[Effect of irradiation on the iron uptake of liver cells in vitro].
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Biomedical subjects
Publications and source records attributed to G Adám.
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According to our earlier results, non-painful, weak afferent visceral signals may exert a steady influence on brain processes, including cognitive functions. In the present series colonic impulses of irritable bowel syndrome (IBS) subjects served as a model of chronic impact from the gut. Hemispheric preference, as well as cognitive style of information processing served as indicators of covert changes in brain functions. In twenty-one IBS patients and in ten control subjects of both sexes, the thresholds of minimal colonic distension sensitivity has been measured following the determination of hemispheric preference and of advantage in verbal or spatial information processing of the subjects. In IBS patients distension thresholds proved to be higher in verbals than in spatials, whereas in healthy controls the relationship of colonic thresholds and verbal versus spatial advantage was reversed. Among the normal controls with left hemisphere preference a significantly higher distension threshold has been observed than in those with right hemisphere preference, whereas in the IBS group such threshold-differences were not observable.
The GABA-ergic and opioid modulation of neurally induced muscle responses was studied in isolated guinea-pig taenia coli and human colonic circular muscle, using identical field stimulation parameters (rectangular pulses of 0.5 ms duration, 9 V x cm(-1) intensity, trains of 3 pulses at 0.5 Hz, repeated every 1/3/5 min). The stimulation-induced contractions were inhibited in both preparations by GABA and baclofen; the IC50 values in human colonic circular muscle were approximately 100 and 31.0 microM, respectively. In guinea-pig taenia coli, the inhibition by 10(-4) M GABA was dose-dependently reversed by 10(-4)-10(-3) M of GABA(B) receptor antagonist CGP 35348; antagonism by phaclofen was less effective in the same concentration range. In human colonic circular muscle, inhibition by 3 x 10(-5) M baclofen was fully reversed by 10(-3) M CGP 35348. With the exception of caecum, the delta 2 opioid receptor agonist deltorphin II was a potent inhibitor in human colonic circular muscle. 10(-8) M Deltorphin caused a 74.4 +/- 9.6% (n = 4) inhibition which was reversed by 10(-6) M of delta receptor selective peptide antagonist BOC-Tyr-Pro-Gly-Phe-Leu-Thr(OtBu). Deltorphin II was ineffective in guinea-pig taenia coli even at 10(-6) M; the same concentration caused an 84.3 +/- 7.9 (n = 4) inhibition in human preparations. It is concluded that: 1) GABA-ergic modulatory mechanisms are present both in human colonic circular muscle and guinea-pig taenia coli; 2) the GABA receptors involved are of type B; and 3) delta opioid receptor-mediated modulation functions only in human colonic circular muscle in regions other than the caecum.
Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.
The influence of chronic arterial hypertension upon the permeability to albumin of the cerebral capillaries, i.e. the blood-brain barrier, was studied in normotensive Wistar and spontaneously hypertensive Wistar rats with experimental subarachnoid hemorrhage. The blood-brain barrier permeability to albumin was assessed quantitatively by spectrophotometric determination of Evans blue extravasation. Subarachnoid hemorrhage was produced by injecting autologous blood into the cortical subarachnoid space. A significant increase of Evans blue albumin extravasation was found in the spontaneously hypertensive rats with subarachnoid hemorrhage as compared with normotensive animals suffering from subarachnoid hemorrhage. Subarachnoid hemorrhage in this model alone caused a significant Evans blue extravasation, whereas sham-operation did not. These findings emphasize the necessity for effective attempts to reduce the leakage of the capillary system in the early stage of subarachnoid hemorrhage.