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Biomedical subjects

C J Robinson

Publications and source records attributed to C J Robinson.

At least 73 records · Page 4Linked to original sources
PubMed1987

Naloxone efficacy in bladder rehabilitation of spinal cord injury patients.

Naloxone has been reported to facilitate detrusor activity by blocking the inhibitory action of the enkephalins. We tested the urodynamic effects of intravenous naloxone (0.4 to 0.8 mg.) in 15 patients with spinal cord injury via rapid fill carbon dioxide cystometry and perineal electromyography. Fourteen patients had suprasacral lesions (3 complete), while 1 had an incomplete lower cord lesion. The average interval from injury was 4.2 months. Most of the patients were managed with intermittent catheterization and most had chronic bacteriuria. Initially, 10 patients had detrusor areflexia and 5 had detrusor hyperreflexia (2 with dyssynergia). Of the 15 patients 14 had no neuropathic condition as noted on baseline electromyography. After naloxone injection no significant cystometrographic changes occurred but 11 patients (73 per cent) had decreased electromyographic activity. The vesicourethral pattern of the 2 patients with dyssynergia did not change after naloxone, even though the electromyographic response decreased in both. The patients showed no other effects of the naloxone administration. Contrary to other studies, naloxone seemed to diminish pelvic floor (electromyographic) activity but it did not change bladder (cystometrographic) function during bladder rehabilitation of spinal cord injury patients.

Adult↗
PubMed1987

Responses in the first or second somatosensory cortical area in cats during transient inactivation of the other ipsilateral area with lidocaine hydrochloride.

Simultaneous recordings were obtained from the primary and secondary somatosensory cortical areas (SI and SII) in cats anesthetized with ketamine or pentobarbital. A total of 40 individual neurons were studied (29 in SII and 11 in SI) before, during, and following injections of microliter quantities of lidocaine hydrochloride in the other ipsilateral cortical area. Activity in the cortex injected with the local anesthetic was monitored with single-neuron, multi-neuron, or evoked potential responses to determine the time course of inactivation within 0.5-2 mm of the injection sites. Recording sites in both cortical locations were in the representations of the distal forelimb. Responses were elicited by transcutaneous electrical stimulation across the receptive fields with needle electrodes. Short-latency responses were synchronously activated, and, in those circumstances where single neurons were isolated in both areas, no overall differences in latency were noted. Anesthetization of either cortical area never blocked access of somatosensory information to the intact area, even when the injected cortex was completely silenced in the vicinity of the injection mass. In 15 SII neurons and 7 SI neurons, changes were seen in short-latency evoked responses to stimulation of their receptive fields or in background activity following local anesthesia of the other area through several cycles of injection and recovery. In 7 of these 15 SII cells, changes were noted in the timing and/or firing rates of the short-latency responses; changes were noted in the short-latency responses of 2 of these 7 SI cells while SII was silenced. In 11 SII and 6 SI cells, "background" activity that was recorded during the interstimulus intervals either increased (most cases) or decreased during local anesthesia of the other area. The results are discussed in reference to the hypothesis that primary sensory cortical areas feed information forward to secondary areas, and these feed back modulatory controls to the primary regions.

Animals↗
PubMed1986

Olfactory adenylate cyclase of the rat. Stimulation by odorants and inhibition by Ca2+.

Membranes prepared from the olfactory mucosa of the rat show a high level of adenylate cyclase activity. The activity increases up to 2-fold in the presence of physiologically relevant concentrations of odorants and is inhibited by Ca2+. The level of cyclase activity found is sufficient to explain the speed of olfactory transduction, which occurs on a time scale of tens of milliseconds.

Acetophenones↗
PubMed1986

Mercuric chloride-, gold sodium thiomalate-, and D-penicillamine-induced antinuclear antibodies in mice.

Inducibility of antinuclear antibodies (ANA) by mercuric chloride (HgCl2) was studied in various strains of mice. High response to the treatment was observed in strains A.SW (H-2s), A.CA (H-2f), A.TH (H-2t2), B10.S (H-2s), DBA/1J (H-2q), and P/J (H-2p); strains A.BY (H-2b), B10.M (H-2f), and C3H/HeSnJ (H-2k) showed a low response, while strains A/WySn (H-2a), A/J (H-2a), A.TL (H-2tl), BALB/cJ (H-2d), C57BL/10SnJ (H-2b), B10.A (H-2a), and PL/J (H-2u) did not produce any detectable ANA. Thus, the H-2a haplotype determines resistance to the treatment regardless of the genetic background; the H-2s determines susceptibility, while the H-2b and H-2f are intermediate haplotypes whose effect depends on the interaction with the background genes. Our results with intra-H-2 recombinant strains indicate that the I region of the H-2 complex is the major genetic factor controlling this response. The function of the I region is to control cellular cooperation in the immune response that finally results in production of antibodies specific for a particular antigen. Therefore, we postulated that the I region controls the antibody response to a nuclear antigen released as a result of HgCl2 toxicity in mice. A genetic study of an A.SW X C57BL/10 cross confirmed this observation, showing that resistance to ANA induction by HgCl2 in this strain combination is determined by interaction of a semidominant H-2-linked gene and one or more unlinked genes. The two drugs tested, gold sodium thiomalate and D-penicillamine, also induced ANA in A.SW mice, while other strains tested resisted this treatment.

Animals↗
PubMed1986

Changes in micturition volume thresholds in conscious dogs following spinal opiate administration.

Micturition difficulties appear as an often-reported side effect of the clinical use of opiates for spinal analgesia. Only a few experimental studies have focused specifically on this problem, especially in an unanesthetized animal model where chronic pharmacological studies can be carried out. The changes in micturition volume thresholds that occurred following spinal intrathecal injections of 1 mg of morphine sulphate were measured in 11 conscious dogs and compared with threshold changes produced in these same dogs by i.v. injections of various doses of morphine sulphate and by intrathecal and i.v. injections of naloxone HCl. In all cases, intrathecal or systemic morphine at doses of 1.0 mg or greater significantly (P less than 0.05) increased the bladder volume at which micturition took place. Naloxone, injected intrathecally to reverse the effects of intrathecal morphine, significantly reduced the micturition volume threshold, in most cases to below control volumes. A 400 microgram dose of naloxone, injected intrathecally without prior injection of morphine, significantly lowered the volume threshold in 9 dogs, even though two of these dogs had elevated thresholds following naloxone injection. The reduction in volume thresholds by i.v. naloxone not preceded by morphine injection was not statistically significant over that of control. These results are interpreted in light of recent findings concerning localization of endogenous opiate receptors within the micturition reflex pathway.

Anesthesia, Spinal↗
PubMed1985

Renal osteodystrophy and metastatic calcification in long-term continuous ambulatory peritoneal dialysis.

The biochemical data and drug histories related to bone disease were extracted from the case records of 47 patients who had been treated by continuous ambulatory peritoneal dialysis (CAPD) for more than two years. These data were reviewed in conjunction with the skeletal surveys done over the same period in all patients, with particular reference to secondary hyperparathyroidism, osteomalacia and non-visceral metastatic calcification. Paired bone biopsies were available in 20 of these patients and the histology was quantitated. In the majority of our patients secondary hyperparathyroidism was controlled or improved on CAPD. Osteomalacia also improved in two of the three patients in whom it was initially present and did not develop in any patient whilst on CAPD. We did, however, note a high incidence of non-visceral metastatic calcification. Small vessel calcification developed in 19.6 per cent of patients, large vessel calcification developed in 23.9 per cent and soft tissue calcification developed in 21.7 per cent of patients. We conclude that CAPD, as a form of treatment for end-stage renal disease, satisfactorily controls the osteodystrophy associated with renal failure in the majority of patients. The significance of the high incidence of non-visceral metastatic calcification remains to be established.

Adult↗
PubMed1984

The importance of fortification of flour with calcium and the sources of Ca in the diet of 375 English adolescents.

The contribution of the fortification of flour with calcium carbonate to the Ca intake of 375, 11-14-year-old Northumbrian children has been calculated. Mean Ca intakes were above those currently recommended for children of this age. The fortification of flour supplied 16% of the total Ca intakes. Without the fortification, the percentage of these children with intakes below the recommended intake would be more than double. This would include the majority of girls (particularly those of social classes III, IV and V). The recommendation to stop fortifying flour with calcium carbonate should be reviewed.

Adolescent↗
PubMed1984

Peripheral neural correlates of magnitude of cutaneous pain and hyperalgesia: simultaneous recordings in humans of sensory judgments of pain and evoked responses in nociceptors with C-fibers.

The peripheral neuronal correlates of heat pain elicited from normal skin and from skin made hyperalgesic following a mild heat injury were studied by simultaneously recording, in humans, evoked responses in C mechanoheat (CMH) nociceptors and the magnitude estimations of pain obtained from the same subjects. Subjects made continuous magnitude ratings of pain elicited by short-duration stimuli of 39-51 degrees C delivered to the hairy skin of the calf or foot before and at varying intervals of time after a heat injury induced by a conditioning stimulus (CS) of 50 degrees C, 100 s or 48 degrees C, 360 s. The stimuli were applied with a thermode pressed against the nociceptor's receptive field. For heat stimulations of normal skin, that is, uninjured skin, pain thresholds in 14 experiments with nine subjects ranged from 41 to 49 degrees C, whereas response thresholds for most of the 14 CMH nociceptors were 41 degrees C (in two cases, 43 degrees C). The latter suggested that spatial summation of input from many nociceptors was necessary at pain threshold. An intensity-response function was obtained for each CMH by relating the total number of nerve impulses evoked per stimulus to stimulus temperature. A corresponding magnitude scaling function for pain was obtained by relating the maximum rating of pain elicited by each stimulus to stimulus temperature. The relation between the subject's scaling function and the intensity-response function of his CMH nociceptor varied somewhat from one experiment to the next, regardless of whether the results were obtained from the same or from different subjects. However, when averages were computed for all 14 tests, there was a near linear relationship between the mean number of impulses elicited in the CMHs and the median ratings of pain, over the range of 45-51 degrees C. It was concluded that the magnitude of heat pain sensation was more closely related to the magnitude of response in a population of CMH nociceptors than in any individual nociceptor. At 0.5 min after the CS, the pain thresholds of most subjects were elevated, and the magnitude ratings of pain elicited by supra-threshold stimuli were lower than pre-CS values (hypoalgesia). Corresponding changes were seen in the increased thresholds and decreased responses (fatigue) of most CMHs. By 5-10 min after the CS, the pain thresholds of most subjects were lower, and their magnitude ratings of suprathreshold stimuli were greater than pre-CS values (hyperalgesia).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

Time-intensity profiles of cutaneous pain in normal and hyperalgesic skin: a comparison with C-fiber nociceptor activities in monkey and human.

Contributions of evoked discharge in nociceptors with C-fibers to the temporal profiles of magnitude judgments of pain by humans were determined for heat stimulations of the skin before and after the development of hyperalgesia (increased sensitivity to pain) produced by a mild heat injury. Human subjects continuously rated the magnitude of pain evoked by short-duration heat stimuli of 39-51 degrees C delivered to the hairy skin of the arm or leg (calf or foot) before and after the development of hyperalgesia produced by a conditioning stimulus (CS) of either 50 degrees C for 100 s or 48 degrees C for 360 s. During heat stimulations of the leg in humans, magnitude judgments of pain were obtained simultaneously with recordings of evoked discharges in single C-fiber mechanoheat (CMH) nociceptive afferent fibers. Seven fibers were studied before and after the CS. In other experiments, magnitude ratings of pain evoked by heat stimulations of the arm were compared with heat-evoked discharges in 21 CMH nociceptive afferent fibers innervating the hairy skin of the wrist or hand in anesthetized monkeys. From CMH responses obtained in each species, median response latencies were calculated as well as poststimulus time (PST) histograms--the latter plotting mean frequency of discharge versus time during each stimulus. In these analyses, the times of action potentials in CMHs were calculated as they would occur at entry to the lumbar or cervical spinal cord in humans, taking into account the temporal dispersion that should occur because of differing conduction velocities. These results were then compared with response latencies for pain and the temporal profiles of pain ratings made by individual subjects. Comparisons were made for data obtained before the CS (normal skin) and those obtained 10 min after the CS in heat-sensitized (hyperalgesic) skin. For normal skin, PST histograms of mean frequencies of discharge were similar for CMHs with similar heat thresholds (41-43 degrees) in the anesthetized monkey and the awake human. Despite minor discrepancies, there were similarities in the changes in these histograms for monkey and human CMHs following heat sensitization after the CS. It was concluded that CMHs in monkeys and humans have similar response magnitudes and temporal profiles of response to heat. The major differences in the temporal profiles of CMH responses and human pain ratings were the latencies at which CMH responses and pain ratings began, reached maximum, and ended.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Induction of anti-nuclear antibodies by mercuric chloride in mice.

Mercuric chloride (HgCl2) was administered parenterally to outbred Swiss ICR mice of both sexes and to inbred A/J male mice. In repeated experiments both male and female ICR mice developed anti-nuclear antibodies (ANA) giving a distinctive nucleolar fluorescence pattern in response to HgCl2 treatment. Within 1 week after the start of treatment, many of the mice had serum ANA of the IgG class directed against nucleolar antigen(s). Maximum ANA induction was reached by week 4. Inbred A/J male mice were resistant to the induction of ANA by HgCl2.

Animals↗
PubMed1983

Psychophysical detection and pain ratings of incremental thermal stimuli: a comparison with nociceptor responses in humans.

The capacity of humans to detect and scale the magnitude of pain elicited by small increments in temperature, delivered by a contact thermal stimulator to localized areas of the arm or leg, was measured on non-painful and painful adaptation temperatures. Subjects continuously rated the magnitude of any pain sensation elicited by heat increments superimposed on base temperatures of 38, 44, 47 or 48 degrees C. Detection threshold was also measured using a two-alternative forced choice method. The increment detection thresholds were lower for a continuously painful base of 47 degrees C than for a non-painful base of 38 degrees C in normal skin, and likewise were lower for a base of 38 degrees C following hyperalgesia induced by a mild burn. Incremental pain thresholds were nearly equal to detection thresholds on the base of 47 degrees C. The sensitivity with which subjects could scale the magnitude of pain was 2-7 times better for increments delivered on a 48 degrees C as opposed to a 38 degrees C base. Evoked responses in 6 single C-fiber mechanoheat nociceptive afferents (CMHs) were recorded percutaneously from the peroneal nerves of 3 humans, who were simultaneously judging pain magnitude. For a base of 38 degrees C, both the pain and the neural response thresholds were an order of magnitude higher than corresponding thresholds on a base of 48 degrees C. For a base of 47 degrees C, response thresholds of the CMHs ranged from 0.1 to 0.5 degrees C and were comparable to detection thresholds of 0.1 to 0.3 degrees C. The sensitivity with which most nociceptors could signal increment size was 3-4 times better on a 48 degrees C than a 38 degrees C base. Incremental pain sensitivity was not altered by a compression block of activity in myelinated afferents that eliminated the sense of cool and touch. Thus, activity in unmyelinated fibers alone could account for the sensitivity to incremental thermal stimuli that were superimposed on a painful base temperature. Further, it is likely that CMH nociceptors alone could provide the peripheral information necessary to detect and to make magnitude judgments of pain elicited by these stimuli.

Hot Temperature↗
PubMed1983

Procainamide-induced antinuclear antibodies in beagle dogs.

Procainamide produces a high incidence of autoimmune reactions in humans. To establish an animal model, we treated three groups of beagle dogs with increasing doses of procainamide HCl (100 to 200 mg/kg) for 11 to 14 months. Sera were examined before and during treatment for antinuclear antibodies (ANA) at a 1:10 dilution by an indirect immunofluorescence assay. The first group of six dogs, which were 1 year old and born in our colony, remained generally negative for ANA. In the second group of four dogs, which were of the same origin but were 3 to 6 years old, two developed ANA after 4 months of treatment. The third group of four dogs were 3 to 6 years old and had been born in the FDA colony to parents originating from another source. These dogs developed ANA after 1 to 2 months and remained generally positive throughout the 11 months of treatment. Dogs of the control groups remained negative except for one that was ANA-positive on several occasions. Three of the ANA-positive treated dogs and the ANA-positive control dog had circulating immune complexes. Serum procainamide concentrations were comparable in dogs of each group; acetylprocainamide was not detected. No alterations were found in serum proteins or in the hemograms, and no clinical signs were seen. The data suggest that age plays a contributory role in the development of this autoimmune response in the dog.

Aging↗
PubMed1982

Drug-induced antinuclear antibodies in the guinea pig.

Antinuclear antibodies (ANA) development was studied in male guinea pigs in response to chronic treatment with procainamide, hydralazine, acetanilide or caffeine. Acetanilide and caffeine have not previously been associated with ANA induction. Fifty-one weanling Hartley guinea pigs were divided into five groups which received either procainamide, hydralazine, acetanilide, caffeine or saline sc for 55 weeks; drug dosage was 10 mg/kg initially and was increased incrementally to 40 mg/kg by 10 months except for hydralazine, which was increased to 20 mg/kg. Two weeks before initiation of treatment, 1 mg of the appropriate drug in 0.4 ml of buffered Freund's complete adjuvant (FCA-PBS) was administered intradermally. Controls received FCA-PBS only. Sera ANA were assayed at 6, 10 and 13 months. After 13 months of treatment, those sera which were ANA positive were assayed for anti-deoxyribonucleoprotein antibodies and were titered for ANA. Chi-square analyses were performed on results of the 10- and 13-month ANA screening results. ANA induction was significant at P = 0.05 only for the group receiving procainamide at both 10 and 13 months of treatment. When the cumulative results of all ANA screens were analyzed, ANA induction was significant for procainamide, acetanilide and caffeine. The test system did not prove to be promising for unambiguous identification of drugs with ANA-inducing potential, but may be useful for studies of mechanisms of ANA induction by chemicals.

Acetanilides↗
PubMed1982

Role of prolactin in vitamin D metabolism and calcium absorption during lactation in the rat.

Intestinal calcium absorption and plasma levels of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were measured in lactating and non-lacting rats and the effects of bromocriptine and exogenous prolactin treatment were evaluated. In lacting rats calcium absorption and plasma levels of parathyroid hormone, 1,25(OH)2D3 and alkaline phosphatase activity were significantly increased. Bromocriptine treatment significantly reduced the enhanced calcium absorption and levels of plasma 1,25(OH)2D3 and alkaline phosphatase but had no significant effect on plasma levels of parathyroid hormone. Prolactin administered with bromocriptine to lactating animals prevented all the changes observed with bromocriptine treatment alone. It was concluded that the increased plasma levels of prolacting during lactation lead to high plasma levels of 1,25(OH)2D3 which are responsible for the enhanced intestinal calcium absorption.

Alkaline Phosphatase↗