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Biomedical subjects

A Romani

Publications and source records attributed to A Romani.

At least 109 records · Page 6Linked to original sources
PubMed1991

EEG changes and platelet aggregation in experimental cerebral focal ischemia in rabbits.

Nine white New Zealand rabbits were submitted to internal carotid embolization with microspheres which caused a histologically verified focal cerebral ischemia. Six animals were sham-operated. EEG, QEEG, ECG, blood pressure, rectal temperature and platelet aggregation were monitored in basal conditions and one hour after ischemia. Embolized animals showed an increase in power density spectrum (PDS) and delta activity (0.15-3.70 Hz) and the appearance of platelet aggregation. The QEEG changes were correlated to the degree of platelet aggregation after ischemia.

Animals↗
PubMed1991

Prestimulus EEG influence on late ERP components.

Ten healthy volunteers were submitted to an auditory oddball event related potentials (ERP) paradigm. Single trial 500 ms poststimulus ERPs (Pz, Cz, Fz--linked earlobes) along with the correspondent 1000 ms prestimulus EEG (O1-Cz) were stored. EEG epochs were submitted to spectral analysis and a slow wave index (SWI = delta + theta/total) was computed. Three selective ERP averages corresponding to low, medium and high SWI were computed. N2 latency was longer and P3a amplitude was lower in high SWI averages as compared to low SWI averages.

Analysis of Variance↗
PubMed1991

Effect of stimulus mode on middle latency auditory evoked potentials in humans.

Middle Latency Auditory Evoked Potentials (MLAEPs) were recorded in 35 healthy subjects; all underwent monaural stimulation and 18 of them additionally underwent binaural stimulation. The aim of the study was to determine the effect of stimulus mode on MLAEP Na, Pa and Nb components and to assess normative data for clinical purposes. MLAEPs were respectively obtained from Cz-ipsilateral ear lobe (monaural mode) and from Cz-A1 and Cz-A2 (binaural mode) by twice averaging 1000 responses to 65 dBHL alternating clicks delivered at a repetition rate of 8.1 Hz. Time base was 100 msec; analogical band-pass filter setting was 5-1000 Hz (off-line digital badpass: 20-100 Hz). The statistical analyses (paired t-test, repeated measures analysis of variance) were not able to demonstrate any differences that derived from differing sides of stimulation (monaural mode) or from differing recording derivations (binaural mode); on the contrary, we demonstrated a slight increase in waveform amplitudes when the binaural mode was employed. In particular, we observed an increase in Na-Pa peak-to-peak amplitude, whereas Pa-Nb amplitude was unmodified. This finding is explicable in terms of a binaural interaction effect. Finally, we propose some guidelines for the correct performance and evaluation of MLAEPs in clinical practice.

Acoustic Stimulation↗
PubMed1990

Hormonal control of Mg2+ transport in the heart.

Magnesium is abundant in the mammalian body and the second most abundant cation in cells. Because the concentration of intracellular free Mg2+ is relatively high (0.2-1 mM), Mg2+ is unlikely to act as a second messenger, like Ca2+, by rapidly changing its cytosolic concentration. But changes in Mg2+ do have profound effects on cellular metabolism, structure and bioenergetics. Key enzymes or metabolic pathways, mitochondrial ion transport, Ca2+ channel activities in the plasma membrane and intracellular organelles, ATP-requiring reactions, and structural properties of cells and nucleic acids are modified by changes in Mg2+ concentration. Yet, although some information is available from giant cells and bacteria, little is known about the regulation of intracellular Mg2+ in mammalian cells. Here we report a new transport mechanism for Mg2+ across the sarcolemma of cardiac cells in both intact hearts and dissociated myocytes. We show that noradrenaline, through beta-adrenergic stimulation and increase of cyclic AMP, stimulates a large efflux of Mg2+ from cardiac cells. This transport is of major dimensions and can move up to 20% of total cellular Mg2+ within a few minutes.

Animals↗
PubMed1990

Norepinephrine evokes a marked Mg2+ efflux from liver cells.

The addition of norepinephrine to perfused rat livers and to collagenase isolated hepatocytes induced a marked and dose-dependent magnesium efflux. The addition of beta-adrenergic receptor antagonists, but not alpha-antagonists, completely blocked the Mg2+ efflux. The Mg2+ efflux could also be induced by forskolin and by permeable cAMP analogues. By contrast, the addition of carbachol or vasopressin induced a Mg2+ influx into isolated hepatocytes. These results indicate that a significant Mg2+ efflux from liver cells can be induced through the beta-adrenergic receptors and that it is mediated through the cytosolic cAMP levels.

Animals↗
PubMed1990

Glucose 6-phosphate stimulation of MgATP-dependent Ca2+ uptake by rat kidney microsomes.

(1) The features of MgATP-dependent Ca2+ accumulation under stimulation with glucose 6-phosphate were studied in rat kidney microsomes. (2) Ca2+ accumulated in the presence of MgATP alone does not exceed approx. 2 nmol/mg protein. (3) Glucose 6-phosphate markedly stimulates Ca2+ accumulation, up to steady-state levels approx. 15-fold higher than in its absence. (4) The hydrolysis of glucose 6-phosphate by glucose-6-phosphatase is essential for the stimulation, as shown by inhibiting the glucose 6-phosphate hydrolysis with adequate concentrations of vanadate. Inorganic phosphate is accumulated in microsomal vesicles during glucose 6-phosphate-stimulated Ca2+ uptake in equimolar amounts with respects to Ca2+. (5) Increasing concentrations of glucose 6-phosphate result in increasing stimulations of Ca2+ uptake, until a maximal Ca2(+)-loading capacity of approx. 27 nmol/mg microsomal protein is reached. It is suggested that the enlargement of the kidney microsomal Ca2+ pool induced by glucose 6-phosphate (an important metabolite in kidney) might play a role in the regulation of Ca2+ homeostasis in kidney tubular cells.

Adenosine Triphosphate↗
PubMed1990

Effects of capsaicin, tachykinins, calcitonin gene-related peptide and bradykinin in the pig iris sphincter muscle.

Capsaicin-sensitive sensory neurons of the rabbit iris, by releasing tachykinins, exert a major role in the control of pupil motility in response to various noxious stimuli. However, the contribution of sensory innervation to the regulation of iris smooth muscle tone in other mammals species is not known. We have studied the effects produced by electrical field stimulation, capsaicin, substance P, neurokinin A, calcitonin gene-related peptide (CGRP), and bradykinin in the isolated iris sphincter muscle of the pig. Capsaicin (10 microM): a) contracted the isolated sphincter muscle and; b) released immunoreactivity for substance P (SP-LI) and CGRP (CGRP-LI) from this preparation. These two effects were no longer observed at the second exposure to the drug. Electrical field stimulation (10 Hz, 60 V, 0.5 ms for 5 s) produced a biphasic contractile response. The rapid component was inhibited by atropine (1 microM), while the delayed response was blocked by previous exposure to capsaicin (10 microM). Substance P and neurokinin A consistently produced contraction of the pig iris sphincter muscle, substance P being more potent than neurokinin A. CGRP induced a contractile response in more than 50% of the preparations. The tachykinin antagonist [D-Arg1, D-Trp7,9, Leu11]-substance P (3 microM) blocked: a) the effect of substance P (1 nM); b) the delayed response to electrical field stimulation and; c) reduced by more than 50% response to capsaicin. Bradykinin (10 microM) failed to release either SP-LI or CGRP-LI. The contractile response evoked by bradykinin was unaffected by in vitro pretreatment with capsaicin (10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Liver cytosolic non-dialysable factor(s) can counteract GTP-dependent Ca2+ release in rat liver microsomal fractions.

Readdition to rat liver microsomes of dialysed liver post-microsomal supernatant resulted in an almost complete inhibition of the Ca2+-releasing effect of GTP. Such inhibition was heat-labile, and was associated with non-ultrafiltrable supernatant components with a molecular weight higher than 30,000 D. A preliminary fractionation of liver supernatant showed that the inhibitory effect is recovered in the 40-50% ammonium sulfate-precipitated proteins, with an approx. 10-fold enrichment. The active ammonium sulfate fraction did not modify the GTP-induced Ca2+ increase of passive Ca2+ efflux from microsomes, nor did it affect microsomal GTP hydrolysis, which is likely required for its Ca2+ releasing effect. The active ammonium sulfate fraction appears to markedly favour the translocation of GTP-released Ca2+ into a microsomal GTP-insensitive pool. Separation of liver microsomes in smooth and rough fractions revealed that such GTP-insensitive Ca2+ pool is almost completely associated with smooth microsomes.

Animals↗
PubMed1989

Ca2+ mobilization by vasopressin and glucagon in perfused livers. Effect of prior intoxication with bromotrichloromethane.

Perfused livers isolated from rats treated with BrCCl3 for up to 15 min were used as an experimental tool to investigate the role of the hepatic endoplasmic reticulum in Ca2+ mobilization elicited by vasopressin and glucagon. BrCCl3-treatment caused extensive impairment (37 to 92%) of Ca2+ pumps of isolated liver microsomes, while Ca2+ pumps of mitochondria and plasma membrane vesicles remained undamaged. In perfused livers of BrCCl3-treated rats, the efflux of Ca2+ and the concomitant stimulation of O2 consumption and glucose release induced by vasopressin were decreased. The extent of the decrease paralleled the duration of BrCCl3-treatment. The decrease of Ca2+ efflux following vasopressin addition was closely correlated with the decrease of active Ca2+ accumulation by isolated microsomes (r = 0.99, P less than 0.001). The Ca2+ efflux elicited by glucagon was also decreased after BrCCl3-treatment, whereas stimulation of O2 consumption and glucose release were retained. The possibility that BrCCl3-treatment might impair the production of the intracellular Ca2+-mobilizing messenger IP3 is unlikely, since vasopressin still induced the formation of inositol phosphates, including IP3, in isolated hepatocytes obtained from BrCCl3-treated rats. Thus, this work supports the hypothesis that the Ca2+ stored in the liver ER is the major pool of intracellular Ca2+ available for mobilization by vasopressin, glucagon and other effectors.

Animals↗
PubMed1989

Clinical and biochemical responses to therapy in Alzheimer's disease and multi-infarct dementia.

Memory performance, central monoaminergic function and sympathetic nerve activity were studied in patients with dementia of the Alzheimer type (DAT) or with multi-infarct dementia before and after 4 weeks with single or combined drug therapy (choline-piracetam). Analysis of the levels of 3-methoxy-4-hydroxyphenylglycol (MHPG), 3-methoxy-4-hydroxyphenylacetic acid (HVA) and 5-hydroxyindolacetic acid in the cerebrospinal fluid (CSF) and also in urine (plus 3-methoxy-4-hydroxy mandelic acid) showed that the basal values of HVA in the CSF and urine were lower in the more severely demented compared with the mildly demented subjects in both groups. The combined drug treatment resulted in a statistically significant increase in the MHPG level in the CSF of mildly demented subjects of the DAT group, while it seemed not to influence the other monoamine metabolites. The sympathetic nerve activity was similar in both patient groups and was unchanged after therapy. These findings suggest a dopaminergic deficit in advanced stages of the disease and a possible enhancement of the central noradrenergic output with therapy. No effects of therapy on memory performance or correlations between monoamine levels and memory test scores were noted.

Aged↗
PubMed1989

Event-related potentials in chronic alcoholics during withdrawal and abstinence.

Twenty-one chronic alcoholics were submitted to an "oddball" auditory event-related potentials (ERP) paradigm and to the Wechsler Memory Scale (WMS) after four weeks' abstinence. Eight of these patients were also submitted to the same ERP procedure and to two WMS items (digit span and associations) during a minor withdrawal state in the first days of hospitalization. Alcoholics showed reduced N1-P3 and N2-P3 amplitudes as compared to control subjects. Three alcoholics showed a P3 latency that exceeded the age-corrected control range (2 SE). There was no correlation between neuropsychological performances and electrophysiological measures, but the three subjects with abnormal P3 latencies had lower WMS scores. During withdrawal, greater N1-P2 amplitudes and shorter P3 latencies were observed as well as poorer performances on the two WMS items. The results are discussed in view of the possible contributions of ERPs in the understanding of the effects of chronic alcohol intake and alcohol withdrawal on CNS functions.

Adult↗
PubMed1989

Somatosensory evoked potentials by tibial nerve stimulation in the rabbit.

Somatosensory evoked potentials by tibial nerve stimulation were obtained in ten New Zealand rabbits. The subcortical or cortical source of the three negative and three positive peaks present in the first 55 ms is discussed viewing the results obtained by different surface electrode locations and by stereotaxic recordings. The authors report interanimal, interhemispheric and test-retest variability of latencies and amplitudes of subcortical and cortical components.

Animals↗
PubMed1988

4-Hydroxynonenal and other lipid peroxidation products are formed in mouse liver following intoxication with allyl alcohol.

Some recent reports indicate that lipid peroxidation might play a crucial role in the production of allyl alcohol hepatotoxicity. Previous work from our laboratory has suggested that in the case of bromobenzene, a hepatotoxin sharing the ability of allyl alcohol to induce a marked depletion of liver glutathione, liver injury is likely to be mediated by lipid peroxidation. In particular, we demonstrated that 4-hydroxynonenal and other aldehydes derived from lipid peroxidation can be detected in the liver of bromobenzene-poisoned mice. In the present study, we report also the in vivo formation of 4-hydroxynonenal and other aldehydes after allyl alcohol poisoning. 24-h-fasted mice were intoxicated with allyl alcohol (1.5 mmol/kg body wt., i.p.) and killed 1-3 h later. 4-Hydroxynonenal and other carbonyls were looked for in liver extracts in the form of 2,4-dinitrophenylhydrazone derivatives. After fractionation of liver extracts by means of thin-layer chromatography (TLC), a well-resolved peak corresponding to standard 4-hydroxynonenal was obtained in the high-pressure liquid chromatography analysis. Total carbonyls (as 2,4-dinitrophenylhydrazones) were separated by TLC into three fractions, according to their different polarity. The amounts of carbonyls present in each fraction were determined by ultraviolet-visible spectroscopy. In addition, several products were identified in the fraction of the 'non-polar carbonyls' corresponding to alkanals and alk-2-enals.

1-Propanol↗
PubMed1988

MgATP-dependent glucose 6-phosphate-stimulated Ca2+ accumulation in liver microsomal fractions. Effects of inositol 1,4,5-trisphosphate and GTP.

Ca2+ release triggered by inositol 1,4,5-trisphosphate (IP3) and/or GTP has been studied with rough and smooth microsomes isolated from rat liver. Microsomes were loaded with Ca2+ in the presence of MgATP and in the presence or in the absence of glucose 6-phosphate (glucose-6-P) which markedly stimulated the MgATP-dependent Ca2+ accumulation in rough and smooth microsomes (5- and 10-fold, respectively). Upon addition of IP3 (5 microM), rough and smooth microsomes rapidly release a part (not exceeding 20%) of the Ca2+ previously accumulated both in the absence and in the presence of glucose-6-P. Under the same experimental conditions, inositol 1,3,4,5-tetrakisphosphate was ineffective in triggering any Ca2+ release. Upon addition of GTP (10 microM) both the microsomal fractions progressively release the Ca2+ previously accumulated in the presence of glucose-6-P, when 3% polyethylene glycol was also present. In the absence of polyethylene glycol, GTP released Ca2+ from rough microsomes only, and GTP plus IP3 caused a Ca2+ release which was the sum of the Ca2+ releases caused by GTP and IP3 independently. Both IP3 and GTP, added to microsomes at the beginning of the glucose-6-P-stimulated Ca2+ uptake, reduced the Ca2+ accumulation into rough and smooth microsomes without modifying the initial rate (3 min) of Ca2+ uptake. Also in these conditions, the effects of GTP and IP3 were merely additive. These results indicate that both rough and smooth liver microsomes are responsive to IP3 and GTP with respect to Ca2+ release and that IP3 and GTP likely act independently.

Adenosine Triphosphate↗
PubMed1988

Intraocular pressure changes in secondary positions of gaze in normal subjects and in restrictive ocular motility disorders.

One hundred normal Caucasian eyes and 29 eyes with restrictive disorders of ocular motility were studied in order to delineate intraocular pressure changes in secondary positions of gaze. Applanation tonometry was performed in the primary position and at an angle of 22 degrees. In patients with restrictive syndromes the changes of intraocular pressure in the secondary positions of gaze were significantly higher (p less than 0.0001) than in normal subjects. The range of variation in normal subjects was 0, +3 mmHg for supraduction and -3, +1 mmHg for abduction. Patients with restrictive syndromes showed changes between +1 and +15 mmHg for supraduction and between +3 and +10 mmHg for abduction. Results obtained in the two groups showed the existence of false negatives. This test is thus a practical and useful diagnostic tool, but its results must be evaluated cautiously.

Adolescent↗
PubMed1988

MgATP-dependent, glucose 6-phosphate-stimulated liver microsomal Ca2+ accumulation: difference between rough and smooth microsomes.

Some features of the MgATP-dependent Ca2+-accumulating capacity of rough as compared to smooth liver microsomal fraction were studied. Smooth microsomes accumulate somewhat higher amounts of Ca2+ than rough ones in the presence of MgATP. In the presence of glucose 6-phosphate, which markedly stimulates MgATP-dependent Ca2+ accumulation in both fractions, smooth microsomes exhibit a much higher Ca2+-accumulating capacity than rough ones. Possible reasons of the differences observed between the two fractions were investigated. Smooth microsomes exhibit a higher Ca2+-dependent ATPase activity, suggesting a higher Ca2+ inward transport into smooth vesicles. Also, following the inhibition of active Ca2+ transport by means of vanadate, smooth microsomes appear to release the Ca2+ previously accumulated--both in the absence (i.e., with MgATP only) and in the presence of glucose 6-phosphate--at a lower rate than rough ones. This indicates a lower passive backflux of Ca2+ accumulated in smooth vesicles. On the basis of these data, differences can be envisaged with respect to cellular Ca2+ handling by different domains of endoplasmic reticulum in the liver.

Adenosine Triphosphate↗
PubMed1988

Prestimulus spectral EEG patterns and the evoked auditory vertex response.

A vigilance-related index (slow wave index, SWI) representing the relative delta + theta amplitude of the 1 sec prestimulus EEG spectrum has been related to latencies and amplitudes of the auditory cortical evoked response (EP) in 12 volunteers. Stimuli were 70 dB SL tone bursts delivered at 10 sec ISI. Four selective averages were obtained for each subject according to the subdivision of the SWI into quartiles. The subjects were divided into 2 groups having individual mean SWI values above or below the group's median SWI. Repeated measures MANOVA showed that N1 latency increased within subjects from the first to the fourth SWI quartile and that it was longer in subjects with high mean SWIs. N1-P2 amplitude decreased within subjects from the first to the fourth SWI quartile, but only in the group with high mean SWI.

Adult↗