Respiratory care units for non-invasive mechanical ventilation in motor neurone disease.
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Delivery of Health Care↗
Biomedical subjects
J Marín
Publications and source records attributed to J Marín.
Pattern formation and optimization in army ant raids.
Army ant colonies display complex foraging raid patterns involving thousands of individuals communicating through chemical trails. In this article we explore, by means of a simple search algorithm, the properties of these trails in order to test the hypothesis that their structure reflects an optimized mechanism for exploring and exploiting food resources. The raid patterns of three army ant species, Eciton hamatum, Eciton burchelli, and Eciton rapax, are analyzed. The respective diets of these species involve large but rare, small but common, and a combination of large but rare and small but common food sources. Using a model proposed by Deneubourg et al. [4], we simulate the formation of raid patterns in response to different food distributions. Our results indicate that the empirically observed raid patterns maximize return on investment, that is, the amount of food brought back to the nest per unit of energy expended, for each of the diets. Moreover, the values of the parameters that characterize the three optimal pattern-generating mechanisms are strikingly similar. Therefore the same behavioral rules at the individual level can produce optimal colony-level patterns. The evolutionary implications of these findings are discussed.
Algorithms↗
Home mechanical ventilation in amyotrophic lateral sclerosis patients is not always a problem.
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Home Care Services↗
Regulation of beta-adrenoceptor-mediated relaxation of the rat aorta is modulated by endogenous ovarian hormones.
The aim of this study was to assess the influence of the endogenous status of ovarian hormones on the relaxation induced by the beta-adrenoceptor agonists isoprenaline (isoproterenol) and dobutamine in thoracic aorta segments, precontracted with noradrenaline, from age-matched (13-week-old) virgin (oestrus) and ovariectomized (OVX) prepubertal female Wistar rats. Isoprenaline-induced relaxation was decreased in intact aortic segments from OVX rats compared with that in segments from oestrus rats. Relaxation was significantly reduced by endothelium removal, 1 micromol/l propranolol or 100 micromol/l N(G)-nitro-L-arginine methyl ester (L-NAME). The beta(1)-adrenoceptor agonist dobutamine induced less relaxation in intact arteries from oestrus rats than did isoprenaline, and dobutamine-induced relaxation was markedly less in intact segments from OVX compared with oestrus rats. This dobutamine-induced relaxation was abolished by endothelium removal, and reduced by 1 micromol/l propranolol, 100 micromol/l L-NAME or 1 micromol/l yohimbine. Cholera toxin (an activator of the stimulatory G-protein G(s)) caused relaxation in intact arteries from oestrus rats; this relaxation was decreased by both deprivation of ovarian hormones and endothelium removal. Forskolin (a direct activator of the catalytic subunit of adenylate cyclase) and sodium nitroprusside (a nitric oxide donor and cGMP-dependent vasodilator agonist) induced similar endothelium-independent relaxation in arteries from both oestrus and OVX rats. These results suggest that the relaxation elicited by endothelial beta-adrenoceptor activation in the rat thoracic aorta is impaired by deprivation of female ovarian hormones; this impairment is caused, at least in part, by decreases in both the endothelial release of NO and G(s) function.
Adrenergic beta-Agonists↗
Role of protein kinase C in electrical-stimulation-induced neuronal nitric oxide release in mesenteric arteries from hypertensive rats.
This study examines the influence of hypertension on neuronal nitric oxide (NO) release and its modulation by protein kinase C (PKC). For this purpose, mesenteric segments without endothelium were obtained from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs), and neurogenic NO release induced by electrical field stimulation (EFS) was examined in these segments. EFS induced frequency-dependent contractions. The NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) and the sensorial neurotoxin capsaicin increased EFS-induced contractions in SHR segments, but did not affect these contractions in segments from WKY rats. In segments from SHRs, the increase in EFS-induced response by capsaicin was further increased by the combination of capsaicin and L-NAME. EFS-induced contractions in SHR arteries were unaltered by the protein synthesis inhibitor cycloheximide or by 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), an inhibitor of inducible NO synthase, and increased by the guanylate cyclase inhibitor Methylene Blue. In these arteries, capsaicin plus the PKC inhibitor calphostin C increased the contractions elicited by EFS; the addition of L-NAME did not affect this increase. Phorbol 12,13-dibutyrate (PDBu) did not modify the response to EFS in these arteries pretreated with capsaicin, although a combination of PDBu and L-NAME was effective. These results indicate that, in mesenteric arteries, EFS induces the release of NO from perivascular nitrergic nerves and of neuropeptides from sensory nerves, but only in hypertensive rats. The NO released is synthesized by constitutive neuronal NO synthase in a manner that is positively modulated by PKC, an enzyme that seems to be activated in hypertension.
Animals↗
[Isolation of Scedosporium prolificans from the air in the room of a patient with leukemia and disseminated infection with this fungus].
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Air Microbiology↗
Superoxide anion and K+ channels mediate electrical stimulation-induced relaxation in the rat basilar artery.
Electrical field stimulation (a single pulse, 0.2 ms) caused a rapid relaxation of rat basilar artery segments precontracted with different agents, but not with 30 mM KCl. This relaxation was not modified by endothelium removal, 10 microM tetrodotoxin, 1 microM propranolol, 1 microM atropine, 30 microM indomethacin, 10 microM methylene blue, 100 microM N(G)-nitro-L-arginine methyl ester or 1 microM cimetidine but it was significantly reduced by 50 and 100 U/ml superoxide dismutase. Charybdotoxin (0.1 and 0.2 microM), a blocker of large-conductance Ca2+-activated K+ channels (BK(Ca)), decreased the relaxation elicited by electrical stimulation, whereas it was unaltered by 10 microM glibenclamide or 1 microM apamin, blockers of ATP-sensitive (K(ATP)) or small-conductance K(Ca) channels, respectively. Thapsigargin (0.01 and 0.1 microM), an inhibitor of sarcoplasmic reticulum Ca2+-ATPase, increased the electrical stimulation-induced relaxation, which was nearly abolished by charybdotoxin. These results show that electrical stimulation induces endothelium-independent and non-neurogenic relaxations in the rat basilar artery. This response appears to involve generation of superoxide anion, increase of cytosolic free Ca2+ concentration and subsequent activation of BK(Ca) channels.
Acetylcholine↗
Asthma visits to emergency rooms and soybean unloading in the harbors of Valencia and A Coruña, Spain.
Soybean unloading in the harbor of Barcelona, Spain, has been associated with large increases in the numbers of asthma patients treated in emergency departments between 1981 and 1987. In this study, the association between asthma and soybean unloading in two other Spanish cities, Valencia and A Coruña, was assessed. Asthma admissions were retrospectively identified for the period 1993-1995, and harbor activities were investigated in each location. Two approaches were used to assess the association between asthma and soybean unloading: One used unusual asthma days (days with an unusually high number of emergency room asthma visits) as an effect measure, and the other estimated the relative increase in the daily number of emergency room visits by autoregressive Poisson regression, adjusted for meteorologic variables, seasonality, and influenza incidence. No association between unusual asthma days and soya unloading was observed in either Valencia or A Coruña, except for one particular dock in Valencia. When the association between unloaded products and the daily number of emergency asthma visits was studied, a statistically significant association was observed for unloading of soya husk (relative risk = 1.50, 95% confidence interval 1.16-1.94) and soybeans (relative risk = 1.31, 95% confidence interval 1.08-1.59) in A Coruña. In Valencia, a statistical association was found only for the unloading of soybeans at two particular docks. Although these findings support the notion that asthma outbreaks are not a common hidden condition in most harbors where soybeans are unloaded, the weak associations reported are likely to be causal. Therefore, appropriate control measures should be implemented to avoid soybean dust emissions, particularly in harbors with populations living in the vicinity.
Air Pollutants↗
Mechanisms involved in the cellular calcium homeostasis in vascular smooth muscle: calcium pumps.
The regulation of cytosolic Ca2+ homeostasis is essential for cells, and particularly for vascular smooth muscle cells. In this regulation, there is a participation of different factors and mechanisms situated at different levels in the cell, among them Ca2+ pumps play an important role. Thus, Ca2+ pump, to extrude Ca2+; Na+/Ca2+ exchanger; and different Ca2+ channels for Ca2+ entry are placed in the plasma membrane. In addition, the inner and outer surfaces of the plasmalemma possess the ability to bind Ca2+ that can be released by different agonists. The sarcoplasmic reticulum has an active role in this Ca2+ regulation; its membrane has a Ca2+ pump that facilitates luminal Ca2+ accumulation, thus reducing the cytosolic free Ca2+ concentration. This pump can be inhibited by different agents. Physiologically, its activity is regulated by the protein phospholamban; thus, when it is in its unphosphorylated state such a Ca2+ pump is inhibited. The sarcoplasmic reticulum membrane also possesses receptors for 1,4,5-inositol trisphosphate and ryanodine, which upon activation facilitates Ca2+ release from this store. The sarcoplasmic reticulum and the plasmalemma form the superficial buffer barrier that is considered as an effective barrier for Ca2+ influx. The cytosol possesses different proteins and several inorganic compounds with a Ca2+ buffering capacity. The hypothesis of capacitative Ca2+ entry into smooth muscle across the plasma membrane after intracellular store depletion and its mechanisms of inhibition and activation is also commented.
Animals↗
Nitric oxide-dependent and -independent mechanisms in the relaxation elicited by acetylcholine in fetal rat aorta.
The aim of the present study was to analyze the mechanisms involved in the relaxation induced by 1 microM acetylcholine (ACh) in aortic segments from fetal rats at term precontracted with 3 microM prostaglandin F2alpha (PGF2alpha) and incubated with 1 microM indomethacin. The endothelium-dependent relaxation caused by ACh was reduced by the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 0.1 mM), such an effect was reversed by 0.1 mM L-arginine (L-Arg). After precontraction of segments with 50 mM KCl the relaxant response to ACh was smaller than that after precontraction with PGF2alpha; this reduction was increased by L-NMMA, whereas L-NMMA plus L-Arg potentiated the relaxation. Thiopentone sodium (0. 1 mM), ouabain (10 microM), tetraethylammonium (TEA, 0.5 mM) and apamin (1 microM), inhibitors of cytochrome P450 monooxygenases, Na+ pump, Ca2+-activated (KCa) and small-conductance (SKCa) K+ channels, respectively, reduced the relaxation to ACh, which was unaffected by charybdotoxin (0.1 microM) and glibenclamide (1 microM), inhibitors of large-conductance BKCa and ATP-sensitive K+ channels. The L-NMMA/indomethacin-resistant relaxation to ACh was markedly reduced by thiopentone sodium, and similarly decreased by either ouabain or TEA. The endothelium-independent relaxation induced by exogenous NO (10 microM) in segments precontracted with PGF2alpha was unaltered by ouabain, glibenclamide, TEA and after precontraction with 50 mM KCl, and potentiated by L-NMMA. The potentiation of NO responses by L-NMMA was also observed in segments precontracted with KCl. These results suggest that ACh relaxes the fetal rat aorta by endothelial release of both NO and endothelium-derived hyperpolarizing factor (EDHF), a metabolite derived from cytochrome P450 monooxygenases, that hyperpolarizes smooth muscle cells by activation of KCa, essentially SKCa channels, and Na+ pump. It seems that when the effect of EDHF is abolished, the formation of NO could be increased.
Acetylcholine↗
Changes in plasma oxidative state with age and their influence on contractions elicited by noradrenaline in the rat tail artery.
The present study analyzes the changes in plasma oxidative state with age and their influence on the contractions induced by noradrenaline (NA) in endothelium-denuded segments from the tail artery of 6- (young), 24- (old) and 30- (very old) month-old Sprague Dawley rats. The sensitivity (-log EC50) to NA increased with age, this increase being higher in old than in very old animals. Moreover, the maximum response (Emax) to NA did not change in old rats, whereas decreased in very old animals. We also found a progressive increase in the plasma oxidative state with age, measured as malondialdehyde (MDA) levels, that was accompanied by a decrease in the plasma antioxidative state, measured as glutathione peroxidase activity. In addition, MDA (0.5, 1 and 10 microM) potentiated the NA responses in 6-, 24- and 30-month-old rats, respectively, without affecting Emax. In young animals, catalase (1000 U/ml) or dimethylsulfoxide (7 mM), scavengers of hydrogen peroxide or hydroxyl radicals, respectively, did not modify either the contractions induced by NA in control situation or the potentiation of these responses caused by MDA. However, the superoxide anion scavenger, superoxide dismutase (SOD, 150 U/ml), completely reversed the increase in sensitivity to NA caused by MDA, without affecting NA responses in control situation. These results suggest that the increase in NA sensitivity with age could be due, at least in part, to the enhancement of plasma oxidative state during aging. In addition, in this alteration of the responses to NA caused by MDA, the generation of superoxide anions appears to be involved. This study supports the hypothesis that the enhancement of plasma oxidative state could play an important role in the increase of vascular resistance with age.
Aging↗
Vascular sodium pump: endothelial modulation and alterations in some pathological processes and aging.
The vascular Na+ pump maintains intracellular ionic concentration and controls membrane potential. Its inhibition by cardiac glycosides enhances the intracellular Na+ concentration. This in turn activates the Na+-Ca2+ exchange mechanism, which induces intracellular Ca2+ increase, membrane depolarization, and noradrenaline release from perivascular adrenergic nerve endings; mechanisms that promote vasoconstriction. This article reviews the relevance of the Na+ pump in vascular tone regulation and the modulation of its activity by the endothelium. The endothelium negatively modulates the vasoconstriction elicited by Na+ pump inhibition by the release of nitric oxide, according to some authors, or an unknown factor, as suggested by others. The possible existence of endogenous digitalis-like factors is also reviewed, as is the involvement of the vascular Na+ pump in some cardiovascular disorders and aging.
Aging↗
[Acute respiratory insufficiency as initial manifestation of brain stem lesions].
We describe three patients with different brainstem lesions (bulbar angioma, bulbar infarct, and Arnold-Chiari malformation) who debuted with acute respiratory insufficiency. Other neurological manifestations had gone unobserved in all three cases. Respiratory insufficiency worsened notably during sleep to the point that mechanical ventilation was required or death occurred (Ondine s curse). The patient with a bulbar angioma is stable with only assisted ventilation by a nasal route at night, with good quality of life. Our conclusions are that: a) central nervous system anomalies need to be investigated as possible causes of respiratory insufficiency when lungs are normal; b) the respiratory control of patients with brainstem lesions should be studied, particularly at night (polysomnography), and c) even when awake-state ventilation is adequate, nighttime assisted ventilation may be required.
Acute Disease↗
[The patterns of use and factors associated with the patient admission of hospital emergencies for asthma and chronic obstructive pulmonary disease].
The aim of this study was to describe the epidemiological characteristics of emergencies caused by asthma and chronic obstructive pulmonary disease (COPD) at the Hospital Clínico Universitario of Valencia (Spain) and to analyze factors related to hospital admissions for the same causes. Emergency room medical records for 1993 to 1995 of patients older than 14 years of age were examined to identify those due to asthma or COPD, according to established protocol. Demographic variables were described, followed by Poisson regression analysis of time and seasonal factors affecting emergencies. Factors related to hospital admission were analyzed by logistic regression, taking into account age group, sex, place of residence, and the year, month, day and hour of emergency room arrival. Asthma patients amounted to 1% of emergencies, while COPD patients accounted for 2%. The admission rate for women with asthma was higher than for men (F/M ratio = 0.78), whereas the rate for men with COPD was higher than for women (F/M ratio = 3.14). The largest age groups with asthma emergencies included young people aged 15 to 24 years old and those over 60. Hospital admissions or transfers to other hospitals were ordered for 17.4% of asthma patients and 38.8% of COPD patients. Nearly a third of COPD patients and a fifth of asthma patients were readmitted within the ten days following the first emergency. Clear temporal patterns of COPD emergency were observed for month (most occurring in winter), day of the week (most on Monday) and hour of the day (most during daytime hours, with fewer at midday). The time patterns were less evident for asthma emergencies, although the likelihood of admission because of asthma varied by month and day of the week. Emergency room records may be useful for studying the patterns of respiratory disease presentation. Other possible uses are epidemiologic monitoring and evaluation of health care quality.
Adolescent↗
Role of K+ channels and sodium pump in the vasodilation induced by acetylcholine, nitric oxide, and cyclic GMP in the rabbit aorta.
The endothelium-dependent relaxation caused by acetylcholine (ACh) in rabbit aorta segments was reduced by the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine methyl ester and by blockade of: Na+ pump with ouabain, large-conductance Ca2+-activated K+ (BK(Ca)) channels with charybdotoxin (ChTx), or voltage-dependent K+ (Kv) channels with 4-aminopyridine (4-AP). ACh relaxation was unaltered by glibenclamide, apamin, and Ba2+, blockers of ATP-sensitive K+ channels, small-conductance Ca2+-activated K+ channels, and inward rectifier K+ channels, respectively. The relaxation induced by exogenous NO and 8-bromocyclic GMP (8-BrcGMP) was similar in intact and endothelium-denuded segments, and it was reduced or unaltered by the same drugs used in the case of ACh. However, a 4-AP concentration 20-fold higher was necessary to reduce exogenous NO relaxation. These data suggest a resemblance in the mechanisms implicated in the relaxation elicited by ACh, exogenous NO, and 8-BrcGMP. Therefore, the relaxation caused by ACh is mainly mediated by endothelial NO, which in turn, enhances cGMP levels; this messenger appears to be the major one responsible for the smooth muscle cell hyperpolarization in the relaxation elicited by ACh, which is mediated by activation of the Na+ pump and ChTx- and 4-AP-sensitive K+ channels, likely BK(Ca) and Kv channels.
Acetylcholine↗
Age-related changes in vascular responses.
Aging causes changes in the structure and function of the vessels that leads to an increase in the incidence of certain cardiovascular diseases, such as hypertension, coronary artery disease, heart failure, and postural hypotension with enhancement of both morbidity and mortality. When aging is associated with hypertension, these changes are increased. Aging alters endothelial cells, and so the vascular tone regulation, reducing the endothelium-dependent relaxations, probably by a decrease in endothelial synthesis or release of nitric oxide. In addition, endothelium-independent relaxations are essentially unaltered, those elicited by beta-adrenoceptor agonists being usually reduced. Aging scarcely modifies the contractions induced by different agents, such as 5-hydroxytryptamine, histamine, high potassium, and angiotensin, whereas reduces those elicited by noradrenaline or endothelin. Vascular Ca(2+) homeostasis appears to be altered in aging. The extracellular Ca(2+) dependence of contractile responses elicited by agonists is enhanced, which explains the increased sensitivity to Ca(2+) antagonists in elderly. Finally, Na(+) pump activity, that controls cellular ionic homeostasis, seems to be reduced in aging. The contractions elicited by Na(+) pump inhibition with ouabain are negatively modulated by the release of a diffusible endothelial factor, an effect lost in aging, being replaced by an endothelium-dependent contracting factor that facilitates ouabain responses.
Aging↗
Relationship between induced sputum cell counts and fluid-phase eosinophil cationic protein and clinical or physiologic profiles in mild asthma.
BACKGROUND: Sputum analysis is the only non-invasive method to examine airway inflammatory processes in subjects with asthma. The aim of this study was to investigate the relationship between cell counts and fluid phase levels in induced sputum in subjects with mild asthma, and the severity of asthma as assessed by clinical, physiologic and blood measurements. METHODS: Forty patients with mild asthma, aged 17 to 49 years were studied (good sputum sample only from 31). On the first day, spirometry and methacholine challenges were performed. After 2 to 4 days, venous blood for absolute eosinophil count and eosinophil cationic protein (ECP) measurement was obtained and sputum was induced by inhalation of hypertonic saline. For the next 15 days subjects recorded their peak expiratory flow (PEF), symptom scores, and beta2-agonist requirements twice daily. Differential counts of leukocytes were done on cytospin preparations of homogenized sputum and the supernatant was examined for eosinophil cationic protein (ECP). RESULTS: Sputum eosinophil counts and not neutrophil, epithelial cells, macrophages, or lymphocytes, were inversely correlated to FEV1/FVC % (r = -.57, P = .0008) and to PC20-methacholine (r = -.40, P = .024). No statistical relationship was obtained between eosinophil counts and either symptom scores, bronchodilator requirements, or daily PEF variability. Sputum ECP values were correlated to FEV1/FVC% (r = -.41, P = .026) but not to PC20 (r = -.32, P = .08) or clinical scores or PEF variation. A trend to significance was appreciated between peripheral blood and sputum eosinophil counts (r = .34, P = .067) and no relationship was found between sputum and serum ECP values (r = .10, P = .38). CONCLUSIONS: Although sputum markers give some information about disordered lung function and physiologic changes in the airways, they are not the only factors concerned in the clinical expression of mild asthma.
Adolescent↗
Role of iNOS in the vasodilator responses induced by L-arginine in the middle cerebral artery from normotensive and hypertensive rats.
1. The substrate of nitric oxide synthase (NOS), L-arginine (L-Arg, 0.01 microM - 1 mM), induced endothelium-independent relaxations in segments of middle cerebral arteries (MCAs) from normotensive Wistar-Kyoto (WKY) and hypertensive rats (SHR) precontracted with prostaglandin F2alpha (PGF2alpha). These relaxations were higher in SHR than WKY arteries. 2. L-N(G)-nitroarginine methyl ester (L-NAME) and 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), unspecific and inducible NOS (iNOS) inhibitors, respectively, reduced those relaxations, specially in SHR. 3. Four- and seven-hours incubation with dexamethasone reduced the relaxations in MCAs from WKY and SHR, respectively. 4. Polymyxin B and calphostin C, protein kinase C (PKC) inhibitors, reduced the L-Arg-induced relaxation. 5. Lipopolysaccharide (LPS, 7 h incubation) unaltered and inhibited these relaxations in WKY and SHR segments, respectively. LPS antagonized the effect polymyxin B in WKY and potentiated L-Arg-induced relaxations in SHR in the presence of polymyxin B. 6. The contraction induced by PGF2alpha was greater in SHR than WKY arteries. This contraction was potentiated by dexamethasone and polymyxin B although the effect of polymyxin B was higher in SHR segments. LPS reduced that contraction and antagonized dexamethasone- and polymyxin B-induced potentiation, these effects being greater in arteries from SHR. 7. These results suggest that in MCAs: (1) the induction of iNOS participates in the L-Arg relaxation and modulates the contraction to PGF2alpha; (2) that induction is partially mediated by a PKC-dependent mechanism; and (3) the involvement of iNOS in such responses is greater in the hypertensive strain.
Animals↗