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Biomedical subjects

B I Lee

Publications and source records attributed to B I Lee.

83 records · Page 5Linked to original sources
PubMed1984

Pathophysiologic concentrations of lysophosphoglycerides quantified by electron microscopic autoradiography.

Lysophosphoglycerides accumulate in ischemic myocardium and appear to contribute to malignant dysrhythmia. Exposure of normoxic isolated Purkinje fibers or ventricular muscle strips to exogenous lysophosphatidyl choline (LPC) results in rapid, yet reversible, electrophysiologic derangements analogous to changes associated with ischemia in vivo. However, subcellular, local concentrations required for induction of electrophysiologic effects have not yet been elucidated unambiguously. The present study was designed to delineate the subcellular distribution and the sarcolemmal concentration of LPC by quantitative electron microscopic autoradiography after exposure of canine ventricular muscle strips to 3H-methyl LPC (200 microM) for 10 minutes. Tissue was processed for electron microscopy with a new procedure developed specifically to spatially fix choline phosphatides and render them insoluble in lipid solvents. Grain distributions were analyzed in the same group of cells that had been monitored electrophysiologically while superfused with LPC. LPC significantly decreased the resting membrane potential, action potential amplitude, duration, Vmax of phase 0, and conduction time. Grains were concentrated in the membranous organelles of cardiac myocytes. Myocyte sarcolemma exhibited the highest grain density (129 grains/100 micron2 versus a background of 0.27 grains/100 micron2). Calculations based on grain densities, emulsion sensitivity, exposure time, and specific activity indicated that the sarcolemma incorporated 5.4 X 10(6) LPC molecules/micron3 of membrane volume corresponding to approximately 1% of total sarcolemmal phospholipid. Since incorporation of only this small amount of lysophosphoglyceride into the sarcolemma was sufficient to elicit electrophysiologic disturbances, the observed accumulation of lysophosphoglycerides induced by ischemia appears to be sufficient to contribute to malignant dysrhythmia in vivo.

Animals↗
PubMed1983

Alpha adrenergic-mediated accumulation of calcium in reperfused myocardium.

Reperfusion of ischemic myocardium is associated with increases in total myocardial calcium (Ca+2), which may influence the ultimate extent of ischemic damage as well as the development of arrhythmias. Since reperfusion is also associated with enhanced alpha-adrenergic responsivity, this study was performed to determine the potential interactions between alpha-adrenergic receptors and myocardial calcium during reperfusion. Cats were subjected to 35 min of left anterior descending coronary artery occlusion and 10 min of reperfusion. Total myocardial calcium was measured by atomic absorption spectrometry. Intracellular calcium was calculated from measurements of extracellular space [( 3H]inulin). In control animals with reperfusion, total calcium increased from 0.32 +/- 0.03 to 0.65 +/- 0.05 mmol/100 g dry tissue (P less than 0.0001), while intracellular calcium increased from 0.15 +/- 0.03 to 0.40 +/- 0.05 mmol/100 g dry tissue (P less than 0.001). Pretreatment with the alpha-adrenergic blocking agents phentolamine or prazosin prevented the increase in total and intracellular calcium. Phentolamine and the aqueous soluble alpha 1-adrenergic antagonist BE-2254 administered as late as 2 min before reperfusion similarly attenuated the increase in tissue calcium. Although administration of BE-2254 2 min before reperfusion failed to block the reperfusion-induced increase in extracellular space, the increase in calculated intracellular calcium was prevented. beta-Adrenergic blockade with propranolol partially attenuated but did not prevent an increase in total tissue calcium. Labetalol, a combined alpha- and beta-adrenergic blocking agent completely blocked the increase in tissue calcium during reperfusion. Additional experiments performed after 70 min of ischemia with reperfusion demonstrated a 49% attenuation of the increase in tissue calcium with alpha-adrenergic blockade. Electron microscopy with pyroantimonate and x-ray microprobe analysis demonstrated a large increase in calcium precipitate in mitochondria after reperfusion in untreated animals. Though alpha-adrenergic blockade prevented the calcium deposition in mitochondria, other criteria of ischemia persisted. Thus, alpha-adrenergic blockade specifically prevents the increase in intracellular calcium during reperfusion in reversibly injured tissue, independent of alterations in extracellular space and tissue water.

Adrenergic alpha-Antagonists↗
PubMed1982

The arachidonic acid metabolic capacity of canine myocardium is increased during healing of acute myocardial infarction.

The relative capacity for metabolizing [14C]arachidonic acid into biologically active products was studied in microsomes prepared from both normal and infarcted regions of myocardium at three different times after circumflex coronary artery occlusion in the dog. At 3 days after infarction, when polymorphonuclear leukocytes were the predominant invading cell, the ability of infarcted left ventricle microsomes to produce arachidonic acid metabolites was greater than that of microsomes from normal areas of the same hearts. At 3 weeks after infarction, when macrophages were the predominant infiltrating cell and there was a proliferation of blood vessels and fibroblasts, there continued to be significant increases in the production of both prostacyclin (measured as 6-keto PGF1 alpha) and thromboxane (measured as TxB2). This enhanced production was still seen at 3 months after infarction at a time when histological examination of the tissue showed that it was still healing with both blood vessels and fibroblasts present. The production of 6-keto PGF1 alpha was 31.7 +/- 4 picomoles per milligram protein per hour (pmol/mg per hr) in noninfarcted regions of left ventricle, whereas the production was significantly increased to 71.7 +/- 15 at 3 days, 64.1 +/- 10 at 3 weeks, and 67.2 +/- 15 even at 3 months after infarction. The thromboxane synthetase activity rose significantly from 30.1 +/- 5 pmol mg per hr in noninfarcted regions to 73.7 +/- 18 at 3 days, 71.2 +/- 5 at 3 weeks, and 92.4 +/- 40 at 3 months. The enhanced ability to metabolize arachidonic acid may result from the inflammatory cell invasion or fibroblast activation which accompany healing of acute infarcts.

Animals↗
PubMedDate not supplied

HIPDM single photon emission computed tomography brain imaging in partial onset secondarily generalized tonic-clonic seizures.

HIPDM-Single photon emission computed tomography brain imaging was performed during interictal and ictal stages in three patients with complex partial seizures and secondarily generalized tonic-clonic seizures. In all three patients, interictal studies demonstrated decreased regional cerebral perfusion (rCP) and ictal studies showed increased rCP in the epileptogenic region. The demonstration of focal hyperperfusion by SPECT performed during secondarily generalized tonic-clonic seizures suggests that rCP in the epileptic focus remains higher than in other cerebral regions during immediate postictal stages, even in secondarily generalized seizures.

Adolescent↗
PubMedDate not supplied

Regional cerebral perfusion in PLEDs: a case report.

[123I]N,N,N'-trimethyl-N'-(2 hydroxy-3-methyl-5-123I-iodobenzyl)- 1,3-propane-diamine 2HCl single-photon-emission computed tomography (HIPDM-SPECT) brain imaging in one patient with periodic lateralized epileptiform discharges (PLEDs) on the EEG demonstrated increased regional cerebral perfusion in the PLEDs focus suggesting that PLEDs are the manifestation of abnormally enhanced neuronal activities. This may explain the frequent association of mental confusion, focal neurologic signs, and occurrence of seizures in association with PLEDs.

Adult↗
PubMedDate not supplied

Prolonged ictal amnesia with transient focal abnormalities on magnetic resonance imaging.

A previously healthy woman had a prolonged amnestic state caused by complex partial status epilepticus with bilateral mesiotemporal lobe involvement confirmed by EEG with nasopharyngeal electrodes. A magnetic resonance imaging (MRI) scan obtained shortly after recovery from the amnesia showed reversible focal abnormalities consisting of increased signal intensity on T2-weighted scan in the mesiotemporal lobe.

Adult↗
PubMedDate not supplied

Healing after arterial dilatation with radiofrequency thermal and nonthermal balloon angioplasty systems.

Thermal balloon angioplasty has been proposed as a means of reducing acute and delayed reclosure of arteries after percutaneous transluminal balloon angioplasty. A radiofrequency (rf) balloon catheter was used to perform thermal balloon angioplasty on canine arteries in vivo. The histologic appearance of rf-treated sites was compared with that of control sites treated by conventional percutaneous transluminal angioplasty. Acutely, rf-treated sites showed a reduced medial cellularity with preservation of internal elastic lamina except at the transitional zone between thermal injury and normal artery, where localized internal elastic lamina disruption was found. Nonthermal sites showed generalized disruption of internal elastic lamina and normal medial cellularity. Both thermal and nonthermal sites displayed a return of intimal cover commencing at 1 to 2 weeks and completed by 4 weeks. Diffuse myointimal hyperplasia appeared by 2 weeks after injury at breaks in the internal elastic lamina along the nonthermal vessels but was localized to the transitional zone in thermal injury sites. In rf-treated vessels, repopulation of the acellular thermally modified media had commenced by 4 weeks, and by 8 weeks the media was diffusely repopulated by spindle-shaped cells resembling smooth muscle cells lying between and aligned with preserved connective tissue laminae. Overall, the distribution and extent of the proliferative response after rf thermal balloon angioplasty were less than those seen after nonthermal balloon angioplasty. Thermal sites, which underwent reintimalization before medial cells returned, were considerably less prone to the development of myointimal hyperplasia. These results suggest that this modality may have beneficial effects on arterial healing after angioplasty.

Angiography↗