981 resultados para tidal volume
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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In most reptiles, the ventilatory response to hypercapnia consists of large increases in tidal volume (V-T), whereas the effects on breathing frequency (f(R)) are more variable. The increased V-T seems to arise from direct inhibition of pulmonary stretch receptors. Most reptiles also exhibit a transitory increase in ventilation upon removal of CO2 and this post-hypercapnic hyperpnea may consist of changes in both V-T and f(R). While it is well established that increased body temperature augments the ventilatory response to hypercapnia, the effects of temperature on the post-hypercapnic hyperpnea is less described. In the present study, we characterise the ventilatory response of the agamid lizard Uromastyx aegyptius to hypercapnia and upon the return to air at 25 and 35 degreesC. At both temperatures, hypercapnia caused large increases in V-T and small reductions in f(R), that were most pronounced at the higher temperature. The post-hypercapnic hyperpnea, which mainly consisted of increased fR, was numerically larger at 35 compared to 25 degreesC. However, when expressed as a proportion of the levels of ventilation reached during steady-state hypercapnia, the post-hypercapnic hyperpnea was largest at 25 degreesC. Some individuals exhibited buccal pumping where each expiratory thoracic breath was followed by numerous small forced inhalations caused by contractions of the buccal cavity. This breathing pattern was most pronounced during severe hypercapnia and particularly evident during the post-hypercapnic hyperpnea. (C) 2002 Published by Elsevier B.V.
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To study the effects of environmental hypercarbia on ventilation in snakes, particularly the anomalous hyperpnea that is seen when CO(2) is removed from inspired gas mixtures (post-hypercapnic hyperpnea), gas mixtures of varying concentrations of CO(2) were administered to South American rattlesnakes, Crotalus durissus, breathing through an intact respiratory system or via a tracheal cannula by-passing the upper airways. Exposure to environmental hypercarbia at increasing levels, up to 7% CO(2), produced a progressive decrease in breathing frequency and increase in tidal volume. The net result was that total ventilation increased modestly, up to 5% CO(2) and then declined slightly on 7% CO(2). on return to breathing air there was an immediate but transient increase in breathing frequency and a further increase in tidal volume that produced a marked overshoot in ventilation. The magnitude of this post-hypercapnic hyperpnea was proportional to the level of previously inspired CO(2). Administration of CO(2) to the lungs alone produced effects that were identical to administration to both lungs and upper airways and this effect was removed by vagotomy. Administration of CO(2) to the upper airways alone was without effect. Systemic injection of boluses of CO(2)-rich blood produced an immediate increase in both breathing frequency and tidal volume. These data indicate that the post-hypercapnic hyperpnea resulted from the removal of inhibitory inputs from pulmonary receptors and suggest that while the ventilatory response to environmental hypercarbia in this species is a result of conflicting inputs from different receptor groups, this does not include input from upper airway receptors.
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The tegu lizard Tupinambis merianae exhibits an episodic ventilatory pattern when dormant at 17 degrees C but a uniform ventilatory pattern when dormant at 25 degrees C. At 17 degrees C, ventilatory episodes were composed of 1-22 breaths interspaced by non-ventilatory periods lasting 1.8-26min, Dormancy at the higher body temperature was accompanied by higher rates of O-2 consumption and ventilation. The increase in ventilation was due only to increases in breathing frequency with no change observed in tidal volume. The air convection requirement for O-2 did not differ at the two body temperatures. The respiratory quotient was 0.8 at 17 degrees C and 1.0 at 25 degrees C. We found no consistent relationship between expired gas composition and the start/end of the ventilatory period during episodic breathing at 17 degrees C. However, following non-ventilatory periods of increasing duration, there was an increase in the pulmonary O-2 extraction that was not coupled to an equivalent increase in elimination of CO2 from the lungs. None of the changes in the variables studied could alone explain the initiation/termination of episodic ventilation in the tegus, suggesting that breathing episodes are shaped by a complex interaction between many variables. The estimated oxidative cost of breathing in dormant tegus at 17 degrees C was equivalent to 52.3% of the total metabolic rate, indicating that breathing is the most costly activity during dormancy.
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Tupinambis merianae increased minute ventilation by increasing both tidal volume and breathing frequency during sustained locomotion at 0.17 m s(-1). Animals in which the post-hepatic septum (PHS) had been surgically removed were not able to increase tidal volume during locomotion. Tegus without PHS compensated, in part, by increasing breathing frequency above the levels observed for tegus with intact PHS, but minute ventilation remained less than in the control animals. The rate of oxygen consumption and the air convection requirement, however, were not significantly different between animals with and without PHS, nor at the tested speeds was endurance affected by the removal of the PHS. These data suggest that the PHS facilitates ventilation by acting as a mechanical barrier, preventing the viscera from moving cranially during physical exertion.
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In order to study the relative roles of receptors in the upper airways, lungs and systemic circulation in modulating the ventilatory response of caiman (Caiman latirostris) to inhaled CO2, gas mixtures of varying concentrations of CO2 Were administered to animals breathing through an intact respiratory system, via a tracheal cannula by-passing the upper airways (before and after vagotomy), or via a cannula delivering gas to the upper airways alone. While increasing levels of hypercarbia led to a progressive increase in tidal volume in animals with intact respiratory systems (Series 1), breathing frequency did not change until the CO2 level reached 7%, at which time it decreased. Despite this, at the higher levels of hypercarbia, the net effect was a large and progressive increase in total ventilation. There were no associated changes in heart rate or arterial blood pressure. on return to air, there was an immediate change in breathing pattern; breathing frequency increased above air-breathing values, roughly to the same maximum level regardless of the level of CO2 the animal had been previously breathing, and tidal volume returned rapidly toward resting (baseline) values. Total ventilation slowly returned to air breathing values. Administration of CO2 via different routes indicated that inhaled CO2 acted at both upper airway and pulmonary CO2-sensitive receptors to modify breathing pattern without inhibiting breathing overall. Our data suggest that in caiman, high levels of inspired CO2 promote slow, deep breathing. This will decrease deadspace ventilation and may reduce stratification in the saccular portions of the lung.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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The Locus coeruleus (LC) has been suggested as a CO2 chemoreceptor site in mammals. In the present study, we assessed the role of LC noradrenergic neurons in the cardiorespiratory and thermal responses to hypercapnia. To selectively destroy LC noradrenergic neurons, we administered 6-hydroxydopamine (6-OHDA) bilaterally into the LC of male Wistar rats. Control animals had vehicle (ascorbic acid) injected (sham group) into the LC. Pulmonary ventilation (plethysmograph), mean arterial pressure (MAP), heart rate (HR), and body core temperature (T-c, data loggers) were measured followed by 60 min of hypercapnic exposure (7% CO2 in air). To verify the correct placement and effectiveness of the chemical lesions, tyrosine hydroxylase immunoreactivity was performed. Hypercapnia caused an increase in pulmonary ventilation in all groups, which resulted from increases in respiratory frequency and tidal volume (V-T) in sham-operated and 6-OHDA-lesioned groups. The hypercapnic ventilatory response was significantly decreased in 6-OHDA-lesioned rats compared with sham group. This difference was due to a decreased V-T in 6-OHDA rats. LC chemical lesion or hypercapnia did not affect MAP, HR, and T-c. Thus, we conclude that LC noradrenergic neurons modulate hypercapnic ventilatory response but play no role in cardiovascular and thermal regulation under resting conditions.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Esta revisão teve por objetivo destacar os principais achados publicados nos últimos dez anos sobre os efeitos da respiração frenolabial (RFL) em pacientes com doença pulmonar obstrutiva crônica (DPOC). A busca dos artigos foi realizada nas bases de dados Lilacs, IBECS, MEDLINE e SciELO, por meio dos seguintes descritores da área da saúde (DeCS): doença pulmonar obstrutiva crônica, reabilitação, respiração, hiperinsuflação e dispneia, e suas respectivas versões na língua inglesa (MeSH), além do termo pursed-lip breathing. Após a eliminação dos títulos repetidos, foram selecionados somente os estudos que abordavam a RFL como tema principal, resultando em 12 artigos científicos, 10 ensaios clínicos e 2 revisões bibliográficas. Segundo os achados, a RFL proporciona: alterações sobre a gasometria arterial, caracterizada pelo aumento da saturação e pressão parcial de oxigênio; padrão ventilatório, com diminuição da frequência respiratória e aumento de tempo expiratório e do volume corrente; mecânica ventilatória, por meio do recrutamento de musculatura abdominal expiratória e dos músculos da caixa torácica e acessórios da inspiração; diminuição no consumo de oxigênio; alterações na modulação autonômica cardíaca induzida pelo aumento da atividade parassimpática e, por fim, melhora na qualidade de vida destes pacientes. A RFL é considerada uma manobra de grande importância, por repercutir de forma positiva em diversos sistemas e sobre a qualidade de vida de pacientes portadores da DPOC.
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O objetivo deste estudo foi verificar a influência das diferentes dimensões corporais de meninos de 11 a 13 anos de idade, nas respostas cardiorrespiratórias, ao longo dos estágios de um teste incremental de esforço máximo em cicloergômetro. Vinte meninos realizaram um teste incremental máximo em cicloergômetro com carga inicial de 30 W e incrementos subsequentes de 30 W a cada três minutos. As variáveis respiratórias foram medidas respiração-a-respiracão através de um analisador metabólico de gases. A frequência cardíaca foi constantemente monitorada durante o teste. Os grupos foram divididos a posteriori em função da carga máxima atingida no teste incremental (90 ou 120 W) e em função da massa corporal (maior ou menor que 45 kg). As seguintes variáveis foram mensuradas continuamente: frequência respiratória, volume corrente, ventilação, consumo de oxigênio absoluto e relativo, produção absoluta de gás carbônico, frequência cardíaca e equivalente ventilatório de oxigênio. Foi concluído que as variáveis antropométricas, especialmente estatura e massa corporal, mostram-se estreitamente relacionadas às respostas cardiorrespiratórias, apresentando-se como fatores determinantes e limitantes do desempenho, devendo ambas ser consideradas para a prescrição e prática de exercícios físicos desta população pediátrica.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Objetivou-se com este experimento avaliar os efeitos do butorfanol precedido ou não pela levomepromazina sobre a freqüência cardíaca (FC), as pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM, respectivamente), a freqüência respiratória (f), a concentração de dióxido de carbono ao final da expiração (ETCO2), a saturação da oxihemoglobina (SpO2), o volume corrente (VC) e o volume minuto (VM), em cães. Para tal, foram empregados vinte animais adultos, clinicamente saudáveis, distribuídos igualmente em dois grupos (GC e GL). Ao GC administrou-se solução salina a 0,9% (Controle), no volume de 0,2mL kg-1, pela via intravenosa (IV). Decorridos 15 minutos, administrou-se butorfanol na dose de 0,3mg kg-1 pela mesma via. Aos animais do GL foi adotada a mesma metodologia, porém substituindo-se a solução salina pela levomepromazina na dose de 1mg kg-1. As medidas das variáveis cardiorrespiratórias iniciaram-se imediatamente antes da aplicação dos fármacos (M1). Novas mensurações foram realizadas 15 minutos após a administração da solução salina a 0,9% ou levomepromazina (M2) e 10 minutos após a administração de butorfanol (M3). As demais colheitas foram realizadas a intervalos de 10 minutos, durante 30 minutos (M4, M5 e M6, respectivamente). Os dados numéricos colhidos foram submetidos à Análise de Variância (ANOVA), seguida pelo teste de Tukey (p<0,05) para as comparações das médias. O emprego do butorfanol promoveu diminuição significativa das freqüências cardíaca e respiratória e do volume minuto no grupo previamente tratado pela levomepromazina; entretanto, essas alterações foram discretas, não comprometendo os demais parâmetros circulatórios e respiratórios.
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There is evidence that serotonin [ 5- hydroxytryptamine ( 5- HT)] is involved in the physiological responses to hypercapnia. Serotonergic neurons represent the major cell type ( comprising 15 - 20% of the neurons) in raphe magnus nucleus ( RMg), which is a medullary raphe nucleus. In the present study, we tested the hypothesis 1) that RMg plays a role in the ventilatory and thermal responses to hypercapnia, and 2) that RMg serotonergic neurons are involved in these responses. To this end, we microinjected 1) ibotenic acid to promote nonspecific lesioning of neurons in the RMg, or 2) anti- SERT- SAP ( an immunotoxin that utilizes a monoclonal antibody to the third extracellular domain of the serotonin reuptake transporter) to specifically kill the serotonergic neurons in the RMg. Hypercapnia caused hyperventilation and hypothermia in all groups. RMg nonspecific lesions elicited a significant reduction of the ventilatory response to hypercapnia due to lower tidal volume ( V-T) and respiratory frequency. Rats submitted to specific killing of RMg serotonergic neurons showed no consistent difference in ventilation during air breathing but had a decreased ventilatory response to CO2 due to lower VT. The hypercapnia- induced hypothermia was not affected by specific or nonspecific lesions of RMg serotonergic neurons. These data suggest that RMg serotonergic neurons do not participate in the tonic maintenance of ventilation during air breathing but contribute to the ventilatory response to CO2. Ultimately, this nucleus may not be involved in the thermal responses CO2.
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Eight non-lactating Alpine goats, averaging 57kg, were paired according to weight and assigned randomly to 2 groups of 4 animals, control (CG) and treatment (TG) with feed and water ad libitum. An adjustment period of 7 days with all animals at thermoneutral conditions was followed by a 28-day period when TG was exposed to air temperatures averaging 35.0 degrees C, from 0800 to 1700h, including simulated solar radiation, and thermoneutral conditions from 2700 to 0800h. CG remained under thermoneutral conditions. Respiratory frequency was greater, tidal volume lower, and respiratory minute volume greater for TG than CG (176 vs 30 breaths/min, P<.001, 105 vs 293ml, P<.01; 18.4 vs 9.21, P<.05). Respiratory evaporation and sweating rate as well as rectal and skin temperatures were greater for TG than CG (14.59 vs 6.32 kcal h(-1), P<.01; 43.97 vs.00 g m(-2) h(-1), P<.001; 40.0 vs 38.9 degrees C, P<.001; 39.3 vs 35.8 degrees C, P<.01). There was no difference between groups for hematocrit and feed intake, but water consumption was greater for stressed goats than control ones (28.3 vs 29.7%; 1.44 vs 1.49 kg/day; 3.07 vs 1.26 I/day, P<.05), Final body weights of both groups were similar to initial ones. It was concluded that non-lactating goats tolerated well a 35 degrees C day temperature which is 5 degrees C above the upper critical temperature, with a black-globe temperature of 39.1 degrees C and a Botsball temperature of 28.3 degrees C, though a certain degree of hyperthermia may occur, as long as thermoneutral conditions have prevailed during the night.