Search PubMed⌕ Search

Biomedical subjects

J Kucharczyk

Publications and source records attributed to J Kucharczyk.

At least 37 records · Page 2Linked to original sources
PubMed1994

Severe brain edema associated with cumulative effects of hyponatremic encephalopathy and ischemic hypoxia.

Hyponatremia in cats produced brain edema, detectable by both magnetic resonance imaging (MRI) and increased brain water, with a compensatory decrease of brain sodium. Sodium transport was measured in synaptosomes from hyponatremic cat cerebral cortex. The sodium efflux via Na(+)-K(+)-ATPase was significantly higher (144%) than control, while sodium influx via the Na+/H+ antiporter was significantly decreased (74%). Both responses tend to decrease brain intracellular sodium and thus, brain cell osmolality. Ischemia following unilateral middle cerebral artery occlusion also resulted in brain edema. However, the efflux of sodium via both Na(+)-K(+)-ATPase and sodium channels actually decreased, both maladaptive responses. Furthermore, when ischemia was superimposed upon hyponatremia, all of the cerebral adaptive changes which had been induced by hyponatremia alone were rendered ineffective. This resulted in further elevations of brain water and sodium. Hyponatremia superimposed upon ischemia thus worsens the brain edema associated with ischemia alone. Thus, ischemia impairs the ability of the brain to adapt to hyponatremia, probably by eliminating the compensatory mechanisms of brain sodium transport initiated by hyponatremia.

Animals↗
PubMed1994

Diffusion-weighted magnetic resonance imaging of acute focal cerebral ischemia: comparison of signal intensity with changes in brain water and Na+,K(+)-ATPase activity.

Diffusion-weighted magnetic resonance (MR) images from rats during acute cerebral ischemia induced by middle cerebral artery occlusion were analyzed for correspondence with changes in brain water, cation concentrations, and Na+,K(+)-ATPase activity measured in vitro after 30 or 60 min of ischemia. In the ischemic hemisphere, signal intensity was increased at 30 min (p < 0.05 vs contralateral hemisphere) and further increased at 60 min. Na+,K(+)-ATPase activity was 34% lower in ischemic cortex and 40% lower in ischemic basal ganglia after 30 min (p < 0.05), but water content and Na+ and K+ concentrations were not significantly different between hemispheres. After 60 min, water content and Na+ concentration were increased, and both Na+,K(+)-ATPase activity and K+ concentration were decreased in the ischemic hemisphere (p < 0.05). These findings are consistent with the hypothesis that the early onset of signal hyperintensity in diffusion-weighted MR images may reflect cellular edema associated with impaired membrane pump function. Early in vivo detection and localization of potentially reversible ischemic cerebral edema may have important research and clinical applications.

Acute Disease↗
PubMed1994

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairs brain adaptation to hyponatremia, worsening brain edema, we performed in vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or hypoxic hypoxia. Mortality with hypoxic hypoxia was 0%; with hyponatremia, 22%; and with hyponatremia+hypoxia, 100%. Hyponatremia in cats produced brain edema, with a compensatory decrease of brain sodium. Ischemic hypoxia also resulted in brain edema, but with elevation of brain sodium. However, when ischemic hypoxia was superimposed upon hyponatremia, there was elevation of brain sodium with further elevation of water. Outward sodium transport in cat cerebral cortex synaptosomes was measured via three major pathways through which brain osmolality can be decreased. After hyponatremia, sodium transport was significantly altered such that brain cell osmolality would decrease: 44% increase in Na(+)-K(+)-ATPase transport activity (ouabain inhibitable); 26% decrease in amiloride-sensitive sodium uptake. The change in veratridine-stimulated sodium uptake was not significant (P > 0.05). When ischemic hypoxia was superimposed upon hyponatremia, all of the cerebral adaptive changes induced by hyponatremia alone were eliminated. Thus, hypoxia combined with hyponatremia produces a major increase in brain edema and mortality, probably by eliminating the compensatory mechanisms of sodium transport initiated by hyponatremia that tend to minimize brain swelling.

Amiloride↗
PubMed1993

High-speed MR imaging of ischemic brain injury following stenosis of the middle cerebral artery.

Magnetic susceptibility contrast-enhanced and diffusion-weighted echo planar magnetic resonance (MR) imaging was performed using a cat model of acute regional cerebral ischemia induced by partial stenosis of the right middle cerebral artery (MCA). The imaging data were correlated with triphenyltetrazolium chloride (TTC)-stained histopathologic coronal brain sections to determine the prognostic efficacy of high-speed MR imaging techniques in differentiating mild, moderate, and severe cerebral hypoperfusion. Brains of animals without cortical injury on TTC staining were found to have a reduction in peak contrast enhancement of 32 +/- 6% (mean +/- SD) below control values with no significant change in the apparent diffusion coefficient (ADC), determined from the diffusion-weighted MR images. In cases where moderate ischemic injury was observed in the TTC-stained sections, a 10-20% drop in the ADC was found over the 6-h study period, accompanied by a much wider variation in peak contrast enhancement. Finally, where TTC staining showed severe ischemic brain damage, a 40-50% drop in ADC and a reduction in peak contrast enhancement effect of > 95% were observed as early as 1 h following MCA stenosis. The significant correlation between imaging observations and histologically confirmed cerebral ischemia indicates that magnetic susceptibility contrast-enhanced echo planar MR imaging is sensitive to slight reductions in cerebral perfusion that fall below the threshold for reliably detectable ischemia-induced alterations in ADC. First-pass perfusion-sensitive imaging may thus be diagnostically useful in differentiating severely hypoperfused permanently injured tissue from the mildly hypoperfused ischemic penumbra.

Animals↗
PubMed1993

Echo-planar perfusion-sensitive MR imaging of acute cerebral ischemia.

T2*-sensitive echo-planar magnetic resonance imaging was used with first-pass magnetic susceptibility contrast enhancement in a cat model of acute regional stroke to evaluate the relationship between cerebral hypoperfusion and ischemic brain damage. In normal brain, dose-dependent decreases in signal intensity were observed after intravenous injection of 0.15-0.50 mmol/kg dysprosium-diethylenetriaminepentaacetic acid bismethylamide or gadodiamide injection. Shortly after unilateral occlusion of the middle cerebral artery, foci of signal hyperintensity on diffusion-weighted images were observed in the ipsilateral basal ganglia. Sixty minutes after occlusion, perfusion deficits in the ipsilateral parietal and temporal cortical gray matter were observed to be spatially correlated with areas of hyperintensity on diffusion-weighted images. When reflow was attempted after 60 minutes, delayed contrast agent transit suggestive of partial ischemic tissue injury was demonstrated. Attempts to produce reflow after 2 hours did not restore normal brain perfusion and resulted in image hyperintensity and histopathologic brain damage. Six-hour occlusion was associated with pronounced perfusion deficits in the ischemic territory.

Acute Disease↗
PubMed1993

Early detection of regional cerebral ischemia using high-speed MRI.

BACKGROUND AND PURPOSE: Diffusion-weighted magnetic resonance imaging (MRI) has been shown to be effective in detailing regions of cerebral ischemia in which water proton translations or motions have been slowed. The corresponding perfusion patterns, however, have not been correlated. Further, the hemodynamics of normal and ischemic tissues and the changes due to mild insults are also not clear. This study describes high-speed MRI techniques and observations found in the early detection of regional cerebral ischemia in the cat. METHODS: Gradient-echo and spin-echo-planar MRI was used with middle cerebral artery balloon occluders to induce transient ischemia and reperfusion. RESULTS: Apparent diffusion fell within minutes after middle cerebral artery occlusion and correlated with near-total or total perfusion deficits. Reactive hyperemia, apnea, and vasodilatation appeared to be changed in ischemic and normal brain. CONCLUSIONS: Characterization of early ischemic events is dramatically improved when the motions of water (apparent diffusion), delivery of water (perfusion), and response to hemodynamic perturbations (regulatory response) are measured. All can be accomplished with high-speed MRI techniques described herein.

Animals↗
PubMed1992

Hypercarbia-induced changes in cerebral blood volume in the cat: a 1H MRI and intravascular contrast agent study.

Cerebral blood volume changes with arterial carbon dioxide were monitored by proton T1-weighted MR images following administration of the intravascular contrast agent Gd-DTPA labeled with human serum albumin. Without MR contrast, no significant image intensity changes were observed with PaCO2. Following contrast, regional brain image intensities increased significantly over control (0% inspired CO2) in cortical gray, white, and basal ganglia regions with increasing PaCO2 and returned to control intensities upon return to 0% inspired CO2. Imaging of through-plane and in-plane phantoms was performed to assess flow effects. Signal losses of 2 and 6% (relative to no flow) were observed for bulk velocities of 5 mm/s at TE values of 15 ms. An intravascular contrast agent may be useful for MRI monitoring of local cerebral blood volume changes during cerebral perturbations.

Adipose Tissue↗
PubMed1992

Iron-dextran as a magnetic susceptibility contrast agent: flow-related contrast effects in the T2-weighted spin-echo MRI of normal rat and cat brain.

Iron-dextran (1 mmol Fe/kg) was used as an intravascular, paramagnetic contrast agent in rat and cat brain in conventional spin-echo T2-weighted (TR 2800/TE 100) 1H magnetic resonance imaging. The resulting images displayed differential decreases (30-50%) in intensity whose pattern was similar to that obtained with the superparamagnetic particulate iron oxide AMI-25 (0.18 mmol Fe/kg). Postcontrast images displayed improved anatomic detail, and contrast effects were observed to be greater in cortical and subcortical gray matter than in adjacent white matter. Intravenous injection of acetazolamide after administration of iron-dextran caused a small additional decrease in image intensity. Measurement of whole blood and plasma at 5 min postinjection of either contrast agent revealed significant increases in their volume magnetic susceptibilities. The contrast effect appears to be related to magnetic susceptibility changes brought about by the iron-dextran; it has both blood volume and blood flow components. The static model of magnetic susceptibility effects in brain capillaries is modified to include bolus flow of erythrocytes, providing a mechanism for the observed flow effects.

Acetazolamide↗
PubMed1992

Hyponatremic encephalopathy: is central pontine myelinolysis a component?

PURPOSE: Severe hyponatremia is often associated with permanent brain damage. There has been substantial controversy about whether central pontine myelinolysis (CPM), a rare neurologic disorder of uncertain etiology, can complicate either hyponatremia or its therapy. This study was undertaken to determine how often hyponatremic patients with the clinical diagnosis of CPM actually have the disorder as an integral structural component of their encephalopathy. PATIENTS: Analyses were carried out in 20 patients who had severe symptomatic hyponatremia and a presumptive diagnosis of CPM, based on clinical and/or neuroradiologic findings. All had been referred for neuroradiology consultation. The mean age (+/- SD) was 47 +/- 14 years, the lowest serum sodium level was 104 +/- 8 mM, and 85% of the patients were female. The etiologies were diverse and included postoperative status, thiazide diuretics, polydipsia, infection, acute renal failure, chronic alcoholism with emesis, and beer potomania. METHODS: The original and subsequent films of 20 patients were reevaluated retrospectively by two neuroradiologists. The clinical course was also reevaluated, and in eight patients, the postmortem brain findings were reviewed. The diagnosis of CPM was made only on the basis of strict criteria relating to either (1) pathologic findings of CPM on postmortem examination; or (2) computed tomographic scan and/or magnetic resonance imaging findings diagnostic of CPM. RESULTS: No pontine lesions were present in 15 of 20 patients in whom the diagnosis of CPM had initially been made. All 15 had extrapontine demyelinating lesions but the pons was normal. Two others had only lateral pontine lesions, so that only three of 20 patients had definite CPM. All but one of the 20 hyponatremic patients had a definite hypoxic event prior to any therapy with intravenous sodium chloride. The involved brain areas included basal ganglia, thalamus, cortical gray matter, and periventricular white matter, areas often affected by hypoxia. Each of the three patients in whom unequivocal findings of CPM were present had long histories of chronic alcoholism and hepatic cirrhosis. CONCLUSIONS: These results suggest that: (1) Neither hyponatremic encephalopathy nor its therapy is commonly associated with CPM; (2) Patients with chronic alcoholism who also become hyponatremic can develop pontine demyelinating lesions; (3) Most patients with symptomatic hyponatremia who are diagnosed as having CPM in fact have diffuse cerebral demyelinating lesions with a normal pons; (4) The distribution of cerebral demyelinating lesions in patients with hyponatremic encephalopathy is compatible with hypoxic damage.

Adult↗
PubMed1992

Cytotoxic brain edema: assessment with diffusion-weighted MR imaging.

To determine whether cytotoxic brain edema is associated with a decrease in diffusion, it was induced in rats, in the absence of ischemia, with an established model of acute hyponatremic encephalopathy. Cytotoxic brain edema secondary to acute hyponatremia was induced with intraperitoneal injections of 2.5% dextrose in water and subcutaneous injection of arginine-vasopressin. Coronal spin-echo magnetic resonance (MR) images were obtained with and without strong diffusion-sensitizing gradients before and after induction of acute hyponatremia. The apparent diffusion coefficient (ADC) was measured at two coronal section locations. In hyponatremic rats, the brain ADC was significantly reduced (P = .0153 and .0001) and was positively correlated with increased total brain water content (P = .0011). Plots of ADC versus total brain water showed a statistically significant inverse linear relationship between ADC and increasing brain water at the anterior coronal section location. The results indicate that the ADC may be a sensitive indicator of cytotoxic brain edema and thus may enable quantitative evaluation of such edema with diffusion-weighted MR imaging.

Animals↗
PubMed1992

MR imaging of the pituitary gland in infants and children: changes in size, shape, and MR signal with growth and development.

It has been reported that on MR images of the brain in neonates the entire pituitary gland is hyperintense. This is quite different from the well-established observation that portion is isointense. To better understand the development of the neonatal pituitary gland, we studied the timing and magnitude of changes in the size, shape, and MR signal of the pituitary gland in early childhood and infancy. The study included 76 infants and children ages 3 days to 4 years old. In each MR study, the signal intensity of the pituitary gland on T1-weighted coronal (n = 24) and sagittal (n = 76) images was compared with the signal intensity of the pons by using region-of-interest methods. The size and shape of the pituitary glands were recorded. Statistical comparisons were made for signal intensity and size of the pituitary gland between boys and girls and among age groups. The results showed that the MR signal of the posterior lobe remained hyperintense relative to the pons for all age groups represented in our study (through 4 years). However, the signal intensity of the anterior lobe gradually diminished and by approximately age 2 months was isointense with the pons. Thus, by approximately age 2 months the MR signal intensity of the infant's pituitary gland has changed from being entirely hyperintense (as seen in neonates) to isointense in the anterior lobe and hyperintense in the posterior lobe (as seen in adults). In the first 2 months of life the pituitary gland is bulbous in shape; later it has a flatter upper surface. We found no significant changes in the length or signal intensity of the pituitary gland; no differences among sexes in size, shape, or signal intensity were demonstrated. Findings of a bulbous pituitary gland and high MR signal of the entire pituitary are normal in neonates up to 2 months of age. After that, the gland gradually flattens and the MR signal of the anterior lobe decreases until it has characteristics similar to the adult pituitary. Lack of high signal or discovery of a small pituitary gland in a neonate should alert the radiologist to the possibility of pituitary malformation or dysfunction.

Child, Preschool↗
PubMed1991

Diffusion/perfusion MR imaging of acute cerebral ischemia.

In vivo echo-planar MR imaging was used to measure apparent diffusion coefficients (ADC) of cerebral tissues in a comprehensive noninvasive evaluation of early ischemic brain damage induced by occlusion of the middle cerebral artery (MCA) in a cat model of acute regional stroke. Within 10 min after arterial occlusion, ADC was significantly lower in tissues within the vascular territory of the occluded MCA than in normally perfused tissues in the contralateral hemisphere. Sequential echo-planar imaging was then used in conjunction with bolus injections of the magnetic susceptibility contrast agent, dysprosium DTPA-BMA, to characterize the underlying cerebrovascular perfusion deficits. Normally perfused regions of brain were identified by a dose-dependent 35-70% loss of signal intensity within 6-8 s of contrast administration, whereas ischemic regions appeared relatively hyperintense. These data indicate that sequential diffusion/perfusion imaging may be useful in differentiating permanently damaged from reversibly ischemic brain tissue.

Animals↗
PubMed1991

Anisotropy in diffusion-weighted MRI.

Diffusional anisotropy of water protons, induced by nonrandom, directional barriers which hinder or retard water motion, is measurable by MRI. Faster water diffusion was observed when the diffusion-sensitizing gradient direction paralleled the long axes of white matter tracts, indicative of fewer barriers to water motion. Diffusion perpendicular to this axis was as much as four times slower. Anisotropy was seen pre- and postmortem in all axial, sagittal, and coronal planes, with and without cardiac gating. Ordering has also been observed in feline optic nerve and in human peripheral nerves. Utilization of this technique can greatly improve understanding and assessment of demyelinating disorders, of white matter infarcts and neoplasms, and of neonatal brain and spinal cord development.

Animals↗
PubMed1991

In vivo diffusion-perfusion magnetic resonance imaging of acute cerebral ischemia.

We compared the anatomic extent and severity of ischemic brain injury shown on diffusion-weighted magnetic resonance (MR) images, with cerebral tissue perfusion deficits demonstrated by a nonionic intravascular T2*-shortening magnetic susceptibility contrast agent used in conjunction with standard T2-weighted spin-echo and gradient-echo echo-planar images. Diffusion-weighted images displayed increased signal intensity in the vascular territory of the middle cerebral artery 25-40 min after permanent occlusion, whereas T2-weighted images without contrast were negative or equivocal for at least 2-3 h after stroke was induced. Contrast-enhanced T2-weighted and echo-planar images revealed perfusion deficits that were spatially closely related to the anatomic regions of ischemic tissue injury. These data indicate that diffusion-weighted MR images are very sensitive to early onset pathophysiologic changes induced by acute cerebral ischemia. Combined sequential diffusion-perfusion imaging enables noninvasive in vivo examination of the relationship between hypoperfusion and evolving ischemic brain injury.

Acute Disease↗