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A de Mendonça

Publications and source records attributed to A de Mendonça.

At least 19 recordsLinked to original sources
PubMed2006

Does caffeine modify corticomotor excitability?

AIMS: To test the influence of caffeine on the lower and upper motor neuron excitability. METHODS: In Experiment A, 18 healthy subjects received 200 mg of caffeine or placebo, in a randomized, double-blind, placebo-controlled design protocol. Mean F-waves amplitude, amplitude of the motor response evoked by magnetic stimulation (MEP), MEP duration, cortical silent period (CSP), central conduction time, and cortical threshold were evaluated. In Experiment B, 6 healthy controls received 400 mg of caffeine, the peripheral silent period (PSP) and CSP were evaluated. CSP was recorded bilaterally in biceps brachii (intensity 10% above threshold) and abductor digiti minimi (ADM) (intensity at 10% and 50% above threshold). Muscle contraction was above 50% of the maximum force in both experiments. Latencies were defined by a technician who was not aware of this investigation. Serum caffeine level was evaluated. RESULTS: In Experiment A, only the CSP, recorded in both ADM with intensity at 10% above threshold showed a significant change after caffeine (decrease of 17.1+/-34.0 ms, about 12% reduction). In Experiment B, PSP did not change, but CSP tested with intensities 10% above threshold was significantly decreased by 20.8+/-34.4 ms in ADM and 13.5+/-13.8 ms in biceps (about 13 and 16%, respectively). Serum caffeine level clearly increased after consumption but no correlation could be found between these levels and CSP reduction. CONCLUSIONS: In our investigation, caffeine elicited a consistent decrease of the CSP, suggesting that caffeine increases cortical neuronal excitability.

Adult↗
PubMed2006

Mild cognitive impairment: deficits in cognitive domains other than memory.

Patients with mild cognitive impairment (MCI) typically present with memory complaints, but may have mild deficits in other cognitive domains. We compared the neuropsychological profiles of a series of consecutive MCI patients (n = 116) with a control group of healthy elderly subjects (n = 63). The presence of a memory deficit on delayed recall was consistent in the MCI sample, as it was an inclusion criterion in the study. Impairment on immediate recall was present in 62.6% of the patients on paragraph recall of the logical memory test and in 63.1% of the patients on the word paired-associate learning test. Remarkably, patients with MCI frequently had deficits in cognitive domains beyond memory. As much as 68.7% of the patients had deficits in temporal orientation, 30.2% had deficits in semantic fluency, 33.7% in the Token test, 23.4% in calculation, and 23.9% in motor initiative. If detailed neuropsychological testing is performed, the majority of MCI patients will have deficits in cognitive domains other than memory.

Aged↗
PubMed2006

Hypoxia-induced desensitization and internalization of adenosine A1 receptors in the rat hippocampus.

Activation of A1 adenosine receptors is important for both the neuromodulatory and neuroprotective effects of adenosine. However, short periods of global ischemia decrease A1 adenosine receptor density in the brain and it is not known if a parallel loss of functional efficiency of A1 adenosine receptors occurs. We now tested if hypoxia leads to changes in the density and efficiency of A1 adenosine receptors to inhibit excitatory synaptic transmission in rat hippocampal slices. In control conditions, the adenosine analog 2-chloroadenosine, inhibited field excitatory post-synaptic potentials with an EC50 of 0.23 microM. After hypoxia (95% N2 and 5% CO2, for 60 min) and reoxygenation (30 min), the EC50 increased to 0.73 microM. This EC50 shift was prevented by the presence of the A1 adenosine receptor antagonist 8-phenyltheophyline, but not by the A(2A)R antagonist 7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c] pyrimidine, during the hypoxic period. This decreased efficiency of A1 adenosine receptors was not paralleled by a global change of A1 adenosine receptor density or affinity (as evaluated by the binding parameters obtained in nerve terminal membranes). However, the density of biotinylated A1 adenosine receptors at the plasma membrane of nerve terminals was reduced by 30% upon hypoxia/reoxygenation, in a manner prevented by the A1 adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine and mimicked by prolonged (60 min) supra-maximal activation of A1 adenosine receptors with 2-chloroadenosine (10 microM). These results indicate that hypoxia leads to a rapid (<90 min) homologous desensitization of A1 adenosine receptor-mediated inhibition of synaptic transmission that is likely due to an internalization of A1 adenosine receptors in nerve terminals.

2-Chloroadenosine↗
PubMed2005

Clinical significance of subcortical vascular disease in patients with mild cognitive impairment.

Patients with mild cognitive impairment (MCI) typically present with memory complaints. Some of these patients have subcortical vascular disease on computed tomography (CT) scan, namely white matter changes and lacunar infarcts, however it is not known whether these findings are associated with more pronounced cognitive deficits. In the present study we compare demographic, clinical and neuropsychological characteristics of MCI patients according to the presence or the absence of subcortical vascular disease. Forty consecutive patients with memory complaints, at least one neuropsychological memory test below 1 SD the normal for age and education, and maintained activities of daily living, were included. Patients with dementia, history of stroke or transient ischemic attack, or other brain disorders, were excluded. Twenty-five (62.5%) patients with MCI had no ischemic lesions on CT scan, and 15 (37.5%) were found to have subcortical vascular changes. MCI patients with subcortical vascular changes were older (77.1 +/- 6.8 vs. 70.8 +/- 7.5 years old), and more often males. The number of vascular risk factors, the frequency of neurological signs, the Hachinski score and the neuropsychological tests scores were not significantly different. The presence of subcortical vascular disease on CT scan is frequent in older patients with MCI, but does not appear to be associated with the severity of cognitive deficits.

Aged↗
PubMed2003

Purinergic P2 receptors trigger adenosine release leading to adenosine A2A receptor activation and facilitation of long-term potentiation in rat hippocampal slices.

Electrophysiological recordings were used to investigate the effects of ATP analogues on theta-burst-induced long-term potentiation (LTP) in rat hippocampal slices. alpha,beta-Methylene ATP (alpha,beta-MeATP; 20 microM) decreased LTP from 36+/-9% to 17+/-5%, an effect prevented by adenosine A(1) receptor blockade in accordance with the localised catabolism of ATP analogues into adenosine, leading to adenosine A(1) receptor activation. Thus, to probe the role of extracellular ATP, all experiments were performed with the A(1) receptor selective antagonist, 1,3-dipropyl-8-cyclopentylxanthine (50 nM). In these conditions, alpha,beta-MeATP or 5'-adenylylimido-diphosphate (beta,gamma-ImATP; 20 microM) facilitated LTP by 120%, an effect prevented by the P2 receptor antagonists, pyridoxalphosphate-6-azophenyl-2'-4'-disulphonic acid (PPADS; 20 microM) or suramin (75 microM), as well as by the P2X(1/3)-selective antagonist 8-(benzamido)naphthalene-1,3,5-trisulfonate (10 microM). The facilitations of LTP by either alpha,beta-MeATP or beta,gamma-ImATP (20 microM) were also prevented by both 4-(2-[7-amino-2-(2-furyl(1,2,4)-triazolo(2,3a)-(1,3,5)triazin-5-yl-amino]ethyl)phenol (50 nM) or 7-2(-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c] pyrimidine (50 nM), antagonists of facilitatory adenosine A(2A) receptors, were occluded by the A(2A) receptor agonist, CGS 21680 (10 nM) and were prevented by the protein kinase C inhibitor, chelerythrine (6 microM) and unaffected by the protein kinase A inhibitor, H89 (1 microM). Furthermore, beta,gamma-ImATP (20 microM) enhanced [(3)H]adenosine outflow from rat hippocampal slices by nearly 150%, an effect prevented by PPADS (20 microM) or suramin (75 microM). The adenosine transport inhibitors, nitrobenzylthioinosine (5 microM) and dipyridamole (10 microM) also prevented beta,gamma-ImATP (20 microM)-induced [(3)H]adenosine outflow and facilitation of LTP. These results suggest that ATP analogues facilitate LTP through P2 receptor activation that mainly triggers adenosine release leading to the activation of adenosine A(2A) receptors.

Adenosine↗
PubMed2002

Adenosine receptors in the nervous system: pathophysiological implications.

Adenosine is a ubiquitous homeostatic substance released from most cells, including neurones and glia. Once in the extracellular space, adenosine modifies cell functioning by operating G-protein-coupled receptors (GPCR; A(1), A(2A), A(2B), A(3)) that can inhibit (A(1)) or enhance (A(2)) neuronal communication. Interactions between adenosine receptors and other G-protein-coupled receptors, ionotropic receptors and receptors for neurotrophins also occur, and this might contribute to a fine-tuning of neuronal function. Manipulations of adenosine receptors influence sleep and arousal, cognition and memory, neuronal damage and degeneration, as well as neuronal maturation. These actions might have therapeutic implications for neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, as well as for other neurological situations such as epilepsy, idiopathic pain or even drug addition. Peripheral side effects associated with adenosine receptor agonists limit their usefulness in therapeutics; in contrast, adenosine receptor antagonists appear to have less side effects as it is the case of the well-known non-selective antagonists theophylline (present in tea) or caffeine (abundant in coffee and tea), and their emerging beneficial actions in Parkinson's disease and Alzheimer's disease are encouraging. A(1) receptor antagonism may also be useful to enhance cognition and facilitate arousal, as well as in the periphery when deficits of neurotransmitter release occur (e.g. myasthenic syndromes). Enhancement of extracellular adenosine levels through drugs that influence its metabolism might prove useful approaches in situations such as neuropathic pain, where enhanced activation of inhibitory adenosine A(1) receptors is beneficial. One might then consider adenosine as a fine-tuning modulator of neuronal activity, which via subtle effects causes harmonic actions on neuronal activity. Whenever this homeostasis is disrupted, pathology may be installed and selective receptor antagonism or agonism required.

Adenosine↗
PubMed2002

Does caffeine intake protect from Alzheimer's disease?

Caffeine is the most widely consumed behaviourally active substance in the western world. Neuroprotective effects of caffeine in low doses, chronically administered, have been shown in different experimental models. If caffeine intake could protect against neurodegeneration in Alzheimer's disease (AD), then higher levels of caffeine consumption in normal subjects as compared with AD patients should be detectable in the presumably long period before diagnosis when insidious pathogenic changes are taking place. A case-control study was used: cases were 54 patients with probable AD fulfilling the National Institute of Neurologic and Communicative Disorders and Stroke and the AD and Related Disorders Association criteria, in a Dementia Clinics setting. Controls were 54 accompanying persons, cognitively normal, matched for age (+/-3 years) and sex. Patients with AD had an average daily caffeine intake of 73.9 +/- 97.9 mg during the 20 years that preceded diagnosis of AD, whereas the controls had an average daily caffeine intake of 198.7 +/- 135.7 mg during the corresponding 20 years of their lifetimes (P < 0.001, Wilcoxon signed ranks test). Using a logistic regression model, caffeine exposure during this period was found to be significantly inversely associated with AD (odds ratio=0.40, 95% confidence interval=0.25-0.67), whereas hypertension, diabetes, stroke, head trauma, smoking habits, alcohol consumption, non-steroid anti-inflammatory drugs, vitamin E, gastric disorders, heart disease, education and family history of dementia were not statistically significantly associated with AD. Caffeine intake was associated with a significantly lower risk for AD, independently of other possible confounding variables. These results, if confirmed with future prospective studies, may have a major impact on the prevention of AD.

Aged↗
PubMed2001

A functional role for adenosine A3 receptors: modulation of synaptic plasticity in the rat hippocampus.

Adenosine modulates hippocampal synaptic plasticity, namely long-term potentiation (LTP) and long-term depression (LTD), through activation of A1 and A2A receptors. We now report a novel role for the recently described adenosine A3 receptor in the regulation of synaptic plasticity in the CA1 area of hippocampal slices. Activation of adenosine A3 receptors by (1-[2-chloro-6-[[(3-iodophenyl)methyl]amino]-9H-purin-p-yl]-1-deoxy-N-methyl-beta-D-ribofuranuronamide (Cl-IBMECA) (100 nM) increased the magnitude of theta-burst induced LTP (from 1.2+/-0.6% in the control solution to 25.5+/-0.8% in the presence of Cl-IBMECA) and attenuated LTD (from 30.0+/-5.5% decrease in the control solution to 13.6+/-6.6% decrease in the presence of Cl-IBMECA). The selective adenosine A3 receptor antagonist, MRS 1191 (5-10 microM), prevented the effects of Cl-IBMECA. These findings indicate a functional role for adenosine A3 receptors in the modulation of synaptic plasticity.

Adenosine↗
PubMed2000

Long-term potentiation observed upon blockade of adenosine A1 receptors in rat hippocampus is N-methyl-D-aspartate receptor-dependent.

Endogenous adenosine, acting upon A(1) receptors, attenuates long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission in hippocampal slices. Adenosine might exert these effects by inhibiting the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor. Theta burst-induced LTP was larger in the presence of the selective adenosine A(1) receptor antagonist, 1, 3-dipropyl-8-cyclopentylxanthine (DPCPX, 50nM, 40.5+/-6.6% increase in fEPSP) than in the control solution (18.2+/-4.7% increase), and was completely prevented in the presence of DPCPX (50nM) plus the selective NMDA receptor antagonist, DL-2-amino-5-phosphonopentanoate (AP5, 50microM, -3.3+/-7.0% change). In contrast, LTD was induced by low-frequency stimulation in the presence of DPCPX (50nM), even in experiments performed in AP5 (50microM). Thus LTP, but not LTD, observed upon blockade of adenosine A(1) receptors is dependent upon NMDA receptor activation.

2-Amino-5-phosphonovalerate↗
PubMed2000

Presynaptic inhibitory receptors mediate the depression of synaptic transmission upon hypoxia in rat hippocampal slices.

Hypoxia markedly depresses synaptic transmission in hippocampal slices of the rat. This depression is attributed to presynaptic inhibition of glutamate release and is largely mediated by adenosine released during hypoxia acting through presynaptic adenosine A(1) receptors. Paired pulse facilitation studies allowed us to confirm the presynaptic nature of the depression of synaptic transmission during hypoxia. We tested the hypothesis that activation of heterosynaptic inhibitory receptors localized in glutamatergic presynaptic terminals in the hippocampus, namely gamma-aminobutyric acid subtype B (GABA(B)) receptors, alpha(2)-adrenergic receptors, and muscarinic receptors might contribute to the hypoxia-induced depression of synaptic transmission. Field excitatory postsynaptic potentials were recorded in the CA1 area of hippocampal slices from young adult (5-6 weeks) Wistar rats. Neither the selective antagonist for alpha(2)-adrenergic receptors, rauwolscine (10 microM), nor the antagonist for the GABA(B) receptors, CGP 55845 (10 microM), modified the response to hypoxia. The selective adenosine A(1) receptor antagonist, DPCPX (50 nM), reduced the hypoxia-induced depression of synaptic transmission to 59.2+/-9.6%, and the muscarinic receptor antagonist, atropine (10 microM), in the presence of DPCPX (50 nM), further attenuated the depression of synaptic transmission to 49.4+/-8.0%. In the same experimental conditions, in the presence of DPCPX (50 nM), the muscarinic M(2) receptor antagonist AF-DX 116 (10 microM), but not the M(1) receptor antagonist pirenzepine (1 microM), also attenuated the hypoxia-induced depression to 41.6+/-6.6%. Activation of muscarinic M(2) receptors contributes to the depression of synaptic transmission upon hypoxia. This effect should assume particular relevance during prolonged periods of hypoxia when other mechanisms may become less efficient.

Animals↗
PubMed2000

Acute renal failure in the ICU: risk factors and outcome evaluated by the SOFA score.

OBJECTIVES: To describe risk factors for the development of acute renal failure (ARF) in a population of intensive care unit (ICU) patients, and the association of ARF with multiple organ failure (MOF) and outcome using the sequential organ failure assessment (SOFA) score. DESIGN: Prospective, multicenter, observational cohort analysis. SETTING: Forty ICUs in 16 countries. PATIENTS: All patients admitted to one of the participating ICUs in May 1995, except those who stayed in the ICU for less than 48 h after uncomplicated surgery, were included. After the exclusion of 38 patients with a history of chronic renal failure requiring renal replacement therapy, a total of 1411 patients were studied. MEASUREMENTS AND RESULTS: Of the patients, 348 (24.7%) developed ARF, as diagnosed by a serum creatinine of 300 micromol/l (3.5 mg/dl) or more and/or a urine output of less than 500 ml/day. The most important risk factors for the development of ARF present on admission were acute circulatory or respiratory failure; age more than 65 years, presence of infection, past history of chronic heart failure (CHF), lymphoma or leukemia, or cirrhosis. ARF patients developed MOF earlier than non-ARF patients (median 24 vs 48 h after ICU admission, p < 0.05). ARF patients older than 65 years with a past history of CHF or with any organ failure on admission were most likely to develop MOF. ICU mortality was 3 times higher in ARF than in other patients (42.8% vs 14.0%, p < 0.01). Oliguric ARF was an independent risk factor for overall mortality as determined by a multivariate regression analysis (OR = 1.59 [CI 95%: 1.23-2.06], p < 0.01). Infection increased the risk of death associated with all factors. Factors that increased the ICU mortality of ARF patients were a past history of hematologic malignancy, age more than 65 years, the number of failing organs on admission and the presence of acute cardiovascular failure. CONCLUSION: In ICU patients, the most important risk factors for ARF or mortality from ARF are often present on admission. During the ICU stay, other organ failures (especially cardiovascular) are important risk factors. Oliguric ARF was an independent risk factor for ICU mortality, and infection increased the contribution to mortality by other factors. The severity of circulatory shock was the most important factor influencing outcome in ARF patients.

Acute Kidney Injury↗
PubMed2000

Adenosine: does it have a neuroprotective role after all?

A neuroprotective role for adenosine is commonly assumed. Recent studies revealed that adenosine may unexpectedly, under certain circumstances, have the opposite effects contributing to neuronal damage and death. The basis for this duality may be the activation of distinct subtypes of adenosine receptors, interactions between these receptors, differential actions on neuronal and glial cells, and various time frames of adenosinergic compounds administration. If these aspects are understood, adenosine should remain an interesting target for therapeutical neuroprotective approaches after all.

Adenosine↗
PubMed2000

Modification of adenosine modulation of synaptic transmission in the hippocampus of aged rats.

We compared the modulation of synaptic transmission by adenosine A(1) receptors in the hippocampus of aged (24 months) and young adult rats (6 weeks). The adenosine A(1) receptor agonist, N(6)-cyclopentyladenosine, was less potent (P:<0.05) to inhibit synaptic transmission in aged (EC(50)=53 nM) than young adult (EC(50)=14 nM) hippocampal slices, these effects being prevented by the A(1) receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). In contrast with the lower effect of the A(1) receptor agonist, it was observed that blockade of A(1) receptors with DPCPX (50 nM), or removal of endogenous extracellular adenosine with adenosine deaminase (2 u ml(-1)), caused a more pronounced disinhibition of synaptic transmission in aged rats. Also consistent with a more intense A(1) receptor-mediated inhibitory tonus by endogenous adenosine in aged rats was the finding that to fully prevent the depression of synaptic transmission induced by 3 min hypoxia, a higher concentration of DPCPX was required in slices from aged (100 nM) than from young (50 nM) rats. It is concluded that in hippocampal slices of aged rats the efficiency of A(1) receptors to modulate synaptic transmission is reduced, but this may be compensated by an enhanced inhibitory tonus by endogenous adenosine.

Adenosine↗
PubMed1999

Adenosine modulates synaptic plasticity in hippocampal slices from aged rats.

Adenosine is known to modulate synaptic plasticity in the hippocampus of young animals through activation of adenosine A1 receptors. The objective of the present study is to investigate whether the modulatory role of adenosine on phenomena of synaptic plasticity is maintained or modified in the hippocampus of aged animals. We compared the effects of the selective adenosine A1 receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 50 nM), on paired-pulse facilitation (PPF), long-term depression (LTD), long-term potentiation (LTP) and depotentiation elicited in hippocampal slices taken from young adult (5-6 weeks) and old (2 years old) male Wistar rats. DPCPX attenuated PPF both in young (1.64 +/- 0.05 vs. 1.76 +/- 0.05%, n = 6) and in old rats (1.33 +/- 0.05 vs. 1.55 +/- 0.1%, n = 6). LTD was only observed in the presence of DPCPX in both young (21.3 +/- 0.6%, n = 4) and old rats (14.4 +/- 0.9%, n = 6). LTP induced by high-frequency stimulation (HFS) was not significantly different in young and old animals, in the presence or in the absence of DPCPX. A larger depotentiation was observed in the presence of DPCPX in young rats (27.6 +/- 4.4% vs. 16.8 +/- 4.7%, n = 7) as well as in old rats (41.3 +/- 5.1% vs. 16.1 +/- 2.7%, n = 6). LTP induced by theta-burst stimulation was observed only in the presence of DPCPX (53.9 +/- 4.9%, n = 5) in young rats, but could be obtained either in the control solution (81.8 +/- 17.9%, n = 7) or in the presence of DPCPX (98.5 +/- 24.2%, n = 7) in old rats. The modulatory role of endogenous adenosine on synaptic plasticity is generally maintained in aged animals. Drugs interfering with adenosine A1 receptor effects could then be used in old animals to modify synaptic plasticity with relevant behavioural consequences.

Adenosine↗
PubMed1999

N-acetyltransferase (NAT2) genotype and susceptibility of sporadic Alzheimer's disease.

The importance of environmental aggression and individual susceptibility to develop Alzheimer's Disease (AD) has been suggested by epidemiological studies on both typical familial and sporadic AD cases. In order to elucidate functions that can influence the susceptibility to AD pathogenesis, we genotyped a group of 53 sporadic late-onset AD patients, matched control individuals and a larger randomly selected non-demented population for the N-acetyltransferase (NAT2). We determined the relative frequencies of individual allele combinations that define a broad range of acetylator phenotypes. Inter-individual variability in the cytotoxic and genotoxic responses to a wide diversity of environmental chemicals is known to result from the polymorphism of NAT2 as well as other drug-metabolizing-enzyme genes. The results presented are the first to demonstrate a significant difference in the NAT2 genotype profiles of sporadic AD patients compared with the healthy population. A lower frequency of the recessive alleles NAT2*6 (chi-squared 1 d.f. = 12.56, P < 0.0004) and NAT2*5B (chi-squared 1 d.f. = 6.72, P < 0.01) was found among the AD population compared with control individuals, which was concomitant with a significantly higher number of NAT2*4 fully active allele homozygotes and heterozygotes (chi-squared 1 d.f. = 5.69, P = 0.017). The most notable observation was the absence of NAT2*5B/NAT2*6 heterozygotes among cases while being present in 22.5% of control individuals (chi-squared 1 d.f. = 13.08, P = 0.0003). These observations indicate that NAT2 is a potential low-penetrance gene in AD pathogenesis, determining an individual susceptibility trait predisposing to this degenerative disease.

Alzheimer Disease↗
PubMed1998

Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Working group on "sepsis-related problems" of the European Society of Intensive Care Medicine.

OBJECTIVE: To evaluate the use of the Sequential Organ Failure Assessment (SOFA) score in assessing the incidence and severity of organ dysfunction in critically ill patients. DESIGN: Prospective, multicenter study. SETTING: Forty intensive care units (ICUs) in 16 countries. PATIENTS: Patients admitted to the ICU in May 1995 (n = 1,449), excluding patients who underwent uncomplicated elective surgery with an ICU length of stay <48 hrs. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The main outcome measures included incidence of dysfunction/failure of different organs and the relationship of this dysfunction with outcome. In this cohort of patients, the median length of ICU stay was 5 days, and the ICU mortality rate was 22%. Multiple organ dysfunction and high SOFA scores for any individual organ were associated with increased mortality. The presence of infection on admission (28.7% of patients) was associated with higher SOFA scores for each organ. The evaluation of a subgroup of 544 patients who stayed in the ICU for at least 1 wk showed that survivors and nonsurvivors followed a different course. This subgroup had greater respiratory, cardiovascular, and neurologic scores than the other patients. In this subgroup, the total SOFA score increased in 44% of the nonsurvivors but in only 20% of the survivors (p < .001). Conversely, the total SOFA score decreased in 33% of the survivors compared with 21% of the nonsurvivors (p < .001). CONCLUSIONS: The SOFA score is a simple, but effective method to describe organ dysfunction/failure in critically ill patients. Regular, repeated scoring enables patient condition and disease development to be monitored and better understood. The SOFA score may enable comparison between patients that would benefit clinical trials.

Adult↗
PubMed1997

Contribution of metabotropic glutamate receptors to the depression of excitatory postsynaptic potentials during hypoxia.

We tested the hypothesis that activation of metabotropic glutamate receptors (mGluR) might contribute to the depression of excitatory postsynaptic potentials during hypoxia. The experiments were performed on hippocampal slices taken from young (12-14 days old) Wistar rats. The depression induced by hypoxia (14 min) was not modified in the presence of either the non-selective mGluR antagonist (which blocks mainly group I and II mGluR), MCPG (500 microM) or the selective group III mGluR antagonist, MPPG (500 microM). However, in experiments performed in the presence of the selective adenosine A1 receptor antagonist, DPCPX (50 nM), part of the hypoxia-induced depression could be prevented by MPPG (500 microM). Activation of group III mGluR may contribute to the hypoxia-induced depression, but this contribution is only revealed when adenosine A1 receptors are blocked.

Alanine↗