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Biomedical subjects

P Kara

Publications and source records attributed to P Kara.

6 recordsLinked to original sources
PubMed2005

A randomized clinical trial of magnesium sulphate as a vehicle for nebulized salbutamol in the treatment of moderate to severe asthma attacks.

Although it is well known that intravenous administration of MgSO4 as an adjunct to conventional therapy is effective in treating asthma attacks, the effect of nebulized MgSO4 as a vehicle for salbutamol has been less evaluated. The aim of this study was to compare the effects of nebulized salbutamol administrated through either MgSO4 or isotonic saline solution on the 'peak expiratory flow rate' (PEFR), other respiratory and clinical parameters, and hospitalization rate of patients suffering from moderate to severe asthma attacks. Twenty-six patients with asthma attack were enrolled in the study in a randomized single blind fashion. After obtaining initial peak expiratory flow measurements (PEFR) and clinical evaluation, all patients received 1mg/kg corticosteroids and oxygen therapy and then either isotonic MgSO4 (2.5 ml, 6.3%)+salbutamol (2.5 ml) or saline (2.5 ml)+salbutamol (2.5 ml) through a jet nebulizer (group 1 (n=14) vs group 2 (n=12), respectively). The nebulizations were repeated every 20 min for the first hour and every hour for the rest of 4 h. The PEFR measurements and clinical assessment were performed after nebulization at 20th, 60th, 120th, 180th and 240th minutes. Patients were discharged when PEFR reached the target level of 70% of predicted. The baseline PEFRs and clinical parameters were similar between groups 1 and 2 (50.2+/-18.5 vs 44.1+/-13.9, respectively, p>0.05). The mean% increase in PEFR at different measurement levels was similar between the groups. When the treatment response was evaluated within the groups, group 2 showed statistically significant increase in PEFR (% of predicted) 1h earlier than group 1 (60th vs 120th minute, p=0.003 vs p=0.007). The mean duration of achieving target-PEFRs was 105.7+/-72.1 min for group 1 and 118.3+/-96.7 min for group 2 (p>0.05). This study suggested that the additional usage of MgSO4 to nebulized salbutamol has no beneficial effect on the treatment of asthma attacks.

Adolescent↗
PubMed2000

Low response variability in simultaneously recorded retinal, thalamic, and cortical neurons.

The response of a cortical cell to a repeated stimulus can be highly variable from one trial to the next. Much lower variability has been reported of retinal cells. We recorded visual responses simultaneously from three successive stages of the cat visual system: retinal ganglion cells (RGCs), thalamic (LGN) relay cells, and simple cells in layer 4 of primary visual cortex. Spike count variability was lower than that of a Poisson process at all three stages but increased at each stage. Absolute and relative refractory periods largely accounted for the reliability at all three stages. Our results show that cortical responses can be more reliable than previously thought. The differences in reliability in retina, LGN, and cortex can be explained by (1) decreasing firing rates and (2) decreasing absolute and relative refractory periods.

Action Potentials↗
PubMed1999

Arginine analogs modify signal detection by neurons in the visual cortex.

Nitric oxide (NO) modulates neurotransmitter release, induction of long-term synaptic potentiation and depression, and activity levels of neurons. However, it is not known whether NO contributes to the ability of the CNS to distinguish sensory signals from background noise and/or extract sensory information with greater reliability. We addressed these questions in the visual cortex, in vivo, using electrophysiological recording and analysis of signal detection from individual neurons. This was combined with microiontophoretic application of arginine analogs that either upregulate or downregulate the brain's endogenous NO-generating pathways or compounds that produce exogenous NO. Protocols that enhance NO levels generally increased the number of action potentials per trial evoked by visual stimuli, improved signal detection, and decreased the coefficient of variation of visually evoked responses, whereas NO-reducing protocols predominantly had complementary effects. Control experiments demonstrate that these effects are likely attributable to the specific ability of these arginine compounds to modify NO levels versus other nonspecific effects. Differential effects between neighboring cells and between single-cell receptive subfields suggest that these actions have a significant direct neural component versus exclusively operating indirectly on neurons through the central vascular actions of NO.

Action Potentials↗
PubMed1998

Dynamic modulation of cerebral cortex synaptic function by nitric oxide.

Our experiments demonstrate that NO exerts several actions in the cerebral cortex (see Fig. 4). Its production is mediated by neuronal activity through at least two pathways, NMDA receptors and AMPA receptors. By virtue of its diffusion in extracellular space, NO can interact with synapses that are near the production site but not necessarily anatomically connected to the NO source by a conventional synaptic linkage. NO's primary action is amplification of the release of the excitatory neurotransmitter, L-glutamate, thus effectively creating a positive feed-forward gain system. However, a number of effective brakes, presumably activated under physiological conditions, serve to limit the cascade. These include NO's ability to inhibit NMDA receptors, its negative feedback on the rate limiting enzyme, NOS (Rengasamy and Johns, 1993; Park et al., 1994; Ravichandran et al., 1995) and other inhibitory actions (Figs. 3H and L). Under conditions of extremely strong activation or curtailment of the inhibitory feedback mechanisms, as might occur with a change in the local redox milieu (see Lipton, this volume), the amplification cascade may proceed unchecked leading to neurotoxicity (see Dawson, this volume). NO's ability to modulate synaptic function is indicated by both its positive and negative modulatory role in a form of activity-dependent synaptic plasticity, covariance-induced synaptic potentiation. These opposing effects may be due to NO's ability to amplify glutamate release and inhibit NMDA receptors, respectively. The actions of endogenous NO in vivo are primarily facilitatory in visual cortex (Fig. 4). However, inhibitory actions also occur in vivo. The targets for NO in vivo, are potentially more diverse including the neurotransmitter release process, NMDA receptors, other receptors and ion channels and the cerebral vasculature. However, regardless of the signaling pathways, the net result of endogenous NO production in the intact visual cortex is a potent modulation of cells' responses to visual stimulation. Thus, it is likely that this signal plays an important role in ongoing information processing in the mature cerebral cortex, dynamically altering the effective strength of cortical networks.

Animals↗
PubMed1996

Mechanisms for regulating synaptic efficiency in the visual cortex.

Brief epochs of pairing of low frequency synaptic activation and postsynaptic depolarization, in vitro, in supragranular neurons of nature guinea-pig visual cortex lead to a transient (20-60 min) synaptic potentiation. The process is due to a true up-regulation of excitatory synapse efficiency onto the activated neuron. The potentiation requires NMDA receptor activation and a postsynaptic calcium signal for induction and it is modifiable by endogenous nitric oxide (NO) production in the mature cortex. In the cortex of young animals (< PND 21), the pairing-induced potentiation is robust and depends on a postsynaptic calcium signal but it is independent of NMDA receptor activation and NO production. The ability of cortical synaptosomes to release endogenous glutamate is enhanced by NMDA receptor activation and this enhancement is NO-dependent. The NO signal, however, does not amplify the glutamate release of all synapses but only those that have activated voltage-gated calcium channels and were presumably more active at the time of the NO signal. Electrophysiological recordings from visual cortical neurons in anesthetized cats with local iontophoresis of compounds that inhibit or facilitate endogenous cortical NO production reveal the capacity for NO to modulate visual responses in vivo. NO appears to act in the intact cortex by amplifying signals of visual inputs that were co-active at the time of the NO production. The adult visual cortex is capable of dramatic alterations in synaptic efficiency over brief periods suggesting a dynamic cortical network. NMDA receptors and nitric oxide contribute to these processes.

Algorithms↗