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Biomedical subjects

J G Collins

Publications and source records attributed to J G Collins.

At least 127 records · Page 7Linked to original sources

Digestibility of proteins of the histological components of cooked and raw rice.

The aleurone layer, grain coat and embryo which constitute rice bran are rich in vitamins, lipids, protein and lysine compared with the endosperm (milled rice). A method was developed to measure the in vitro protein digestibility of raw and cooked brown rice and their histological components. The protein digestibility of cooked endosperm by the in vitro method agreed with that of other workers using in vivo techniques. The protein digestibility of the aleurone layer and grain coat from raw rice was only 25% but increased to 65% from cooked rice, due to disruption of the cellulosic cell walls at 100 degrees, which was shown by electron microscopy. The decreased protein digestibility due to cooking was not the result of formation of epsilon-lysyl-gamma-glutamyl isopeptide cross-links, but may be due to formation of a cystine-rich core that is resistant to proteases. The protein digestibility of cooked brown rice was approximately the same as that of cooked milled rice, hence it is advantageous for those for whom rice is a staple food to consume brown rather than milled rice.

Amino Acids↗

Interactions of lidocaine and calcium in blocking the compound action potential of frog sciatic nerve.

The exact role of calcium in nerve conduction in neurons that have been blocked by local anesthetics remains controversial. Recently, attention has been drawn to the importance of examining both frequency-dependent and nonfrequency-dependent conduction block, since it is felt that frequency-dependent block provides a model that more closely approximates the normal physiologic state. The present study was designed to examine the effects of calcium on both the nonfrequency-dependent and frequency-dependent components of lidocaine nerve block. Desheathed, whole sciatic nerves from frogs were placed in a sucrose gap chamber and stimulated by trains of 20 impulses at frequencies from 3 to 90 Hz at supramaximal intensity for activation of the compound action potential. After control studies, the nerve was bathed by a frog Ringer's solution containing calcium concentrations, which increased from 0.0 mM to the physiologic value of 2.0 mM with or without 0.5 mM lidocaine. Compound action potentials were measured, and both frequency-dependent block and nonfrequency-dependent block were compared in each solution. Low calcium concentrations significantly enhanced both nonfrequency- and frequency-dependent lidocaine block. The effect of low concentrations of calcium was greater at higher frequencies of stimulation.

Action Potentials↗

Spinally administered epinephrine suppresses noxiously evoked activity of WDR neurons in the dorsal horn of the spinal cord.

This study was designed to determine if spinally administered epinephrine is capable of suppressing noxiously evoked activity of wide dynamic range (WDR) neurons in the dorsal horn of the spinal cord. Extracellular activity was recorded from single WDR neurons in the dorsal horn of decerebrate, spinal cord-transected (T-12) cats. Activity was evoked by the presentation of a noxious radiant heat stimulus (51 degrees C) to the cells' receptive fields on the hind paws. Evoked activity was monitored both before and after the spinal administration of either 50 micrograms (n = 6) or 100 micrograms (n = 6) epinephrine. Both doses of epinephrine produced a significant suppression of noxiously evoked activity, which was dose-dependent. In addition, the 100-microgram dose produced a suppression that was of longer duration than that seen following the 50-microgram dose. Recovery from suppression was recorded following both the 50- and 100-microgram dose. These results indicate that spinally administered epinephrine is capable of suppressing noxiously evoked activity of WDR neurons in the dorsal horn of the spinal cord. Since WDR neurons have been identified as cells of origin for the spinothalamic tract, such an action may block the central transmission of afferent pain information. This may be a mechanism by which spinally administered epinephrine enhances the duration or intensity of spinal anesthesia produced by local anesthetics and may also explain spinal analgesia resulting from the spinal administration of adrenergic agonists. Interactions between spinally administered epinephrine and spinally administered opioids also were studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

Magnesium enhances local anesthetic nerve block of frog sciatic nerve.

The present study was designed to examine the effects of increased magnesium concentration on the nerve block produced by lidocaine, benzocaine, and QX 572 (a quaternary derivative of lidocaine). Desheathed whole sciatic nerves from northern Rana pipiens frogs were placed in a sucrose gap chamber and stimulated at various frequencies at supramaximal intensity for the activation of the compound action potential. After control studies, the nerve was bathed by a calcium-free frog Ringer's solution containing magnesium concentrations of 3.0, 10.0, or 20.0 mM with or without 0.5 mM lidocaine, 0.5 mM benzocaine, or 0.75 mM QX 572. Compound action potentials were measured, and nonfrequency and frequency dependent blocks were compared in each solution. Increased magnesium ion concentration, in the absence of local anesthetics, enhanced the nonfrequency dependent block but did not change the frequency dependent block. All three local anesthetics enhanced both types of block. Increased magnesium concentrations enhanced only the nonfrequency dependent benzocaine block. In contrast, increased magnesium enhanced both types of block produced by QX 572 and lidocaine. These results suggest a potentially important interaction between high magnesium concentrations and local anesthetic nerve blocks.

Action Potentials↗

Alpha-chloralose suppression of neuronal activity.

Alpha-chloralose, an anesthetic agent widely used in neurophysiologic studies, caused a significant and long-lasting suppression of single neuron activity recorded from two areas of the central nervous system in decerebrate cats. A 50 mg/kg dose (an average anesthetic dose used in many neurophysiologic studies) caused suppression of spontaneous and evoked activity of neurons in the dorsal horn of the spinal cord and greater suppression of neurons in the nucleus reticularis gigantocellularis (NRGC) of the medial medullary reticular formation. Many researchers are of the opinion that alpha-chloralose causes less suppression of the central nervous system (CNS) than other commonly used anesthetic agents. The neuronal suppression recorded in this study appears similar in many ways to suppression caused by other anesthetic agents in the same two areas of the CNS. The results of the present study suggest that alpha-chloralose may be capable of producing significant suppression of neurons in the dorsal horn of the spinal cord and NRGC. Its ability to influence other areas of the CNS should not be inferred from these results, but the data do indicate the importance of evaluating the effects of anesthetics upon neurophysiologic systems under study.

Animals↗

The effect of dantrolene on skeletal-muscle sarcoplasmic-reticulum function in malignant hyperpyrexia in pigs.

The effect of the muscle relaxant dantrolene on isolated sarcoplasmic reticulum was studied in control and malignant-hyperpyrexia-susceptible Landrace pigs. The membranes prepared from both sources showed similar Ca2+-dependent ATPase activities, had comparable phospholipid/protein ratios, and their sodium dodecyl sulphate/polyacrylamide-gel patterns were indistinguishable. Membranes from both sources appeared to bind similar amounts of dantrolene. The drug did not stimulate Ca2+-dependent ATPase activity in preparations from either source. The rates of Ca2+ exchange and Ca2+ efflux appeared to be similar in sarcoplasmic reticulum of control and malignant-hyperpyrexia-susceptible pigs. Dantrolene did not affect either the rates or the amount of Ca2+ lost from the vesicles. These results suggest that dantrolene does not directly affect the movement of Ca2+ across the sarcoplasmic-reticulum membrane.

Animals↗

Epidural morphine does not affect the duration of action of epidural 2-chloroprocaine following Caesarean section.

The effect of epidural morphine on the duration of action of epidural 2-chloroprocaine was studied in a double-blind fashion in 30 patients following elective Caesarean section. When compared to epidural saline controls (n = 15), patients (n = 15) who received epidural morphine (4.0-5.0 mg) did not experience a prolongation or reduction in the duration of the somatic or sympathetic nervous system blockades produced by epidural 2-chloroprocaine.

Anesthesia, Epidural↗

Suppression of noxiously evoked WDR dorsal horn neuronal activity by spinally administered morphine.

The present study was carried out in order to examine the ability of spinally administered morphine to suppress noxiously evoked activity of wide-dynamic-range (WDR) neurons in the dorsal horn of the spinal cord in decerebrate, spinal cord-transected cats. All cells (n = 25) responded maximally to high-intensity noxious heat stimulation (51 degrees C) and were classified as wide dynamic range neurons. The spinal administration of 0.1 mg of morphine caused a significant reduction of noxiously evoked activity but did not significantly change spontaneous activity. The 0.25-mg dose caused a significant reduction of both types of activity. Thirty minutes after spinal administration, 0.1 mg of morphine caused a 27% reduction of spontaneous activity and a 43% reduction of noxiously evoked activity. The 0.25-mg dose reduced spontaneous activity by 44% and the evoked activity by 70%. Naloxone partially reversed the morphine-induced neuronal suppression. In addition, in the four neurons in which it was tried, spinally administered epinephrine was found to further suppress the remaining neuronal activity following the spinal morphine effect. These results demonstrate for the first time that spinally administered morphine is capable of suppressing noxiously evoked activity of wide-dynamic-range neurons in the dorsal horn of the spinal cord. They also demonstrate the dose-dependent nature of this effect and the potential importance of the interaction between morphine and adrenergic agonists in blocking information about noxious events. This information provides a probable mechanism of action for spinal opiate analgesia.

Action Potentials↗

Dose-response suppression of noxiously evoked activity of WDR neurons by spinally administered fentanyl.

The present study examined the influence of spinally administered fentanyl on the spontaneous and noxiously evoked activity of wide dynamic range (WDR) neurons in the dorsal horn of decerebrate, spinal cord-transected cats. This work was performed in order to evaluate the dose-response relationship, time course, and naloxone reversibility of fentanyl suppression of neurons that are involved with the transmission of information about pain. Extracellular single neuron recordings were obtained from 18 WDR neurons in the lumbar enlargement. These neurons were activated by a radiant heat stimulus on the footpads of the hindpaw. Fentanyl (10, 15, 25 micrograms in 0.5 ml of physiologic saline) was placed on the spinal cord following control studies of each neuron and the effect was observed. In 12 cats, 31 min after fentanyl administration, naloxone (0.1 mg) was administered intravenously, and its effect on the fentanyl suppression was determined. All three doses of fentanyl suppressed both the spontaneous and evoked activity of all the neurons studied. Thirty minutes after fentanyl the mean evoked activity was reduced to 47, 23, and 11% of control values by 10, 15, and 25 micrograms, respectively. The spontaneous activity was reduced to similar levels. Intravenous naloxone (0.1 mg) caused a significant reversal of the fentanyl suppression. The results of the present study indicate that fentanyl causes a naloxone-reversible, dose-dependent suppression of noxiously evoked WDR neuron activity. Such results support the concept that fentanyl is acting through a specific drug-receptor interaction. The onset of neuronal suppression occurred more rapidly, and the duration of the suppression was longer following fentanyl than that seen following spinal morphine. The onset and duration of this suppression correlates well with human clinical data, providing further evidence that alterations of WDR neuronal activity may be important in the production of spinal opioid analgesia.

Action Potentials↗

Serum morphine levels in cats during dorsal horn neuron suppression by spinally administered morphine.

The degree of serum uptake of morphine following spinal morphine administration was measured in cats. Total serum morphine levels (free plus conjugated) were determined during suppression of noxiously evoked wide dynamic range neuron activity by spinally administered morphine and compared with total serum morphine levels following i.v. administration of similar doses. The serum levels at 30 minutes after spinal application of morphine (a time at which there was significant suppression of noxiously evoked neuronal activity) were low; after 0.1 and 0.25 mg the levels were 6.5 (n=6) and 12.5 (n=5) ng/ml respectively. In contrast, intravenous administration of the same doses (0.1 and 0.25 mg) produced levels at 30 minutes of 24 and 36 ng/ml respectively, while an intravenous dose commonly used in earlier neurophysiologic studies (2 mg/kg) produced serum levels in excess of 400 ng/ml. These results indicate that although there is systemic uptake following spinal administration of morphine, the serum levels achieved are much lower than those following intravenous administration of a comparable dose, and are insufficient to explain the resultant suppression of wide dynamic range neurons.

Animals↗

Thiopental suppression of neurons of the nucleus reticularis gigantocellularis of the cat.

The effects of sodium thiopental on the single-unit activity of cells in the nucleus reticularis gigantocellularis (NRGG) were examined in decerebrated cats. Only cells in the NRGC that responded exclusively to electrical stimulation of A-delta fibers (noxious stimulation) in the superficial radial nerve were studied. Sodium thiopental caused a significant, dose-dependent suppression of spontaneous and evoked neuronal activity of cells in the NRGC. Spontaneous activity was suppressed by 66% and 98% after intravenous administration of sodium thiopental, 2.5 mg/kg and 5.0 mg/kg, respectively. Evoked activity was suppressed by 65% and 79%. These findings, when added to previous reports of the suppressive effects of nitrous oxide, morphine sulfate, ketamine hydrochloride, and halothane, suggest the involvement of the NRGC in nociception and provide evidence that sodium thiopental significantly modifies the neuronal message about a noxious stimulus as recorded at the level of the NRGC.

Action Potentials↗

A comparison of human tactile stimulus velocity discrimination with the ability of S-I cortical neurons in awake rhesus monkeys to signal the same velocity differences before and after non-anesthetic doses of pentobarbital.

Using psychophysical techniques, the ability of human subjects to discriminate the velocity of brush movement across the glabrous skin of the hand was determined. The same stimulus was then used in a series of neurophysiological experiments designed to determine the ability of neurons in the primary somatosensory cortex (S-I) of awake rhesus monkeys to signal differences in the same velocities. Analysis of the data in signal detection theory terms revealed that humans could discriminate two velocities (132 and 182 mm/sec) much better than most of the cortical cells of the monkeys could signal the differences in those same velocities by changes in their stimulus induced mean firing frequency. However, 4 of the 37 cells studied signaled the differences as well as the human observers. Non-anesthetic doses of pentobarbital (1-20 mg/kg) caused a reduction in the firing frequency of the S-I neurons but at the same time enhanced the difference in firing frequency elicited by the two different stimulus velocities. This enhancement in the difference between the firing frequencies was caused by a relatively greater suppression of neuronal activity elicited by the slower velocity. These results not only point out potential problems with the use of barbiturates in neurophysiological studies and by humans who require fine tactile acuity, but they also raise important questions about coding by S-I cells. The reduction in overall neuronal activity accompanied by the enhancement of the difference in firing frequency at the two velocities would suggest that, if firing frequency is coding for stimulus presence or velocity, at 8 mg/kg the monkeys may have a more difficult time detecting the stimulus but an easier time discriminating between different velocities of the stimulus.

Animals↗

Structure of a marsupial-mild trisaccharide.

A trisaccharide, which is a major carbohydrate component of the milk of the tammar wallaby and the grey kangaroo, has been identified by chemical, enzymic, g.l.c.-m.s., and n.m.r. methods as O-beta-D-galactopyranosyl-(1 yields 3)-O-beta-D-galactopyranosyl-(1 yields 4)-D-glucose (3'-galactosyl-lactose).

Animals↗