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Biomedical subjects

A Hakim

Publications and source records attributed to A Hakim.

At least 55 records · Page 3Linked to original sources
PubMed1993

Hypokalemic paralysis.

A case of Hypokalemic paralysis is reported which had an atypical onset and clinical features. The paralysis totally recovered on replacement of potassium.

Adult↗
PubMed1991

Activity of the dihydropyridine calcium channels following cerebral ischemia.

With an in-vivo autoradiographic method the binding of 3H-nimodipine (CAS 66085-59-4) and cerebral blood flow (14C-iodoantipyrine method) were measured in rat brain after occlusion of the middle cerebral and common carotid arteries. The dependence of the binding to neuronal cellular membranes on the duration of ischemia can be interpreted as indicator of the tissue's functional state or its responsiveness to therapy with calcium entry blockers. In the two analyzed structures, dorsolateral caudate and overlying sensorimotor cortex, the appearance of infarction is preceded by an activation of the nimodipine binding sites followed by persistent decline of the binding intensity. Binding to nimodipine may therefore be a useful marker of ischemic but salvageable brain tissue.

Animals↗
PubMed1989

In vivo quantification of blood-brain transfer and binding of [125I]HEAT, an alpha 1-adrenoceptor antagonist.

The uptake and binding constants of [125I]iodo-2-[beta-(4-hydroxyphenyl)-ethyl-amino-methyl]tetralone ( [125I]HEAT) in rat brain were determined in vivo. The initial clearance of the radioligand from blood to brain, K1, was calculated from the initial uptake of the radioligand; it averaged 0.21 +/- 0.01 (SD) ml g-1 min -1, consistent with an initial extraction of 25% (i.e., one-quarter of the blood flow). The most strongly binding regions included the olfactory bulb, thalamic nuclei, medial geniculate body, and cerebral cortical layers. We identified saturable, specific binding in frontal cortex layers 1, 5a, and 5c (motor region), frontal cortex layers 3+4, ventral thalamic nuclei, medial geniculate body, striatum, cerebellum, and olfactory bulb. Addition of unlabeled ligand depressed binding in all regions to the same low level (partition coefficient) of 0.8 ml g-1. Displacement of [125 I]HEAT binding by unlabeled HEAT yielded a global affinity constant (KDVd) of 34 +/- 8 pmol g-1 and receptor densities (Bmax) that varied from 50 pmol g-1 in cerebellar cortex and caudate nucleus to 200 pmol g-1 in the region of highest specific binding, the medial geniculate body.

Adrenergic alpha-Antagonists↗
PubMed1989

Hemodynamic and metabolic effects of extracranial carotid disease.

Cerebral blood flow (CBF), cerebral blood volume (CBV), the CBF/CBV ratio - an index of the hemodynamic reserve capacity - the rate of oxygen metabolism (CMRO2), and the fractional extraction of oxygen by the brain (OEF) were studied by positron emission tomography (PET) in the cortical territory of both internal carotid arteries in 15 cases of transiently symptomatic or progressive extracranial atherosclerotic carotid disease. None of the patients had a major stroke or had a significant neurological deficit except 1 whose damaged hemisphere is excluded from study. All were asymptomatic at the time of PET scanning. Values were obtained in the middle cerebral artery (MCA) distribution, and in the anterior and posterior borderzone regions. Eight cases had unilateral carotid stenosis of 80% or greater and 7 had unilateral or bilateral occlusion of the origin of the internal carotid artery. Results obtained in patients were compared using Student's t-test, to those obtained in neurologically normal, elderly volunteers. Patients with carotid stenosis had a significantly decreased CBF (p less than .025) and CBF/CBV ratio (p less than .025) selectively in the anterior borderzone regions. This was accompanied by a trend toward elevated OEF and declining CMRO2 values. Patients with carotid occlusion had significantly decreased CBF (p less than .005), decreased CBF/CBV ratio (p less than .005) and decreased CMRO2 (p less than .025) in the ipsilateral anterior borderzone and MCA territories. Similar changes were present in the opposite hemisphere of patients with bilateral carotid disease. These results indicate that carotid stenosis is associated with hypoperfusion and diminished hemodynamic reserve capacity in the anterior borderzone, and that carotid occlusion produces more widespread hypoperfusion and metabolic depression.

Aged↗
PubMed1989

Hemodynamic and metabolic effects of cerebral arteriovenous malformations studied by positron emission tomography.

Seventeen patients with an intracranial arteriovenous malformation were studied with positron emission tomography. Cerebral blood flow, cerebral blood volume, oxygen extraction fraction, and glucose and oxygen metabolism were evaluated in both hemispheres, excluding the area of the malformation itself. Patients were divided into three groups according to the size of their malformation, and results obtained were compared with studies in healthy volunteers. The glucose metabolism was significantly (p less than 0.01) decreased in the ipsilateral hemisphere in all patients. The cerebral blood volume was significantly increased (p less than 0.001) ipsilaterally in the three groups, and contralaterally in patients with medium- and large-sized arteriovenous malformations. The cerebral blood volume to cerebral blood flow ration, an index of vascular mean transit time, was significantly increased (p less than 0.005) ipsilaterally in patients with medium- and large-sized malformations and contralaterally in patients with large ones. Cerebral blood flow, oxygen extraction fraction, and oxygen metabolism were within the normal range bilaterally in all three groups, but oxygen extraction fraction tended to be higher in patients with larger lesions. The lack of significant change in oxygen metabolism suggests that oxygen metabolism in cortical areas remote from the arteriovenous malformation has been maintained by compensatory hemodynamic mechanisms. These data reveal widespread metabolic and hemodynamic consequences of arteriovenous malformations and suggest that they are associated with impairment of glucose metabolism, both in ipsilateral regions remote from the lesion and in the contralateral hemisphere in patients with large lesions.

Adult↗
PubMed1988

Toxicity of L-proline toward rat hippocampal neurons.

Intrahippocampal injections of L-proline, a neutral amino acid excitant, non-selectively destroyed pyramidal and granule cells. Co-administration of equimolar kynurenate, an excitatory amino acid antagonist, markedly reduced the extent of neuronal cell death. L-Proline destroyed far more hippocampal neurons than D-proline, in keeping with its greater neuroexcitatory potency. L-Proline must therefore be added to the list of excitotoxins present in brain. Its excitotoxic action may be related to the neurological and cognitive deficits associated with hyperprolinemia.

Animals↗