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Biomedical subjects

T Baker

Publications and source records attributed to T Baker.

At least 109 records · Page 6Linked to original sources
PubMed1980

Development of a cardiac antiarrhythmic screening test utilizing theophylline in the rat.

Cardiac arrhythmias were produced in Sprague-Dawley-derived rats by chloroform challenge. The incidence of cardiac arrhythmias so induced increased with age and as a function of dose after pretreatment with theophylline. The dose-response and time-action parameters of theophylline's predisposing action to chloroform-hypoxia-induced cardiac arrhythmias were determined. This information has been utilized to develop a cardiac antiarrhythmic screening test in unanesthetized rats which is presented in the following paper.

Acetates↗
PubMed1980

A cardiac antiarrhythmic screening test in the rat: the effects of lidocaine, propranolol and quinidine.

The dose-response and time-action parameters for the prototype antiarrhythmic drugs lidocaine, propranolol and quinidine were established using a cardiac antiarrhythmic screening procedure in the rat. This simple screening procedure produces severe cardiac arrhythmias, primarily ventricular fibrillation, in young post-weaning rats which have been pretreated with a single intramuscular injection of theophylline (20 mg/kg) 15 to 45 min prior to their inhalation of chloroform vapors.

Animals↗
PubMed1978

Motor nerve terminal defect following tenotomy.

Post-tetanic potentiation and the underlying post-tetanic repetition in cat soleus muscle require normal motor nerve terminals. These indices of nerve terminal viability are depressed 10 days and absent 15 days after tenotomy of the soleus muscle.

Achilles Tendon↗
PubMed1978

Attenuated dynamic responses of primary endings of muscle spindles: a basis for depressed tendon responses in acrylamide neuropathy.

Depressed or lost tendon reflexes commonly observed in patients with peripheral neuropathies may result partly from attenuation of the dynamic discharge from the primary endings of muscle spindles. This possibility was investigated in cats with an experimental neuropathy induced with acrylamide (30 mg/kg/day intramuscularly). Achilles tendon reflexes and the dynamic discharge from primary muscle spindles were evaluated after five or ten injections of acrylamide. After five injections the animals were moderately impaired neurologically, the Achilles tendon reflex was difficult to elicit in 2 of 5 animals, and the dynamic responses of primary endings of soleus muscle spindles to stretch were depressed. Following ten injections of acrylamide the cats were severely impaired neurologically; tendon responses were either absent or difficult to elicit, and the dynamic responses of their muscle spindles to stretch were reduced by 50% (p less than 0.01). Additionally, the spindels responded to stretch with only 20 to 30% the normal number of afferent impulses. These data suggest that lost tendon responses in acrylamide neuropathy result in part from inadequate activation of motoneurons by spindle afferent discharge.

Acrylamides↗
PubMed1978

The neuropathology of DFP at cat soleus neuromuscular junction.

The fine structure of the cat soleus neuromuscular junction was studied following a single intra-arterial injection of di-isopropylfluorophosphate (DFP) into the right femoral artery. DFP induced separate subacute and delayed morphologic changes in soleus non-myelinated motor nerve terminals. Three days after DFP administration motor nerve terminals were reduced in number. Subacute DFP damage was also noted in the subneural apparatus and in the immediate subjacent muscle. Both pre- and post-junctional subacute changes were resolved two weeks post-DFP. One week following this initial regeneration, soleus motor nerve terminals underwent a delayed transient degeneration, followed by reinnervation of damaged endplates 6--8 weeks following DFP. Quantitative analysis of methylene blue-stained intramuscular nerves indicated that both subacutely and chronically denervated soleus muscle fibres were reinnervated by regeneration of the original motor axon. Reinnervation by means of collateral sprouting was insignificant. This mechanism of reinnervation and the rapidity with which it occurred suggests that both subacute and delayed soleus motor nerve damage is initiated from local actions of DFP on the non-myelinated terminal. The subacute reaction probably results from a direct cytotoxic action of DFP at pre- and post-junctional sites. The delayed nerve terminal degeneration may also stem from an acute effect not immediately detrimental to nerve function.

Animals↗
PubMed1978

The significance of hypotension developing during treadmill exercise testing.

The significance of hypotension developing during treadmill exercise testing was evaluated and correlated with the findings at cardiac catheterization in two groups of patients. Twenty-five patients (Group I) had a fall in systolic pressure during exercise and were compared to 50 consecutive unselected patients (Group II) with a normal blood pressure response. Clinical characteristics were similar in both groups. Females comprised 48 per cent of the patients in Group I and only 30 per cent in Group II. The incidence of significant coronary artery disease was not different when the two groups were compared as a whole, 56 per cent in Group I and 36 per cent in Group II (P = NS). When males and females were considered separately, it was noted that the incidence of coronary artery disease was higher in hypotensive males (77 per cent) when compared to control males (40 per cent) (p less than 0.01). Females in both groups had a lower but comparable incidence of coronary artery disease (25 per cent and 27 per cent, respectively). Resting hemodynamics and angiographic characteristics, such as contraction abnormalities, and the number and distribution of diseased coronary vessels, were similar in both groups of patients. These findings suggest that hypotension in females does not necessarily connote coronary artery disease. Males with hypotension have a higher incidence of coronary artery disease, but the extent and distribution of their disease is no different from that of patients with a normal blood pressure response to exercise.

Adult↗
PubMed1978

Changes in the kinetics of muscle contraction in vitamin D-depleted rats.

Using an in situ rat soleus neuromuscular preparation, changes in the muscle contraction kinetics in response to vitamine D depletion were studied. For a single isometric contraction, the time-to-peak tension (Tp) and the time-for-recovery-half-way-to-resting tension (T1/2r) were recorded. For a 150 Hz, 300 msec tetanus, the T1/2r was determined. Animals raised on high-calcium, high-phosphate, vitamin D-depleted diets showed prolongation of all parameters. Repletion of vitamin D returned Tp and T1/2r values to normal. Neither dietary calcium deficiency nor thyroparathyroidectomy produced an prolongation of Tp or T1/2r values. Therefore, based upon the experimental data, it appears that vitamin D or one of its metabolites, independent of any effect on the serum calcium or serum phosphate concentration, is necessary for normal muscle relaxation.

Animals↗
PubMed1978

Position sensitivity of de-efferented muscle spindles in experimental acrylamide neuropathy.

An experimental neuropathy was induced in cats by injections of acrylamide (7.5, 15 or 30 mg/kg/day) for 2 to 10 days. The responses of primary and secondary endings of soleus muscle spindles to stretch were evaluated and correlated with the appearance of ataxia and incoordinated motor movements. Animals that received 15 or 30 mg/kg/day became ataxic and demonstrated poor motor coordination on the 7th or 4th day, respectively. At these times, both primary and secondary endings of muscle spindles had elevated thresholds and diminished discharge frequencies. Continued acrylamide administration resulted in exacerbation of the clinical symptoms and further attenuation of spindle responses. The discontinuation of acrylamide was followed by slow recovery. Only those cats which received a total dose of 75 mg/kg or less remained asymptomatic and had normal spindle function. The coincidence of onset of motor coordination deficits and spindle dysfunction, coupled with a lack of demonstrable motor defect at the same time, suggests that the initial clinical features of acrylamide neuropathy may be partly the consequence of impaired spindle function.

Acrylamides↗
PubMed1977

Effects of a single methylprednisolone dose on a facilitatory response of mammalian motor nerve.

Long-term glucocorticoid dosing directly enhances a facilitatory function of cat soleus motor nerve terminals. Posttetanic potentiation (PTP) of soleus contraction is a manifestation of this prejunctional facilitation. The present study demonstrates that the same enhancement of facilitation is produced with a single large intravenous dose methylprednisolone. The single dosing method, however, showed an initial suppression of facilitation that neared recovery in four hours. Thereafter, the characteristic augmentation of prejunctional facilitation emerged, peaking in 24 hours. Return to control required four days. Knowledge of this time course enabled centrally disconnected motor nerve endings to be identified as the site of both phases of the steroid action. Since the neuromuscular facilitation studied is equivalent to that triggered by neostigmine-like drugs, the results infer that the antimyasthenic effect of glucocorticoids may involve a direct action on motor nerve endings.

Animals↗
PubMed1977

Glucocorticoid effects on the edrophonium responsiveness of normal and degenerating mammalian motor nerve terminals.

An intensive short-term triamcinolone regimen in cats preserves the prejunctional actions of edrophonium in degenerating motor nerves. These edrophonium actions include the induction of a stimulus-dependent afterdischarge and the initiation of fasciculations. The relationship between fasciculations and stimulus-dependent afterdischarge is discussed. The glucocorticoid preservation of these edrophonium effects is like that previously reported for the preservation of posttetanic facilitation in motor nerves equally compromised. The results therefore show that glucocorticoid and facilitatory drug actions synergize to increase facilitation in degenerating but still functional motor nerves. This drug synergy is comparable to that which occurs in normal motor nerves. This interaction may provide a basis for effectively combining glucocorticoid and facilitatory drugs in the treatment of myasthenia gravis.

Animals↗
PubMed1976

Studies on drug-induced neuropathies. III. Motor nerve deficit in cats with experimental acrylamide neuropathy.

To assess motor nerve and motor nerve terminal function in acrylamide neuropathy, cats were given i.m. injections of acrylamide (15 mg/kg) daily for 10 days to induce a peripheral neuropathy. Tests of function were performed on the day of the 10th injection (day 0) and 7, 21 and 35 days thereafter. In untreated animals tetanic conditioning evoked stimulus-bound repetition (SBR) in 85% of soleus alpha-motoneurones. Following administration of acrylamide, the percent of axons elaborating SBR were: day 0 -- 79%, day 7 -- 71%, day 21 -- 31%, day 35 -- 22%. The response of soleus muscle to SBR is normally a post-tetanic potentiation (PTP) of contractile tension which is proportional to the tetanic conditioning frequency; during the development of the neuropathy, PTP in response to all tetanic frequencies progressively declined, concomitant with and as a result of the declining incidence of SBR. These data indicate that initial functional alterations in motor nerves during acrylamide neuropathy occurs at the level of the nerve terminal, preceding alterations in conduction velocities in the axons. However, the motor nerve deficit is not adequate, in either time to onset or severity, to account for the clinical manifestations of the neuropathy. The possible contribution to clinical signs of the neuropathy made by lesions to other peripheral nerves is discussed.

Acrylamides↗
PubMed1975

Glucocorticoids and mammalian motor nerve excitability.

Short-term treatment of cats with high doses of triamcinolone and related steroids strikingly increased the capacity of soleus motoneurons to generate posttetanic stimulus-bound repetition (SBR) and the obligatory postetanic potentiation (PTP) of muscle. The edrophonium chloride (Tensillon)-induced SBR and twitch potentiation were likewise augmented. These effects reflect an increase in the excitability of the motoneuron. This glucocorticoid effect suggests that the motoneuron is the site of the antimyasthenic action of the hormone. Certainly, the enhanced SBR is a neuronal representation of the adverse epileptogenic action of the glucocorticoids. The glucocorticoid effect on motoneuron outlasts the dosing period, suggesting an underlying alteration in the neuron. Other glucocorticoids caused the same effects, but varied in their potencies. Mineralocorticoids were less effective. The single androgen that was tested proved to be minimally effective.

Animals↗
PubMed1975

Motor nerve terminal response to edrophonium in delayed DFP neuropathy.

A localized peripheral neuropathy was induced in cats with di-isopropyl fluorophosphate (DFP). Soleus nerve-muscle preparations, and the motor nerve terminals in particular, were evaluated for responsiveness to edrophonium (200 mug/kg i.v.). Potentiation of contractile strength was absent 24 hr after DFP, and showed a trend toward recovery 7-14 days post-DFP; it then fell to about 25% of normal 3 weeks following DFP administration. During the ensuing 5 weeks this aspect of edrophonium responsiveness was largely regained. The underlying post-drug repetition which gives rise to the potentiated responses was not demonstrable in either the nerve or muscle 3 weeks after DFP, but was again observed 8 weeks after poisoning. These findings suggest a delayed peripheral neuropathy indicative of a trophic deprivation and further illustrate a motor nerve terminal deficit as the initial function alteration in DFP neuropathy.

Action Potentials↗