PubMed Health⌕ Search

Biomedical subjects

F Abad

Publications and source records attributed to F Abad.

At least 19 recordsLinked to original sources
PubMed2002

Subclinical pain and thermal sensory dysfunction in children and adolescents with Type 1 diabetes mellitus.

AIMS: To assess cutaneous thermal and pain thresholds in upper and lower limbs in neurologically asymptomatic children and adolescents, and to study the relationships of clinical parameters and these sensory thresholds in subclinical diabetic neuropathy. METHODS: Thirty-five neurologically asymptomatic patients, aged 8-16 years, diagnosed with Type 1 diabetes mellitus (DM), and a control group of 35 healthy age-matched subjects participated in the study. Warmth, cold, and heat-induced pain thresholds were measured in the dorsum of the right arm and foot, using quantitative sensory testing (QST). Relevant clinical parameters, retrieved from medical records or measured at the QST session, were obtained for each patient. RESULTS: Compared with controls, diabetic patients had increased thresholds for warmth in the hand (P = 0.002), and cold and warmth in the foot (P = 0.015 and P = 0.004, respectively). Of the diabetic patients, 43% showed abnormality of at least one sensory threshold. A significant correlation was observed for duration of diabetes and heat-induced pain threshold in the hand (P = 0.045), but no correlation was found for age, height, weight, pre-test blood glucose, age of onset, current insulin dose, and mean of glycosylated haemoglobin determinations of the previous 18 months. No significant correlation was found for other sensory thresholds. CONCLUSIONS: Using QST, abnormal cutaneous thermal perception is a common finding, in both upper and lower limbs, in neurologically asymptomatic young diabetic patients. Heat-induced pain threshold in the hand was correlated with the duration of the diabetes.

Adolescent↗
PubMed2001

Oral sucrose compares favourably with lidocaine-prilocaine cream for pain relief during venepuncture in neonates.

UNLABELLED: To compare the relative efficacy of oral sucrose versus EMLA cream for pain relief during venepuncture, 51 full-term newborns (38M, 13F; postnatal age <4 d) in a stable condition were randomly allocated to one of four treatment groups: placebo (2 ml spring water); 2 ml sucrose 24% w/v; 1 g lidocaine-prilocaine 5% cream (EMLA); or EMLA plus sucrose. Water or a single dose of sucrose solution was administered orally 2 min before venepuncture. EMLA cream was applied in the antecubital fossa 45-60 min before venepuncture and covered by a Tegaderm dressing. A pacifier was given before skin puncture, but it was not actively held or replaced during the procedure or observation periods. In total, 55 venepunctures were performed blindly, always for clinical reasons. As indicators of pain, the total crying time was recorded and heart rate, respiratory rate and arterial oxygen saturation were measured blindly at baseline, immediately post-venepuncture, and 2 and 4 min afterwards. The main effects observed were: (i) time spent crying decreased significantly in the sucrose alone (p = 0.001) and EMLA plus sucrose (p = 0.008) groups; (ii) the above treatments attenuated significantly (p < 0.05) the immediate heart rate response to pain; and (iii) the concomitant use of EMLA did not increase further the analgesic efficacy of sucrose. CONCLUSION: This study shows that a 24% oral sucrose solution compares favourably with EMLA cream as a safe and cheap analgesic procedure to decrease pain responses to venepuncture in newborns.

Administration, Oral↗
PubMed2000

Altered regulation of calcium channels and exocytosis in single human pheochromocytoma cells.

We established primary cultures of human pheochromocytoma chromaffin cells. We then tried to find what mechanism of their secretory apparatus could be altered to produce the massive release of catecholamines into the circulation and the subsequent hypertensive crisis observed in patients suffering this type of tumor. Their whole-cell Ca2+ channel currents could be pharmacologically separated into components similar to those found in normal human adrenal chromaffin cells: 20% L-type, 30% N-type, and 50% P/Q-type Ca2+ channels. However, modulation of the channels by exogenous or endogenous ATP and opioids, via a G-protein membrane-delimited pathway, was deeply altered; some cells having no modulation or very little modulation alternated with others having normal modulation. This may be the cause of the uncontrolled secretory response, measured amperometrically at the single-cell level. Some cells secreted for long time periods and were insensitive to nifedipine (L-type channel blocker) or to omega-conotoxin MVIIC (N/P/Q-type channel blocker), while others were highly sensitive to nifedipine and partially sensitive to omega-conotoxin MVIIC. Alteration of the autocrine/paracrine modulation of Ca2+ channels may lead to indiscriminate Ca2+ entry and exacerbate catecholamine release responses in human pheochromocytoma cells.

Adenosine Triphosphate↗
PubMed2000

Comparative pharmacoeconomic study of vancomycin and teicoplanin in intensive care patients.

Randomized clinical trials and meta-analyses have not demonstrated any statistically significant differences between teicoplanin and vancomycin with regard to efficacy. A cost-minimization analysis was conducted to compare the economical impact of the treatment with vancomycin and teicoplanin in intensive care patients. Information on resource utilization was retrospectively collected from 100 consecutive clinical histories of patients hospitalized in a Spanish Intensive Care Unit, who had been given a glycopeptide antibiotic (50 teicoplanin and 50 vancomycin) for the treatment of a suspected or proven infection. Although personnel, material, and monitoring costs were higher in the vancomycin group, the acquisition costs and the total costs were much lower in this group, so the resulting total costs per day were 5508 ptas (33 euros) for vancomycin-treated patients and 9893 ptas (59.5 euros) for teicoplanin-treated patients. The savings with vancomycin for a 10-day course of treatment would be approximately 40697 ptas (244.5 euros) per patient. Results were consistent for a variety of conditions that were included in the sensitivity analysis.

Adolescent↗
PubMed1998

Autotomy in rats following peripheral nerve transection is attenuated by preceding formalin injections into the same limb.

The influence of an evolving painful inflammatory lesion on the development of autotomy, a behavioural model of denervation pain, was studied in rats suffering sciatic and saphenous nerves transection 30 or 60 min, and 1, 3, 7 or 14 days after being injected with formalin (50 microl, 5%, s.c). Hindpaws pressure and heat nociceptive thresholds and volume of the injected paw were assessed, in non-operated rats, at the above time-points. The main effects on autotomy were: (1) a significant attenuation when formalin injection preceded the neurectomies by 1 day or more, a period characterized by hypalgesia of the injected paw to both mechanical (during the first week) and thermal (spanning up to the third day after formalin) stimuli and inflammation (lasting for 14 days); (2) a significantly earlier onset when formalin was injected 30 min before neurectomies. Possible mechanisms linking nociceptive responsiveness and inflammation to the development of autotomy are discussed.

Animals↗
PubMed1998

Human adrenal chromaffin cell calcium channels: drastic current facilitation in cell clusters, but not in isolated cells.

Human adrenal medullary chromaffin cells were prepared and cultured from a cystic tumoral adrenal gland whose medullary tissue was unaffected. Adrenaline-containing and noradrenaline-containing cells were identified using a confocal fluorescence microscope and antibodies against dopamine beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT). Current/voltage (I/V) curves performed with the voltage-clamped cells bathed in 10 mM Ba2+ (holding potential, Vh=-80 mV) revealed the presence of only high-threshold voltage-dependent Ca2+ channels; T-type Ca2+ channels were not seen. By using supramaximal concentrations of selective Ca2+ channel blockers, the whole-cell IBa could be fractionated into various subcomponents. Thus, IBa had a 25% fraction sensitive to 1 microM nifedipine (L-type channels), 21% sensitive to 1 microM omega-conotoxin GVIA (N-type channels), and 60% sensitive to 2 microM omega-agatoxin IVA (P/Q-type channels). The activation of IBa was considerably slowed down, and the peak current was inhibited upon superfusion with 10 microM ATP. The slow activation and peak current blockade were reversed by strong depolarizing pre-pulses to +100 mV (facilitation). A drastic facilitation of IBa was also observed in voltage-clamped human chromaffin cell surrounded by other unclamped cells; in contrast, in voltage-clamped cells not immersed in a cell cluster, facilitation was scarce. So, facilitation of Ca2+ channels in a voltage-clamped cell seems to depend upon the exocytotic activity of neighbouring unclamped cells, which is markedly increased by Ba2+. It is concluded that human adrenal chromaffin cells mostly express P/Q-types of voltage-dependent Ca2+ channels (60%). L-Type channels and N-type channels are also expressed, but to a considerably minor extent (around 20% each). This dominance of P/Q-type channels in human chromaffin cells clearly contrasts with the relative proportion of each channel type expressed by chromaffin cells of five other animal species studied previously, where the P/Q-type channels accounted for 5-50%. The results also provide strong support for the hypothesis that Ca2+ channels of human chromaffin cells are regulated in an autocrine/paracrine fashion by materials co-secreted with the catecholamines, i.e. ATP and opiates.

Adenosine Triphosphate↗
PubMed1997

[Reading-induced epilepsy: three new cases].

INTRODUCTION: Primary epilepsy of reading is a rare syndrome in which patients present with mandibular myoclonia when reading texts. Seizures are also frequently provoked by other stimuli. Occasionally they may be followed by generalized tonic-clonic seizures. CLINICAL CASES: We present the clinical features and electroencephalographs of three patients with epilepsy of reading, one of them also had seizures when playing chess and after doing arithmetic and the third after reading music. Treatment with valproic acid and clonazepam completely controlled the seizures in all three patients. In two cases we saw epileptiform activity on EEG whilst they were reading, although the basal EEG was normal. CONCLUSIONS: We believe that epilepsy of reading is under-diagnosed and emphasize the importance of careful questioning of epileptic patients as to factors which may precipitate the seizures. In view of the social problems which may arise, early recognition of the syndrome is important for the patient.

Adult↗
PubMed1996

Effects of omega-conotoxin MVIIC on veratridine-induced cytotoxicity and cytosolic Ca(2+) oscillations.

External Ca(2+) entry through various Ca(2+)-channel subtypes is responsible for the large oscillations of the cytosolic Ca(2+) concentrations, [Ca(2+)](i), and cell death induced by veratridine in primary cultures of bovine chromaffin cells. Blockade by omega-conotoxin GVIA (GVIA) of N-type Ca(2+) channels, by omega-agatoxin IVA (IVA) of P-type Ca(2+) channels, or by furnidipine of L-type Ca(2+) channels did not afford cytoprotection. However, (omega-conotoxin MVIIC (MVIIC), a wide-spectrum blocker of N-, P- and Q-type Ca(2+) channels greatly protected the cells against the cytotoxic effects of veratridine. Furnidipine further enhanced the cytoprotecting effects of MVIIC. MVIIC but not furuidipine, markedly reduced the oscillations of [Ca(2+)](i) induced by veratridine in single fura-2-loaded chromaffin cells. The results suggest that Ca(2+) entry through any of the different Ca(2+) channel subtypes present in bovine chromaffin cells might be cytotoxic. They also support two ideas: (i) that wide-spectrum neuronal Ca(2+) channel blockers (i.e. MVIIC) might be better cytoprotecting agents than more specific neuronal Ca(2+) channel blockers (i.e., GVIA, IVA, furnidipine); and (ii) that combined Ca(2+) channel blockers may provide greater cytoprotection than single compounds.

Adrenal Glands↗
PubMed1996

Oral sweet solution reduces pain-related behaviour in preterm infants.

To evaluate the effectiveness of oral sucrose in the prevention of pain-induced crying in preterm infants, a sample of 28 healthy neonates (15M, 13F; gestational age at procedure less than 37 weeks) who were having routine blood drawn by arm venipuncture was studied. Infants were randomly allocated to receive by mouth, using a syringe, 2 ml of one of three solutions: spring water (group W) and sucrose 12 and 24% w/v (groups S12 and S24, respectively), all in water vehicle. After 2 min, while awake, arm venipuncture was performed and duration of crying was measured. The time spent crying was reduced in the group treated with the sweetest solution (S24, n = 8, mean = 19.1 s). No difference was observed between the S12 group (n = 8, mean = 63.1 s) and W group (n = 12, mean = 72.9 s). Physiological measurements were recorded at different time points to evaluate excessive basal and procedural distress.

Analgesia↗
PubMed1996

[Epileptic seizures during sleep].

UNLABELLED: Introduction. Epileptic crises presenting exclusively during sleep are rare and pose more problems of diagnosis than do crises of diurnal presentation. PATIENTS: We present the clinical and electroencephalographic data of 20 patients with exclusively sleep-induced epileptic crises, evaluating not only the type of crises and the diagnosis of the particular syndrome, but also the response to treatment and prognosis. The patients studied were over 17 years old, had only nocturnal crises and were followed up for a period of three years. An EEG done during sleep and cerebral CT scan were available in all cases and a cranial MR was available in two cases. Diagnosis was made using clinical data and the sleep EEG. RESULTS: The majority (40%) had temporal lobe epilepsy. In two patients (10%) occipital paroxysms were found. In all cases both the neurological examination and the mental state were normal. The sleep EEG was pathological in 75% of the cases. Only three of the twenty patients had changes on the CT scan. Monotherapeutic antiepileptic treatment completely controlled the crises in 15 patients. CONCLUSIONS: We wish to emphasize the usefulness and importance of the sleep EEG in defining the syndrome affecting these patients, the diagnostic difficulties in sleep epilepsy, the good response to antiepileptic treatment and the high incidence of recurrence if antiepileptic treatment is no longer given. In view of all these factors we believe that sleep epilepsy may be considered to be a syndrome of epilepsy.

Adolescent↗
PubMed1995

Pharmacological protection against the cytotoxicity induced by 6-hydroxydopamine and H2O2 in chromaffin cells.

We present in this report the characteristics of the damage induced by 6-hydroxydopamine and H2O2 on bovine chromaffin cells in primary culture. Cytotoxicity was quantified using catecholamine cell contents, lactate dehydrogenase (LDH) release, trypan blue exclusion and morphological appearance. An excellent correlation between these four parameters was found. The cytotoxic effects of 6-hydroxydopamine were Ca(2+)-independent. In spite of this, the Ca2+ channel antagonists R56865 (N-[1-(4-(fluorophenoxy)butyl)]-4-piperidinyl-N-methyl-2-benzo-thiazo lamine) lidoflazine exhibited marked cytoprotective effects against both 6-hydroxydopamine and H2O2. The selective dopamine uptake blocker, bupropion, increased the viability of 6-hydroxydopamine and H2O2-treated cells from 20% to around 80%. Catalase drastically protected against the cytotoxic effects of 6-hydroxydopamine and H2O2. In contrast, desferrioxamine gave better protection against H2O2 cytotoxicity; glutathione and N-acetylcysteine only afforded substantial protection against 6-hydroxydopamine. Three main conclusions emerge from this study. (1st) 6-Hydroxydopamine causes chromaffin cell damage via a mechanism probably related to the production of free radicals, but unrelated to Ca2+ ions. Cytoprotection afforded by R56865 and lidoflazine must be unrelated to their Ca2+ antagonist properties. This suggests a novel component in the cytoprotective mechanism of action of these drugs. (2nd) The strong cytoprotective effects of bupropion seem to be unrelated to its ability to block the plasmalemmal dopamine carrier. (3rd) Bovine adrenal chromaffin cells in primary cultures are a suitable model for adult neurons to study the basic mechanism of cell damage, and to screen new drugs with putative neuroprotective properties.

Acetylcysteine↗
PubMed1995

Activated charcoal increases digoxin elimination in patients.

Digoxin continues to be an important cause of drug toxicity. On the basis of a healthy volunteer study, activated charcoal has been proposed as a treatment for digoxin chronic intoxication. In order to evaluate the effect of activated charcoal on digoxin elimination in intoxicated patients during routine practice, we reviewed all Serum Digoxin Level Requests for adult in-patients from 1991 to 1993, with digoxin levels > 2.5 ng/ml. Of a total of 39 cases, 23 had been treated with activated charcoal while 16 had not. Digoxin elimination half-life during activated charcoal therapy was 36 h (S.D. 14 h; 95% C.I. 30-42 h) while in the non-treated group it was 68 h (S.D. 19 h, 95% C.I. 57-78). Calculated total body clearance of digoxin was 55 ml/min (S.D. 17 ml/min; 95% C.I. 45-64 ml/min) for the non-treated group versus 98 ml/min (S.D. 34 ml/min; 95% C.I. 83-113 ml/min) for the group receiving charcoal, representing an 78% increase in digoxin elimination.

Aged↗
PubMed1994

Effects of Ca2+ channel antagonists on chromaffin cell death and cytosolic Ca2+ oscillations induced by veratridine.

Exposure of bovine chromaffin cells to 30 microM veratridine for 24 h led to 70-80% cell death as reflected by phase contrast microscopy, trypan blue exclusion, lactate dehydrogenase (LDH) release and cell catecholamine contents. Na+ deprivation, Ca2+ deletion or tetrodotoxin (5 microM) prevented the veratridine-induced cell damage. Nimodipine and verapamil, but not omega-conotoxin GVIA afforded 20-30% protection. Flunarizine protected the cells by 80% and R56865 by 60%. Stimulation of fura-2-loaded single bovine chromaffin cells with 30 microM of 1,1-dimethyl-4-phenylpiperazinium (DMPP) or 59 mM K+ caused fast increases in cytosolic Ca2+ concentrations, ([Ca2+]i). The [Ca2+]i rose from 0.1 to peaks of 1.9 microM, which quickly declined to near basal levels with a t1/2 of around 30 s. In spite of sustained stimulation with these two depolarizing agents, the [Ca2+]i remained low and did not undergo oscillations. In contrast, veratridine (30 microM) caused large and frequent oscillatory changes in the [Ca2+]i which were long-lasting and did not disappear even 30 min after washing out the toxin. The [Ca2+]i oscillations were reversibly suppressed by Na+ or Ca2+ removal and by 5 microM tetrodotoxin. Selective L-type Ca2+ channel blockers (10 microM nimodipine or verapamil) or N-type Ca2+ channel blockers (1 microM omega-conotoxin GVIA) did not affect the [Ca2+]i oscillations. In contrast, flunarizine or R56865 (10 microM each) suppressed the oscillations of [Ca2+]i. The results demonstrate that bovine chromaffin cells have the necessary machinery to develop prolonged and repetitive [Ca2+]i oscillations in the presence of veratridine; however, 'physiological' depolarizing stimuli did not cause oscillations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1992

Cross-talk between M2 muscarinic and D1 dopamine receptors in the cat adrenal medulla.

In the study reported here we have reached two conclusions. First, the cat adrenal medulla chromaffin cell possesses a dopamine D1 receptor that seems to be coupled to an adenylyl cyclase. Second, this receptor regulates the muscarinic-mediated catecholamine release response through a negative feed-back loop which uses cyclic AMP as a second messenger. These conclusions are supported by the following findings: (i) SKF38393 (a selective D1 receptor agonist), but not quinpirole (a selective D2 agonist), inhibits the methacholine-mediated catecholamine release responses in a concentration-dependent manner (IC50 of around 1-2 microM). (ii) SCH23390 (a selective D1 antagonist), but not sulpiride (a selective D2 antagonist), reversed by 70% the inhibitory effects of SKF38393. (iii) Dibutyril cyclic AMP (500 microM) inhibited by 80% the secretory effects of methacholine.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

The source of calcium for muscarinic-mediated catecholamine release from cat adrenals.

1. In view of conflicting reports on the source of Ca2+ needed to trigger the secretory response to muscarinic stimulation of chromaffin cells, we have reinvestigated this problem in the cat adrenal gland perfused with oxygenated Krebs solution at 37 degrees C. Above a basal rate of secretion of 60 ng/30 s of total catecholamines, 5 s pulses of 100 microM-methacholine evoked 10-fold increases of secretion. This response was entirely mediated by muscarinic receptors, since it was blocked by submicromolar concentrations of atropine but not by d-tubocurarine. 2. Delayed application of methacholine pulses after Ca2+ removal from the Krebs solution led to a progressive decline of the secretory response with a t1/2 of 15 s. Secretion was blocked by 85% after a 60 s period of Ca2+ deprivation; extension of the external Ca2+ (Ca2+o) wash-out period up to 5 min did not further reduce the secretory response. 3. When EGTA (1 mM) was present in the 0 Ca2+ solution, the rate of decline of methacholine responses, as a function of the time of exposure to 1 mM-EGTA, was similar to that obtained with 0 Ca2+. Again, about 15-20% of the secretory response was resistant even to prolonged periods of washing out with the 0 Ca(2+)-EGTA solution. 4. The Ca2+ ionophore ionomycin (1 microM) first decreased and then accelerated the rate of decline of methacholine responses upon Ca2+o wash-out. Particularly relevant is the complete blockade of secretion when the Ca2+o wash-out is performed in the presence of this ionophore. This suggests the existence of a small intracellular functional Ca2+ store sensitive to ionomycin. 5. After abolition of the secretory response through 60 s periods of wash-out with a 0 Ca(2+)-EGTA-ionomycin solution, followed by delayed 5 s methacholine pulses after Ca2+o reintroduction, the glands instantly recovered their normal muscarinic-mediated secretory response. This suggests that upon muscarinic stimulation, Ca2+ required by the secretory machinery to trigger such response immediately comes from extracellular sources. How Ca2+o gains the cell interior so fast upon muscarinic stimulation is unknown; we have previously suggested that the muscarinic receptor in the cat chromaffin cell could be coupled to an ionophore channel which might be chemically activated by muscarinic agonists. 6. Secretory responses to 5 s pulses with 35 or 100 mM-K+ declined faster (t1/2 of 3 and 6 s, respectively) upon Ca2+o wash-out than those of methacholine.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1992

Ca(2+)-activated K+ channels modulate muscarinic secretion in cat chromaffin cells.

1. This study was aimed at testing the hypothesis that Ca(2+)-dependent K+ channels regulate the release of catecholamines mediated by muscarinic stimulation of cat adrenal chromaffin cells. Two parameters were measured: the secretory response to brief pulses of methacholine (100 microM for 10 s) in intact cat adrenal glands perfused at a high rate with oxygenated Krebs solution; and the changes in cytosolic Ca2+ concentrations, [Ca2+]i, produced by puff applications of methacholine pulses (also 100 microM for 10 s) in isolated single cat adrenal chromaffin cells loaded with Fura-2. 2. A pulse of methacholine released 805 +/- 164 ng of catecholamines (mean of thirty-two pulses). d-Tubocurarine (DTC) increased the secretory response in a concentration-dependent manner. The maximum increase (around 1000 ng catecholamines over control values) was reached at 100 microM-DTC and the EC50 was around 10 microM. 3. The secretory responses to methacholine alone, or to the combination of methacholine plus DTC, were strongly dependent on the extracellular Ca2+ concentration, [Ca2+]o. Thus Ca2+o removal from the perfusing solution for 5-10 min abolished catecholamine release. 4. At 0.1 microM, isradipine (an L-type Ca2+ channel blocker) inhibited by 71% the secretory response to DTC plus methacholine. At 1 microM, Bay K 8644 (an L-type Ca2+ channel activator) increased 2-fold the secretory response to DTC plus methacholine (2746 ng of catecholamines). 5. Apamin (1 microM) increased 3.5-fold the secretory response to methacholine pulses (from 500 to 1800 ng of catecholamines). 6. Methacholine pulses enhanced [Ca2+]i from the resting level of 100 nM to a peak of 1000 nM which quickly declined to basal level. DTC (100 microM) enhanced by 20% the [Ca2+]i peak and substantially prolonged its duration. 7. Apamin (1 microM) increased by 60% the [Ca2+]i peak evoked by methacholine, and delayed the initiation of decline of the [Ca2+]i peak. 8. These results are compatible with the idea that muscarinic stimulation depolarizes the cat adrenal chromaffin cell through an unidentified mechanism. Depolarization is probably counteracted by activation of Ca2+i-dependent K+ channels. Therefore, inhibition of these channels enhances depolarization and firing of action potentials which activate voltage-dependent L-type Ca2+ channels to increase further the Ca2+i signal and the secretory response. Thus Ca2+i-dependent K+ channels, probably of the small-conductance type (SK), seem to be involved in the modulation of muscarinic-evoked catecholamine release responses in cat adrenal chromaffin cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗