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Biomedical subjects

V Iyer

Publications and source records attributed to V Iyer.

At least 55 records · Page 3Linked to original sources
PubMed1988

Electrophysiology of guinea-pig myenteric neurons correlated with immunoreactivity for calcium binding proteins.

Experiments were undertaken to define the electrophysiological characteristics and shapes of neurons in the myenteric plexus of the guinea-pig ileum that are immunoreactive for calcium binding proteins. Recordings were made from the neurons with intracellular microelectrodes containing a mixture of the fluorescent dye Lucifer yellow and KCl solution. The neurons studied were filled with Lucifer yellow so that they could be re-identified after processing the tissue to reveal immunoreactivity for either the calcium binding protein (CaBP), spot 35 protein, or vitamin D-dependent CaBP. Neurons were characterized as being AH-neurons, in which each action potential is followed by a prolonged after-hyperpolarization (greater than 4 s), or S-neurons, in which the prolonged after-hyperpolarizations were not observed and focal stimulation of internodal strands evoked fast excitatory synaptic potentials. S-neurons were never immunoreactive for the CaBPs (108 cells), but most AH-neurons (62 of 74) were immunoreactive. Immunoreactive and non-immunoreactive AH-neurons were indistinguishable on the basis of their electrophysiological properties or their shapes (all the AH-neurons were Dogiel type II in shape, i.e. smooth soma and many long processes). The S-neurons had a variety of shapes, but none could be classified as Dogiel type II. It is concluded that most AH-neurons are immunoreactive for calcium binding proteins, and that these proteins are restricted to AH-neurons.

Animals↗
PubMed1988

Evaluation of spinal evoked potentials: a model for assessment of spinal cord function in isolation.

Spinal evoked potentials were recorded from the dorsal columns of in vitro mouse hemicord preparations. The response of these potentials to different periods of hypoxia was studied. A decrease in amplitude of the potential to 50% and 10% of pre-hypoxia reference occurred after 3.19 +/- 1.36 and 7.3 +/- 2.97 min, respectively. Complete recovery of the potential was seen in specimens exposed to 5 and 10 min of hypoxia. Incomplete recovery occurred with exposure to longer periods of hypoxia. In preparations that remained isoelectric for less than 5 min total recovery was seen.

Animals↗
PubMed1988

Induction using fentanyl to suppress the intubation response in the cardiac patient: what is the optimal dose?

Eighty patients undergoing coronary artery surgery were randomly allocated to receive either 0, 2, 5, 10 or 15 micrograms/kg of fentanyl with induction of anaesthesia. Heart rate and blood pressure were measured before induction, after induction, and after intubation. The effects of fentanyl dose on both heart rate and mean arterial pressure (MAP) were evaluated in terms of both the mean and group responses. At all doses of fentanyl, mean heart rate increased after induction and rose further on intubation. The mean increase after induction was minimal at doses of 5 micrograms/kg and greater. The increase in heart rate after intubation was more difficult to block but with a fentanyl dose of 15 micrograms/kg, 87% of patients had heart rates below 100 bpm. As a group, the percentage of patients in whom the postintubation heart rate remained below 100 bpm increased progressively with the fentanyl dose. In contrast, mean MAP fell at all dose levels after induction, the mean fall being about 30 mmHg at 5 micrograms/kg and greater. Mean MAP exceeded pre-induction values after intubation with 0 and 2 micrograms/kg, and progressive attenuation of the MAP rise was found as the dose of fentanyl increased. The percentage of patients who did not exceed their preinduction MAP rose progressively with increasing dose of fentanyl with an ED50 of 3.7 micrograms/kg. If a minimal fall in mean MAP after induction with no rise above preinduction MAP is the sole criterion, a fentanyl dose of about 3 micrograms/kg is recommended. If heart rate is to be kept below 100 bpm, a dose of at least 10 micrograms/kg should be used.2+ dose or greater will cause the MAP to fall in some patients to less

Blood Pressure↗
PubMed1987

Blepharospasm accompanying hypoxic encephalopathy.

Severe bilateral blepharospasm with left hemiplegia occurred in a 50-year-old woman, who developed cardiac arrest following ventricular aneurysmectomy. The blepharospasm was present constantly, even during sleep, and increased during attempts at voluntary eye opening. CT scan revealed multiple hypodense areas involving basal ganglia bilaterally and the right perisylvian area. The blepharospasm improved gradually over a 6-month period, although the left hemiplegia remained unchanged.

Basal Ganglia Diseases↗
PubMed1987

Unusual neurotoxicity associated with amiodarone therapy.

One hundred two patients with recurrent, drug-refractory tachyarrhythmias were treated with amiodarone for nine +/- eight months (mean +/- SD) (range, one to 50 months). Forty-five patients exhibited some form of neurotoxic reaction that was severe enough in nine patients to require discontinuation of treatment or reduction in dosage of the drug. The most frequent neurotoxic findings were tremor (44 patients), peripheral neuropathy (ten patients), and ataxia (seven patients). Five patients developed unusual neurotoxic manifestations: brainstem dysfunction characterized by downbeat nystagmus, hemisensory loss and ataxia, severe dyskinesia, jaw tremor, and proximal myopathy. Neurophysiologic studies revealed varying degrees of predominantly demyelinating peripheral neuropathy. Neurotoxic symptoms improved after discontinuing treatment or decreasing the dosage of the drug. Age of the patient and total cumulative dose did not seem to be risk factors for development of neurotoxicity. These neurotoxic findings suggest that amiodarone-induced neurotoxic reactions are not only confined to the peripheral nervous system, but also that parts of the central nervous system (eg, basal ganglia, brain stem, or their connections) may also be involved.

Aged↗
PubMed1986

The influence of skeletal muscle reinnervation on experimentally induced myotonia.

Earlier studies have shown that prior denervation of muscle prevents myotonia induced by 2,4-dichlorophenoxy acetic acid (2,4-D) both in vivo and in vitro. This work studied the effect of reinnervation on 2,4-D myotonia. Twenty Sprague-Dawley rats were injected with 2,4-D at specific intervals following unilateral sciatic nerve crushing; the gastrocnemius muscle on both sides was studied electromyographically to assess myotonia and to document denervation and reinnervation. All the rats gradually became amyotonic following denervation; myotonia reappeared during reinnervation. Myotonic discharges were no longer detectable 1 week after nerve crushing, but returned completely within 3 weeks. Blocking axoplasmic transport with colchicine had essentially the same effect on myotonia. A reciprocal temporal relationship was noted between the occurrence of fibrillations and myotonic discharges. These findings substantiate the view that innervation is essential to maintain the muscle membrane in a state that will support myotonic discharges.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1984

Halo-body device.

A halo-body system is described which has been developed at Princess Margaret Rose Orthopaedic Hospital in Edinburgh. The system is easy to apply and consists of a standard halo, linked to malleable plates by two hollow vertical rods. These rods are connected to the ring by swivel joints which allow for the movements of flexion and extension. The malleable plates are incorporated into the plaster jacket which rests upon the iliac crests. The results of 13 patients who have had this system applied are discussed and include patients who have sustained fractures of the cervical spine or who have had bone destruction from metastatic disease or from infection. Using this type of system there have been few complications and the patients have benefitted from easy mobilisation.

Cervical Vertebrae↗
PubMed1977

Neural influence on experimental myotonia.

A transitory myotonic state, lasting for less than 24 hours, was induced in rats within 2 hours of the intraperitoneal injection of 2,4-dichlorophenoxyacetic acid. Neuromuscular blockade, nerve block, nerve section, and cordotomy had no effect on the established myotonic state. However, muscle that had been denervated progressively lost its capacity for a myotonic response to subsequent injections of 2,4-dichlorophenoxyacetic acid. After 10 to 12 days denervation, the injection of 2,4-dichlorophenoxyacetic acid produced a brief increase in the number of fibrillations, but typical myotonic discharges were no longer detectable. Unlike denervation, cordotomy did not impair the capacity of the paralyzed limbs to develop in response to 2,4-dichlorophenoxyacetic acid. While myotonia is the result of a primary defect in the muscle membrane, these experiments indicate the innervation is necessary to maintain the muscle membrane in a state that will support myotonia. We hypothesize that an alteration in ionic conductance secondary to denervation is the critical factor in preventing myotonia.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1977

The effect of denervation on subsequent in vitro induction of myotonia.

In order to study the influence of innervation on myotonia, an attempt was made to induce myotonia in previously denervated rat hemidiaphragm preparations in vitro with use of 2,4-dichlorophenoxy acetic acid (2,4-D) and low chloride solutions. Prior denervation prevented the onset of myotonia in both media except during the first 24 hours after nerve section. On the basis of already available data, we propose that the reduced potassium conductance accompanying denervation may be the main factor preventing induciton of myotonia in denervated muscle.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1976

Normal median nerve proximal latency in carpal tunnel syndrome: a clue to coexisting Martin-Gruber anastomosis.

Five of 65 patients referred for electrodiagnosis because of clinical evidence of carpal tunnel syndrome were found to have near normal latency on proximal stimulation of the median nerve, although the distal motor latency was prolonged. In one patient, the proximal latency was actually shorter than the distal latency. The failure of the proximal latency to be prolonged in proportion to the distal latency results in a spuriously high apparent conduction velocity in the forearm segment of the nerve. This value may even exceed the conduction velocity of the corresponding nerve segment in the unaffected arm. Stimulation studies on the ulnar nerve reveal that this disparity is the result of some of the median nerve fibres destined for the thenar muscles taking an aberrant course through the ulnar nerve and thus escaping compression at the wrist. A median-ulnar communication in the forearm, the 'Martin-Gruber' anastomosis, may occur in up to 15% of the population. The presence of the Martin-Gruber anastomosis in patients with carpal tunnel syndrome results in a partial or total sparing of thenar muscles from denervation and the paradoxical recording of normal proximal latencies in the median nerve when the distal latency is prolonged.

Adult↗
PubMedDate not supplied

Ketorolac (Toradol) induced lithium toxicity.

A case of lithium neurotoxicity in a patient with cluster headache, resulting from coadministration of ketorolac is reported. While lithium interaction with many other NSAIDs is well-known, ketorolac has not been incriminated.

Adult↗