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Anish Bhardwaj

Publications and source records attributed to Anish Bhardwaj.

41 records · Page 3Linked to original sources

Interhemispheric intracranial pressure gradients in massive cerebral infarction.

We report continuous bilateral intracranial pressure (ICP) monitoring immediately after transtentorial herniation in a patient with massive cerebral infarction to: 1) determine presence and time course of compartmental ICP differences, and 2) to study effects of therapy on both hemispheres. A 55-year-old man admitted with watershed infarctions in the left anterior-middle-posterior cerebral arteries distribution. Initial investigations demonstrated highly narrowed left extracranial internal carotid artery. Eight days later he developed unexplained lethargy and anisocoria. Head computerized tomography (CT) showed massive left hemispheric infarction, edema, and midline shift. Bilateral subarachnoid bolts demonstrated equally elevated ICP in both hemispheres. Hyperventilation and osmotic therapy produced near-identical ICP reduction bilaterally with resolution of anisocoria. Later, plateau waves and autonomic instability developed. Shortly before loss of brainstem function, interhemispheric ICP gradients (left greater than right) of 30-40 mm Hg developed. Intracranial pressure did not equalize prior to brain death determination. Bilateral ICP monitoring did not reveal an interhemispheric ICP gradient soon after transtentorial herniation in massive MCA infarction. The presence of interhemispheric ICP gradients in massive stroke remains unproven and further clinical study is necessary.

Dysarthria↗

Suppression of cortical functional hyperemia to vibrissal stimulation in the rat by epoxygenase inhibitors.

Application of glutamate to glial cell cultures stimulates the formation and release of epoxyeicosatrienoic acids (EETs) from arachidonic acid by cytochome P-450 epoxygenases. Epoxygenase inhibitors reduce the cerebral vasodilator response to glutamate and N-methyl-D-aspartate. We tested the hypothesis that epoxygenase inhibitors reduce the somatosensory cortical blood flow response to whisker activation. In chloralose-anesthetized rats, percent changes in cortical perfusion over whisker barrel cortex were measured by laser-Doppler flowmetry during whisker stimulation. Two pharmacologically distinct inhibitors were superfused subdurally: 1) N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide (MS-PPOH), an epoxygenase substrate inhibitor; and 2) miconazole, a reversible cytochrome P-450 inhibitor acting on the heme moiety. Superfusion with 5 micromol/l MS-PPOH decreased the hyperemic response to whisker stimulation by 28% (from 25 +/- 9 to 18 +/- 7%, means +/- SD, n = 8). With 20 micromol/l MS-PPOH superfusion, the response was decreased by 69% (from 28 +/- 9% to 9 +/- 4%, n = 8). Superfusion with 20 micromol/l miconazole decreased the flow response by 67% (from 31 +/- 6% to 10 +/- 3%, n = 8). Subsequent superfusion with vehicle restored the response to 26 +/- 11%. Indomethacin did not prevent MS-PPOH inhibition of the flow response, suggesting that EET-related vasodilation was not dependent solely on cyclooxygenase metabolism of 5,6-EET. Neither MS-PPOH nor miconazole changed baseline flow, reduced the blood flow response to an adenosine A(2) agonist, or decreased somatosensory evoked potentials. The marked reduction of the cortical flow response to whisker stimulation with two different types of epoxygenase inhibitors indicates that EETs play an important role in the physiological coupling of blood flow to neural activation.

8,11,14-Eicosatrienoic Acid↗