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Biomedical subjects

T Baker

Publications and source records attributed to T Baker.

At least 91 records · Page 5Linked to original sources
PubMed1985

Methylprednisolone treatment of an organophosphorus-induced delayed neuropathy.

Diisopropylfluorophosphate (DFP) injected into the femoral artery of cats causes a localized organophosphorus-induced delayed neuropathy (OPIDN). Gait disturbances develop in the treated leg 14 days after DFP exposure and reaches a maximum at 21 to 28 days after DFP. In vivo high-frequency conditioning of soleus motor nerve endings evokes stimulus-bound repetitive neural discharges (SBR) and an obligatory potentiation of the muscle contractile response (PTP). In this OPIDN model, SBR and PTP are maximally suppressed at 21 to 28 days after DFP. A high-dose regimen of methylprednisolone started 30 to 40 min after DFP exposure and lasting for 20 days prevented the development of OPIDN. In the methylprednisolone-DFP treated cats, SBR and PTP functions were not suppressed and not different from those in untreated normal cats.

Action Potentials↗
PubMed1985

Measurement of fasciculations as motor nerve ending discharges in the rat: a dose related effect of neostigmine.

The muscle fasciculations caused by neostigmine and similar agents are the result of a primary drug action on motor nerve endings. Asynchronous, repetitive firing of action potentials are evoked at motor nerve endings which are then transmitted to muscle. A dose-response relationship between neostigmine dose and the rate of/or total neural activity has been established in the rat. This fasciculatory response to neostigmine can serve as an index of motor nerve ending excitability and may be useful in assessing the effects of certain pathological states or drug actions at the neuromuscular junction.

Action Potentials↗
PubMed1985

Pharmacologic excitability of rat motor nerve endings: the effect of adrenalectomy on neostigmine-induced fasciculations.

Neostigmine-induced muscle fasciculations, quantitated as fasciculatory muscle action potentials, served as an indirect in vivo indicator of motor nerve ending (MNE) excitability. By this method, MNE excitability was depressed in adrenalectomized rats compared to matched intact controls. Daily or continuous administration of the mineralocorticoids aldosterone or desoxycorticosterone acetate restored MNE excitability toward normal; corticosterone, the endogenous corticosteroid having both mineralo- and glucocorticoid activity, was variably effective. There was a strong negative correlation (r = -0.95) between log plasma [K+]and the fasciculatory response to neostigmine. Dietary restriction of K in adrenalectomized rats lowered plasma [K+]to near normal and significantly increased MNE excitability. This effect of adrenalectomy on MNE excitability was further demonstrated by recording directly the neostigmine-induced repetitive neural discharges responsible for the muscle fasciculations. In adrenalectomized animals, neostigmine-induced neural discharges were reduced in intensity; restoration of neostigmine responsiveness was attained by lowering plasma [K+]through dietary restriction. Stimulus strength-duration relationships for both ventral and dorsal roots disclosed deficits in axonal excitability after adrenalectomy. These returned toward normal when plasma [K+]was lowered by K withdrawal from the diet. From these studies, it is concluded that 1) in adrenalectomized rats, peripheral nerve excitability, including the unmyelinated endings of motor nerve, is depressed; 2) mineralocorticoids play a significant role in restoring MNE excitability in these animals; 3) mineralocorticoid-induced changes in MNE excitability relate to the lowering of an elevated plasma [K+].

Action Potentials↗
PubMed1984

Disruption of written language in aphasia: a case study.

This study documents the performance of a Wernicke aphasic on production of written discourse. The discourse data consisted of spontaneously produced texts of three different types: narrative discourse, personal and formal letters, and expository discourse. A detailed description of the language of this aphasic at a sentence and discourse level revealed preservation of discourse structure through proper use of cohesive devices despite severe disruption of linguistic structure at a sentence level.

Aphasia↗
PubMed1984

Prejunctional and postjunctional effects of tubocurarine and pancuronium in man.

The effects of small doses of tubocurarine and pancuronium on peak tetanic tension and tetanic maintenance were compared. Forty patients undergoing elective orthopaedic procedures under general anaesthesia were studied. Changes in neuromuscular transmission were measured by recording the isometric contraction of the adductor pollicis muscle evoked by supramaximal stimulation of the ulnar nerve at the wrist. Small doses of pancuronium affected predominantly the peak tetanic tension, while small doses of tubocurarine affected mainly tetanic maintenance. Thus, different degrees of depression of peak tetanic tension and tetanic maintenance were observed with tubocurarine and pancuronium. This clinical study supports Bowman's hypothesis, based upon laboratory findings in the cat, that prejunctional and postjunctional effects of neuromuscular blocking agents depend on their affinity for cholinoceptors at different sites.

Adult↗
PubMed1983

An electrophysiologic and ultrastructural study of the phenylmethanesulfonyl fluoride protection against a delayed organophosphorus neuropathy.

The delayed organophosphorus neuropathy caused by diisopropylfluorophosphate (DFP) can be prevented by pretreatment with phenylmethanesulfonyl fluoride (PMSF). A single injection of DFP (2 mg/kg) into a cat femoral artery produced a delayed neuropathy in the injected leg. Clinical neurotoxic signs in the DFP treated leg were most prominent at 21 to 28 days after DFP administration: a high-step gait with some tip-toe walking. During that time the capacity of the cat soleus alpha-motor nerve terminals to generate a stimulus-evoked repetitive discharge, known as SBR, was greatly attenuated. At that time, the ultrastructure of the motor nerve terminals demonstrated prominent alterations that correlated well with the motor nerve terminal SBR deficit. These alterations included the presence of extensive whorls in nerve terminals and axoplasms, the retraction and disruption of nerve terminals from the synaptic cleft, and a widening of secondary junctional folds. From the sampled population, the incidence of normal terminals in soleus muscles of the DFP-treated leg was only 2%. Cats which received PMSF (30 mg/kg ip) 24 hr before DFP administration did not develop any neurotoxic signs. Motor movements were normal. The SBR function of the soleus alpha-motor nerve terminals was not lost and its incidence approached normal values. Moreover, the ultrastructure was normal in 86% of examined neuromuscular junctions in the PMSF pretreated DFP cats. Thus, in this model, pretreatment with PMSF protected cats against the delayed neurotoxic effects of organophosphorus poisoning.

Animals↗
PubMed1983

Beneficial action of glucocorticoid treatment on neuromuscular transmission during early motor nerve degeneration.

The effects of a short-term, high-dose glucocorticoid pretreatment regimen (triamcinolone diacetate, 8 mg/kg i.m. daily for 7 days) were examined on neuromuscular transmission deficits observed in the in vivo cat soleus nerve-muscle preparation at 48 hr after soleus nerve transection. The pretreated preparations had 20% more functional motor nerve terminals than the untreated. This was evidenced by a significantly (P less than 0.01) lesser difference in the indirectly evoked isometric contractile tensions between the denervated muscle and the contralateral intact preparation as a result of prior glucocorticoid treatment. The glucocorticoid pretreatment also significantly improved the capacity of the trophically deprived soleus motor nerve terminals to maintain transmission during high-frequency activation (100 to 400 Hz for 10 s). Moreover, triamcinolone treatment before nerve transection completely prevented the development of an increased sensitivity to d-tubocurarine neuromuscular block in untreated, 48-h nerve-transected preparations. These results demonstrate an ability of an intensive high-dose glucocorticoid treatment to sustain single and repetitive neuromuscular transmission during early anterograde nerve degeneration.

Animals↗
PubMed1982

A morphological study of the effect of glucocorticoid treatment on delayed organophosphorus neuropathy.

The delayed neuropathy caused by the organophosphate diisopropylfluorophosphate (DFP) can be minimized by a high dose glucocorticoid regimen started after exposure to DFP. In cats 21 days after an intraarterial injection (2 mg/kg) of DFP, morphologic alterations of neuromuscular junctions and myelinated intramuscular axons are evident. These alterations include the presence of extensive lamellar whorls in nerve axons and terminals, the disruption and retraction of nerve terminals from the synaptic cleft and a widening of secondary junctional folds with coincident dispersion of the basal lamina. The pathologic changes while more intense in the DFP-treated leg are also evident in the contralateral leg. Only 2% of motor nerve terminals from the soleus of DFP-treated legs were rated as normal in morphologic evaluations. In contrast 90% were rated normal in cats exposed to DFP and subsequently treated with one dose of methyl prednisolone (90 mg/kg, i.v.) and 7 doses (8 mg/kg, i.m.) of triamcinolone over a 20 day period. The mechanism whereby glucocorticoid therapy exerted this effect during the time interval studied remains unresolved. However, this observation may be important in the further definition of both the normal and diseased state.

Animals↗
PubMed1982

Hyperbaric medicine: state of the art, 1979.

An attempt has been made to determine the clinical usage of hyperbaric oxygen therapy at 83 North American hyperbaric treatment centers from 1971 to 1978. Questions were asked about the conditions or diseases treated, yearly case load for each condition, location of functional hyperbaric chambers, types of chambers used, operating costs, and personnel requirements. Commercial diving chambers that treat decompression sickness and air embolism from diving accidents were included in the last two years of the survey. Fifty-seven responses were received; 30 treatment centers had multiple chambers, 24 had monoplace chambers, and three had both types of chambers. A total of 10,942 patients were treated during the eight-year survey period; 8,408 patients (76%) had category I or II conditions, as defined by the Undersea Medical Society. Of the 20 most commonly treated conditions, 17 were in category I or II. During the survey period, the use of hyperbaric oxygen increased, particularly in the treatment of decompression sickness, carbon monoxide poisoning, and osteomyelitis and osteoradionecrosis.

Brain Ischemia↗
PubMed1981

Correlation between anticurare activity of tetanic stimulation and neostigmine in anesthetized man.

Frequency and dose-dependent changes in neuromuscular transmission were examined in 70 patients undergoing elective surgical procedures requiring the use of muscle relaxants. Anesthesia was induced with sodium thiopental and maintained with N2O-O2 and fractional dose of meperidine or fentanyl. Neuromuscular block was produced and maintained at 80% level with incremental intravenous doses of d-tubocurarine. Neuromuscular function was measured by recording the force of thumb adduction evoked by supramaximal stimulation of the ulnar nerve at the wrist. Single stimuli were applied every 2.5 seconds as square pulses of 0.1-msec duration. In 30 patients tetanic trains of 10-second duration ranging from 10 to 400 Hz were used. In 40 patients neostigmine doses ranging from 0.5 to 5.0 mg were used. Criteria for responses to 10-second tetanic trains during 80% neuromuscular block were determined and compared with responses after neostigmine. At a frequency of 50 Hz a complete tetanic fade was followed by partial posttetanic relief of block. At a frequency of 200 Hz tetanic fade was followed by complete but transient posttetanic decurarization. The original control twitch tension was not exceeded in posttetanic or postdrug responses. It is concluded that the transient after effects of tetanic stimulation are closely related to the anticurare effects of neostigmine.

Adolescent↗
PubMed1980

Muscle spindle function in organophosphorus neuropathy.

The contribution of muscle spindle dysfunction to the neurological signs o-delayed organophosphorus neuropathy was investigated in the hindlimbs of cats intra-arterially injected with 2 mg/kg of diisopropylfluorophosphate (DFP). In this model of a delayed peripheral neuropathy, the animals exhibit a peculiar high-step gait and a sluggish response to noxious stimuli. These signs initially appear 14 days and are maximum 21--28 days after DFP administration. The position sensitivities of secondary but not primary soleus muscle spindles were depressed at 14 days after DFP. At 21 days after DFP, both primary and secondary endings had attenuated position sensitivities and significantly elevated thresholds. Spindle function was normal at 56 days after DFP exposure. The onset, peak and recovery of soleus muscle spindle dysfunction corresponded to those in alpha-motor axons, indicating the mixed sensory motor nature of organophosphorus neuropathy. Thus, impairment of both sensory and motor functions contributes to the neurological signs of this neuropathy.

Afferent Pathways↗
PubMed1980

The effects of phenylmethanesulfonyl fluoride on delayed organophosphorus neuropathy.

A delayed localized neuropathy of peripheral nerves in a single hind leg of the cat develops after a single intraarterial 2 mg/kg injection of diisopropylfluorophosphate (DFP). This neuropathy is manifested by a maximum loss of the capacity of soleus alpha-motor nerve terminals to generate stimulus-bound repetition 21 days after DFP exposure. Phenylmethanesulfonyl fluoride (PMSF) is a protective inhibitor of the neurotoxic esterase which is associated with the development of the delayed organophosphorus neuropathy. Pretreatment of cats with PMSF (30 mg/kg i.p.) 24 h before the DFP injection protected the cats from the delayed neuropathy. No clinical neurotoxic signs were observed at 21 days after DFP. The stimulus-bound repetitive capacity of soleus alpha-motor nerve terminals was not lost at this time and its incidence was much greater than that which occurred in cats not pretreated with PMSF.

Action Potentials↗