, the use of paracetamol as a self-poisoning agent is increasing. As very large doses of the drug cause severe liver injury, which can result in fulminant hepatic failure when left untreated, it is essential that nurses have a complete understanding of the mechanisms of normal paracetamol metabolism, effects of overdosage and treatment strategies to guide the nursing management of clients. This review therefore critically examines the pathophysiology and nursing management of clients with acute paracetamol overdosage.

Acetaminophen↗
PubMedDate not supplied

Magnesium and brain trauma.

Nuclear magnetic resonance (NMR) studies of central nervous system (CNS) trauma have shown that intracellular free magnesium (Mg) concentration declines following injury. This fall in free Mg concentration was associated with a decrease in brain total tissue Mg concentration. Declines in both free and total tissue Mg concentration could be prevented or attenuated by treatments targeted to improve neurologic outcome by inhibition of specific injury factors, such as excitatory amino acids and opioid peptides. Furthermore, the extent of these changes in CNS Mg concentration and their attenuation with a diversity of treatments have been correlated to neurologic outcome. As such, it has been proposed that Mg, and in particular the cytosolic free Mg concentration, plays a critical central role in determining the degree of neurologic deficit expressed following a traumatic injury to the CNS. This mini-review will focus on the evidence suggesting that Mg concentration is important in the development of irreversible tissue damage following traumatic brain injury, and will discuss the relative importance of Mg to this process, and its interrelationship with a number of other proposed injury factors.

Animals↗