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Biomedical subjects

D I Graham

Publications and source records attributed to D I Graham.

At least 307 records · Page 17Linked to original sources
PubMed1976

Triethyltin sulfate-induced neuropathy in rats. Electrophysiologic, morphologic, and biochemical studies.

Adult rats given high orally administered doses of triethyltin (TET) sulfate lost weight, developed hind limb wasting, and became paraplegic or quadriplegic within three weeks of intoxication. A 33% reduction in the motor nerve conduction velocity (MNCV) of the sciatic nerve in the absence of significant demyelination was observed. There was observed, however, intramyelinic edema formation and an increased number of axonal neurofilaments and neurotubules; changes that paralleled the decrease in MNCV during the period of intoxication. Although the animals became asymptomatic and the MNCV normalized within two to three weeks of discontinuing the TET intoxication, the intramyelinic vacuoles and the increased numbers of neurofilaments and neurotubules persisted.

Animals↗
PubMed1976

Melanotic tumours (Blue Naevi) of spinal nerve roots.

Four cases interpreted as intraspinal blue naevi are reported. The patients were adults females with an age range between 22 and 60 yr. In three there was a single tumour arising from the cervical posterior nerve roots and in the fourth there were multiple tumours arising from the posterior nerve roots of the spinal cord and occurring within the cerebello--pontine angle. The histological appearances of the tumours were similar in every way to those of dermal blue naevi. One was of the more common spindle-celled type and three of the cellular variant. The tumours contained melanin-pigment, and spindle cells with dendritic bipolar processes of the type described in dermal blue naevi. One was of the more common spindle-celled type and three of the cellular variant. The tumours contained melanin pigment, and spindle cells with dendritic bipolar processes of the type described in dermal blue naevi. Definite evidence of malignant tranformation was found in two cases and in a third, the appearances were suggestive for early malignant change. Therefore, unlike their dermal equivalents, intraspinal blue naevi appear to have a greater propensity for malignant transformation. In each case a careful clinical examination failed to reveal any evidence of a primary malignant melanoma. In the one case who died and on whom necropsy was performed, the failure to identify a primary cutaneous, mucosal or ocular melanoma substantiated our contention that these tumours were primary.

Adult↗
PubMed1976

Core formation in the muscles of rats intoxicated with triethyltin sulfate.

Young adult Osbourne-Mendel rats intoxicated for up to 23 days with triethyltin sulfate (TET) at a dose of 20 mg/liter of drinking water given ad libitum, developed core-like structures in type 1 extrafusal fibers of the soleus muscles. Frozen sections revealed an absence of oxidative enzyme activity (NADH-tetrazolium reductase) and diminished or absent myosin ATPase (pH 9.4) in the core regions. The main electron microscopic features within the cores were loss of mitochondria and streaming of the Z-disks. The histochemical and electron microscopic similarities and differences between the TET-induced cores, other core models, and those reported in some human neuromuscular disorders are discussed. The present experiments do not clarify whether the cores are produced from a direct effect of TET upon skeletal muscle or upon the neural component of the motor unit.

Animals↗
PubMed1976

Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier.

Acute hypertension was induced in 19 anesthetized cats by the intravenous administration of angiotensin. The caliber of pial arteries was measured by a television image-splitting technique and local cerebral blood flow by the hydrogen clearance technique. As the blood pressure was increased, pail arterioles constricted and cerebral blood flow remained relatively constant, showing that autoregulation of cerebral blood flow was intact. At mean arterial pressures of more than 170 mm Hg arteriolar dilation appeared. In smaller arterioles (initial diameter less than 100 mum) a segmental dilation (the "sausage'string" phenomenon) frequently preceded uniform dilation. This arteriolar dilation was associated with a marked increase in local cerebral blood flow indicating that the upper level of autoregulation had been breached. In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. Hypertension also caused dysfunction of the bloodbrain barrier since, in 17 out of 19 of the cats examined, there was extravasation of protein-bound Evans blue into brain tissue. In only one of the 19 cats subjected to neuropathological analysis was ischemic brain damage identified and this was restricted to minimal ischemic cell change. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. These observations may be of importance in understanding the pathogenesis of hypertensive encephalopathy.

Animals↗
PubMed1975

Patients with head injury who talk and die.

Of 66 patients with head injuries who had talked at some time after injury, 25% did not have intracranial haematoma at necropsy. Most of these had raised intracranial pressure (I.C.P.), and the commonest finding was local swelling related to contusions. Almost half of the non-haematoma cases had ischaemic or hypoxic brain damage, usually without contusions; 3 were children who had had status epilepticus. Fatality without raised I.C.P. was most often due to meningitis. In deteriorating patients without haematoma mortality and morbidity might be reduced by more diagnosis and treatment, particularly of raised I.C.P.

Adolescent↗
PubMed1975

The neurotoxic effects of triethyltin (TET) sulfate on myelinating cultures of mouse spinal cord.

Well myelinated cultures of mouse spinal cord, exposed to varying concentrations of triethyltin sulfate, were examined at different time intervals by light and electron microscopy. At a high concentration of TET (10(-6)M) for 1-2 hours, the myelin sheaths and cells showed marked degenerative changes. At lower concentrations of TET (10(-7)-10(-9) M) intramyelinic and other types of vacuole formation were seen; however, these lesions were always accompanied by changes in the perikarya, dendrites and axons of neurons and in the astrocytes. Also, there was an apparent increased number of neurofilaments and neurotubules in many axons. The findings are discussed in relation to the lesions induced in the experimental animal by alkyl tin intoxication.

Culture Techniques↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 1: Pathophysiology, electroencephalography, cerebral blood flow, blood-brain barrier, and neurological function.

Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 +/- 4.2 ml/100 gm/min to 26.3 +/- 4.4 (p less than .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Animals↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 2: Brain morphology.

The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.

Animals↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 3: Brain energy metabolism.

The authors studied the effect on cortical metabolites of intracranial hypertension produced by the infusion of mock cerebrospinal fluid into the cisterna magna in rabbits subjected to 15 minutes of cerebral oligemia (20 torr) or 15 minutes of complete ischemia. In both groups high-energy metabolites were exhausted within the first 5 minutes of the 15-minute insult. Significant recovery of the high-energy intermediates occurred within 15 minutes of reperfusion, well before return of electroencephalogram (EEG) activity. Continued reperfusion, during which electrical activity and function were returning, brought only moderate improvement in energy metabolites. In contrast, severe lactic acidosis persisted at least 15 minutes after insult, but was reduced by the time EEG activity returned. At no time were there striking differences in metabolites between the oligemic and ischemic groups. These results indicate that recovery in general, and the significantly earlier recovery of oligemic as compared to ischemic animals, cannot be explained on the basis of energy supply. Whether the persistence of lactic acidosis is an important factor limiting return of function requires further study.

Adenosine Triphosphate↗
PubMed1974

The undifferentiated and extended forms of C1300 murine neuroblastoma. An ultrastructural study and detection of concanavalin A binding sites on the plasma membrane.

Mouse neuroblastoma cells (clone neuro-2A) in the undifferentiated and "differentiated" form were compared by light and electron microscopy. "Cytodifferentiation" was induced in monolayer cultures by the addition of dibutyryl-cyclic AMP. The pattern of concanavalin A binding sites was studied after coupling with horseradish peroxidase. The following major differences were observed. The differentiated cells are characterized by numerous and long neurites, aggregation of ribosomes into polysomes, an extensive network of neurofilaments and microtubules, many dense-core neurosecretory-like vesicles, a discontinuous pattern of concanavalin A binding sites on the plasma membrane, and an increase of the specific activities of acetylcholinesterase, choline acetylase and tyrosine hydroxylase. In contrast, the undifferentiated cells grown in suspension culture lack neurites, contain dispersed ribosomes, infrequent neurofilaments and microtubules and dense-core neurosecretory-like vesicles, and exhibit a continuous pattern of concanavalin A binding sites. In addition, the specific activities of the above mentioned enzymes are significantly lower.

Acetylcholinesterase↗
PubMed1973

Arterial spasm and slowing of the cerebral circulation in the ischaemia of head injury.

Carotid angiograms of 33 patients who had died during 1968 and 1969 from blunt head injury were reviewed and assessed for evidence of arterial spasm and slowing of the cerebral circulation. Spasm was found in 57·5%, a prolonged circulation time in 57·5%, and a combination of both features in 42·4% of cases. In the same group of patients there was also a high incidence of ischaemic brain damage. There appeared to be some correlation between arterial spasm and ischaemic damage in the cerebral cortex, but none in the basal ganglia or in the white matter. There was no apparent correlation between a prolonged cerebral circulation time and ischaemic brain damage.

Adolescent↗