Academic literature on the topic 'Diaphragm – Physiology'
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Journal articles on the topic "Diaphragm – Physiology"
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Nguyen, Taitan, Neal A. Rubinstein, Camasamudram Vijayasarathy, Lawrence C. Rome, Larry R. Kaiser, Joseph B. Shrager, and Sanford Levine. "Effect of chronic obstructive pulmonary disease on calcium pump ATPase expression in human diaphragm." Journal of Applied Physiology 98, no. 6 (June 2005): 2004–10. http://dx.doi.org/10.1152/japplphysiol.00767.2004.
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We have previously demonstrated that human diaphragm remodeling elicited by severe chronic obstructive pulmonary disease (COPD) is characterized by a fast-to-slow myosin heavy chain isoform transformation. To test the hypothesis that COPD-induced diaphragm remodeling also elicits a fast-to-slow isoform shift in the sarcoendoplasmic reticulum Ca2+ ATPase (SERCA), the other major ATPase in skeletal muscle, we obtained intraoperative biopsies of the costal diaphragm from 10 severe COPD patients and 10 control subjects. We then used isoform-specific monoclonal antibodies to characterize diaphragm fibers with respect to the expression of SERCA isoforms. Compared with control diaphragms, COPD diaphragms exhibited a 63% decrease in fibers expressing only fast SERCA (i.e., SERCA1; P < 0.001), a 190% increase in fibers containing both fast and slow SERCA isoforms ( P < 0.01), and a 19% increase ( P < 0.05) in fibers expressing only the slow SERCA isoform (i.e., SERCA2). Additionally, immunoblot experiments carried out on diaphragm homogenates indicated that COPD diaphragms expressed only one-third the SERCA1 content noted in control diaphragms; in contrast, COPD and control diaphragms did not differ with respect to SERCA2 content. The combination of these histological and immunoblot results is consistent with the hypothesis that diaphragm remodeling elicited by severe COPD is characterized by a fast-to-slow SERCA isoform transformation. Moreover, the combination of these SERCA data and our previously reported myosin heavy chain isoform data (Levine S, Nguyen T, Kaiser LR, Rubinstein NA, Maislin G, Gregory C, Rome LC, Dudley GA, Sieck GC, and Shrager JB. Am J Respir Crit Care Med 168: 706–713, 2003) suggests that diaphragm remodeling elicited by severe COPD should decrease ATP utilization by the diaphragm.
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Farkas, G. A., and D. F. Rochester. "Functional characteristics of canine costal and crural diaphragm." Journal of Applied Physiology 65, no. 5 (November 1, 1988): 2253–60. http://dx.doi.org/10.1152/jappl.1988.65.5.2253.
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We estimated the in situ force-generating capacity of the costal and crural portions of the canine diaphragm by relating in vitro contractile properties and diaphragmatic dimensions to in situ lengths. Piezoelectric crystals were implanted on right costal and left crural diaphragms of anesthetized dogs, via midline laparatomy. With the abdomen reclosed, diaphragm lengths were recorded at five lung volumes. Contractile properties of excised muscle bundles were then measured. In vitro force-frequency and length-tension characteristics of the costal and crural diaphragms were virtually identical; their optimal force values were 2.15 and 2.22 kg/cm2, respectively. In situ, at residual volume, functional residual capacity (FRC), and total lung capacity the costal diaphragm lay at 102, 95, and 60% of optimal length (Lo), whereas the crural diaphragm lay at 88, 84, and 66% of Lo. Muscle cross-sectional area was 40% greater in costal than in crural diaphragms. Considering in situ lengths, cross-sectional areas, and in vitro length-tension characteristics at FRC, the costal diaphragm could exert 60% more force than the crural diaphragm.
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Bazzy, A. R. "Effect of hypoxia on neuromuscular transmission in the developing diaphragm." Journal of Applied Physiology 76, no. 2 (February 1, 1994): 708–13. http://dx.doi.org/10.1152/jappl.1994.76.2.708.
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To study the effects of hypoxia on neuromuscular transmission in the developing diaphragm, phrenic nerve-hemidiaphragm preparations were obtained from newborn (4–9 days) and older (22–30 days) rats. Diaphragms were stimulated directly or indirectly (via the nerve) for 1 s at frequencies of 10–80 Hz. Force generated in response to stimulation was measured during perfusion of oxygenated Ringer solution (control) and Ringer solution bubbled with 95% N2–5% CO2 (hypoxia). After 45 min of hypoxia, the force response of the older diaphragms to direct stimulation had decreased to approximately 50% of control at > or = 40 Hz; however, when stimulation occurred via the nerve at these frequencies only 15–20% of control force was generated. In the newborn diaphragms, the force decrement after similar or longer periods of hypoxia (< or = 90 min) was 30– 40% irrespective of the route or frequency of stimulation. After 15 min of reoxygenation, the force response to both muscle and nerve stimulation recovered completely in the older diaphragms but only partially in the newborn diaphragms (range 77% of control at 50 Hz to 95% of control at 10 Hz). These data suggest that in the newborn diaphragm 1) neuromuscular transmission is more resistant to the effects of hypoxia than the older diaphragm and 2) the predominant effect of hypoxia is peripheral in the diaphragm muscle fibers, whereas in the older diaphragm the effect is before or at the neuromuscular junction.
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Margulies, S. S. "Regional variation in canine diaphragm thickness." Journal of Applied Physiology 70, no. 6 (June 1, 1991): 2663–68. http://dx.doi.org/10.1152/jappl.1991.70.6.2663.
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To quantify the relationship between both regional and overall diaphragm morphometry and body weight in the dog, diaphragm thickness was measured in five regions of the costal diaphragm and three regions of the crural diaphragm in 40 healthy dogs (8-40 kg). Surface area of the diaphragm, diaphragm weight, and body weight were also determined. Diaphragm surface area and weight varied linearly with body weight, but there was no significant correlation between overall diaphragm thickness and body weight. Diaphragm thickness varied significantly between regions, and three regions had systematic left-to-right differences as well. Because diaphragm geometry influences the diaphragm's function as a pressure generator, regional differences in thickness may alter the relationship between the force developed by the activation of a particular region of the diaphragm and its action on the respiratory system.
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Sugiura, T., S. Morita, A. Morimoto, and N. Murakami. "Regional differences in myosin heavy chain isoforms and enzyme activities of the rat diaphragm." Journal of Applied Physiology 73, no. 2 (August 1, 1992): 506–9. http://dx.doi.org/10.1152/jappl.1992.73.2.506.
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Myosin heavy chain isoforms and enzyme activities were compared between the costal and crural regions of the rat diaphragm. The percentage of heavy chain (HC) IIb in the crural region of the diaphragm was significantly (P less than 0.05) higher than that in the costal region (mean 7.3 vs. 3.0%), and the percentage of HCI was significantly lower in the crural than in the costal diaphragm (22.7 vs. 27.9%). The distributions of HCIIa and HCIId were relatively homogeneous in both regions. Succinate dehydrogenase activity in the costal diaphragm was 21% greater (P less than 0.01) than in the crural diaphragm. In contrast, there was no significant difference in the activity of phosphofructokinase in the crural and costal diaphragms. These results demonstrate that a difference in myosin heavy chain isoforms and oxidative capacity exists between the costal and crural regions of the rat diaphragm.
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Lewis, M. I., W. Z. Zhan, and G. C. Sieck. "Adaptations of the diaphragm in emphysema." Journal of Applied Physiology 72, no. 3 (March 1, 1992): 934–43. http://dx.doi.org/10.1152/jappl.1992.72.3.934.
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In adult male hamsters the influence of emphysema (EMP) on the in vitro contractile and fatigue properties and the histochemical, morphometric, and metabolic properties of muscle fibers in the costal diaphragm was determined 6 mo after the administration of either elastase or saline (controls, CTL). Isometric contractile properties were determined in vitro using supramaximal direct muscle stimulation. Optimal fiber length for force generation was significantly shorter in the EMP than in the CTL diaphragm. Maximum specific force (i.e., force per unit area) was 25% lower than CTL. Fatigue resistance was significantly improved in the EMP diaphragm compared with CTL. Diaphragm muscle fibers were classified as type I or II on the basis of histochemical staining for myofibrillar adenosinetriphosphatase after alkaline preincubation. The proportions of type I and II fibers were similar between the two groups. Cross-sectional areas of type II fibers were 30% larger in EMP than in CTL diaphragms. Succinate dehydrogenase activities of both type I and II fibers were higher in EMP than in CTL diaphragms. The number of capillaries surrounding both type I and II fibers increased with EMP, but in proportion to the hypertrophy of these fibers. Thus, capillary density (number of capillaries per fiber cross-sectional area) remained unchanged. We postulate that these contractile, morphometric, and metabolic adaptations reflect an increased activation of the diaphragm in response to the loads imposed by EMP.
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Matecki, Stefan, Ghiabe H. Guibinga, and Basil J. Petrof. "Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 4 (October 2004): R961—R968. http://dx.doi.org/10.1152/ajpregu.00146.2004.
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Duchenne muscular dystrophy is characterized by myofiber necrosis, muscle replacement by connective tissue, and crippling weakness. Although the mdx mouse also lacks dystrophin, most muscles show little myofiber loss or functional impairment. An exception is the mdx diaphragm, which is phenotypically similar to the human disease. Here we tested the hypothesis that the mdx diaphragm has a defective regenerative response to necrotic injury, which could account for its severe phenotype. Massive necrosis was induced in mdx and wild-type (C57BL10) mouse diaphragms in vivo by topical application of notexin, which destroys mature myofibers while leaving myogenic precursor satellite cells intact. At 4 h after acute exposure to notexin, >90% of diaphragm myofibers in both wild-type and mdx mice demonstrated pathological sarcolemmal leakiness, and there was a complete loss of isometric force-generating capacity. Both groups of mice showed strong expression of embryonic myosin within the diaphragm at 5 days, which was largely extinguished by 20 days after injury. At 60 days postinjury, wild-type diaphragms exhibited a persistent loss (∼25%) of isometric force-generating capacity, associated with a trend toward increased connective tissue infiltration. In contrast, mdx diaphragms achieved complete functional recovery of force generation to noninjured values, and there was no increase in muscle connective tissue over baseline. These data argue against any loss of intrinsic regenerative capacity within the mdx diaphragm, despite characteristic features of major dystrophic pathology being present. Our findings support the concept that significant latent regenerative capacity resides within dystrophic muscles, which could potentially be exploited for therapeutic purposes.
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Supinski, Gerald S., and Leigh A. Callahan. "Diaphragmatic free radical generation increases in an animal model of heart failure." Journal of Applied Physiology 99, no. 3 (September 2005): 1078–84. http://dx.doi.org/10.1152/japplphysiol.01145.2004.
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Heart failure evokes diaphragm weakness, but the mechanism(s) by which this occurs are not known. We postulated that heart failure increases diaphragm free radical generation and that free radicals trigger diaphragm dysfunction in this condition. The purpose of the present study was to test this hypothesis. Experiments were performed using halothane-anesthetized sham-operated control rats and rats in which myocardial infarction was induced by ligation of the left anterior descending coronary artery. Animals were killed 6 wk after surgery, the diaphragms were removed, and the following were assessed: 1) mitochondrial hydrogen peroxide (H2O2) generation, 2) free radical generation in resting and contracting intact diaphragm using a fluorescent-indicator technique, 3) 8-isoprostane and protein carbonyls (indexes of free radical-induced lipid and protein oxidation), and 4) the diaphragm force-frequency relationship. In additional experiments, a group of coronary ligation animals were treated with polyethylene glycol-superoxide dismutase (PEG-SOD, 2,000 units·kg−1·day−1) for 4 wk. We found that coronary ligation evoked an increase in free radical formation by the intact diaphragm, increased diaphragm mitochondrial H2O2 generation, increased diaphragm protein carbonyl levels, and increased diaphragm 8-isoprostane levels compared with controls ( P < 0.001 for the first 3 comparisons, P < 0.05 for 8-isoprostane levels). Force generated in response to 20-Hz stimulation was reduced by coronary ligation ( P < 0.05); PEG-SOD administration restored force to control levels ( P < 0.03). These findings indicate that cardiac dysfunction due to coronary ligation increases diaphragm free radical generation and that free radicals evoke reductions in diaphragm force generation.
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Lewis, M. I., G. C. Sieck, M. Fournier, and M. J. Belman. "Effect of nutritional deprivation on diaphragm contractility and muscle fiber size." Journal of Applied Physiology 60, no. 2 (February 1, 1986): 596–603. http://dx.doi.org/10.1152/jappl.1986.60.2.596.
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The influence of nutritional deprivation on the contractile and fatigue properties of the diaphragm was studied in adult rats. Food access was restricted to one-third of normal daily intake until the body weight of nutritionally deprived (ND) animals was approximately 50% of controls (CTL). Isometric contractile properties were studied in an in vitro nerve muscle strip preparation. Both twitch (Pt) and tetanic (Po) tensions of diaphragms from the ND animals were markedly reduced compared with CTL; however, Pt/Po was higher for the ND group. The shape of the force-frequency curve (normalized to Po) was generally similar between the two groups, except at 5 and 10 pulses/s stimulation, where greater relative tensions were produced in diaphragms from the ND animals. Diaphragm fatigue was induced by repetitive stimulation at either 20 or 100 pulses/s. Endurance time (defined as the time required for tension to fall to 50% of initial) of diaphragms from ND animals was prolonged at both 20 and 100 pulses/s. Immediately after induction of fatigue, force-frequency curves for both ND and CTL diaphragms were shifted to the right. However, this rightward shift was attenuated in the ND group compared with CTL. Nutritional deprivation had no effect on the proportions of different fiber types within the diaphragm but did result in a significant decrease in the cross-sectional area of both fast-and slow-twitch fibers. This decrease in cross-sectional area was significantly greater for fast-twitch fibers. We conclude that these changes in diaphragm contractile and fatigue properties occur as a result of the influence of malnutrition on muscle fiber cross-sectional area.
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Stan, Radu V. "Multiple PV1 dimers reside in the same stomatal or fenestral diaphragm." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 4 (April 2004): H1347—H1353. http://dx.doi.org/10.1152/ajpheart.00909.2003.
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Several of the endothelium-specific structures that have been involved in microvascular permeability [such as caveolae, transendothelial channels (TECs), vesiculovacuolar organelles (VVOs), and fenestrae] can be provided with either a stomatal or fenestral diaphragm. In the case of fenestrae, the diaphragm has the presumed function of creating a permselective barrier for solutes from blood plasma and interstitium. PV1 is an endothelium-specific integral membrane glycoprotein that is associated with both the stomatal diaphragms of caveolae, TECs, and VVOs as well as the diaphragms of endothelial fenestrae. The intimate structure of these diaphragms has been shown to consist of a meshwork formed by radial fibrils. We have recently shown that PV1 is a key structural element of both types of diaphragms, with its expression being sufficient to form de novo stomatal and fenestral diaphragms in both endothelial and nonendothelial cell types in culture. We have further tested the role of PV1 in the structure of the diaphragms and demonstrate here that multiple PV1 homodimers reside in close proximity within the same diaphragm. Our data bring further support to the paradigm by which PV1 dimers would form the fibrils of the diaphragms with a function in the microvascular permeability.
Dissertations / Theses on the topic "Diaphragm – Physiology"
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Orrey, Samantha Taylor. "The relationship between diaphragm thickness, diaphragm strength and diaphragm endurance in young, healthy individuals." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86666.
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Thesis (MScPhysio)--Stellenbosch University, 2014.ENGLISH ABSTRACT: Introduction: In the intensive care unit population, approximately 40% of patients require mechanical ventilation and 20-25% of these patients will encounter difficulties in the discontinuation of mechanical ventilation. As mechanical ventilation affects the diaphragm, a better understanding of the structural and functional changes of the diaphragm is warranted. Method: A scoping review was done to determine whether a relationship between diaphragm thickness, diaphragm strength and diaphragm endurance had been established. Seven databases were searched using a specific search strategy. Papers were identified based on pre-defined inclusion criteria. Data was extracted by the primary investigator (PI) into a self-developed excel spreadsheet. Criteria were developed for a more focused review to inform the planning of a primary study. The primary study investigated the relationship between diaphragm thickness, diaphragm strength and diaphragm endurance in young, healthy individuals. A sample of convenience was used; included healthy individuals (18-24); three activity-levels (sedentary; endurance- and strength related sporting activities); stratified for gender and BMI. Measurements included: Sonographic measurement of diaphragm thickness; mouth pressure manometer measurements for diaphragmatic strength; and fatigue resistance index as a measure of endurance. Participants were instructed to breathe through a pressure threshold device at 60% of PImax until task failure. The fatigue resistance index was calculated as PImax final/PImax initial. Intra-rater reliability was established and testing procedures standardised a priori. Results: 405 full texts were retrieved and assessed for inclusion into the review. Papers identified the evaluation of diaphragm function in a variety of populations. 23 papers were included in the focused review. Six papers were published on diaphragm thickness, six on diaphragm strength and eleven on diaphragm endurance. No papers identified the correlation between diaphragm thickness, diaphragm strength and diaphragm endurance. 55 subjects, males and females, were recruited for the primary study. Groups were similar at baseline with regards to gender, age and BMI. The mean age of the sample was 21.16 years (SD = 1.55), with a mean body mass index (BMI) of 25.43 kg/m2 (SD = 3.70). A moderate positive correlation was established between diaphragm thickness and diaphragm strength measurements (r = 0.52; r2 = 0.27; p < 0.01). Diaphragm thickness was not correlated with diaphragm endurance (r = -0.15; r2 = 0.02; p = 0.29). No relationship was found between the strength of the diaphragm and the endurance of the diaphragm (r= -0.19; r2 = 0.04; p= 0.16). Conclusion: Guidelines for the measurement of diaphragm function do exist, but they are not adhered to by the majority of studies. Study procedures are inconsistently reported and this may affect the reproducibility of techniques in future studies. We further conclude that a correlation exists between diaphragm thickness and diaphragm strength. The use of ultrasound to measure diaphragm thickness proved to be a reliable technology and gave a moderate indication of the strength of the diaphragm. This technology may help clinicians to detect and monitor dysfunction of the diaphragm in the early stages of admission to the acute setting.
AFRIKAANSE OPSOMMING: Inleiding: Ongeveer 40% van pasiente wat in intensiewe sorgeenheid behandel word, benodig intubasie en meganiese ventilasie. Tot 25% van hierdie pasiënte sal probleme ondervind in die staking van meganiese ventilasie. Meganiese ventilasie beïnvloed die diafragma, daarom word n beter begrip van die strukturele en funksionele veranderinge van die diafragma benodig. Metode: 'n Literatuur oorsig is gedoen om te bepaal of daar 'n verhouding bestaan tussen die dikte, krag en uithouvermoë van die diafragma. Sewe databasisse is deurgesoek aan die hand van spesifieke databasis gedefinieerde soektog strategie. Relevante artikels is geïdentifiseer aan die hand van pre-gedefinieerde insluiting kriteria. Data is onttrek en in ‘n self-ontwikkelde datablad opgesom deur die primêre ondersoeker (PI). Hierdie inligting is gebruik in die beplanning van ‘n primêre studie. Die doel van die primêre studie was om die verhouding tussen die diafragma dikte, krag en uithouvermoë in jong, gesonde individue te ondersoek. ‘n Gerieflikheids steekproef is gebruik; insluitend gesonde individue (18-24); drie aktiwiteits vlakke (passief; uithouvermoë- en krag verwante sportaktiwiteite) en breë spektrum vir geslag en ligaamsbou (BMI). Metings ingesluit: sonografiese meting van die diafragma se dikte; monddruk manometer metings vir diafragmatiese krag en ‘n moegheid/weerstand indeks as maatstaf van diafragmatiese uithouvermoë. Deelnemers is opdrag gegee om asem te haal deur toestel met druk maksimum gestel 60% van PImax, tot mislukking. Die moegheid/weerstand indeks is bereken as PImax finale / PImax oorspronlik. Intra-meter betroubaarheid is bepaal en toets prosedures is gestandaardiseer voordat data ingesamel is. Resultate: 405 vol teks artikels is uitgelig vir insluiting in die literatuur oorsig. Diafragmatiese funksie is ge-evalueer in 'n verskeidenheid bevolkings. Drie en twintig artikels is in die finale oorsig ingesluit. Ses artikels wat diafragma dikte evalueer, ses wat diafragmatiese krag evalueer en elf wat die diafragma se uithouvermoë evalueer is ingesluit in die oorsig. Geen van die artikels uitgelig het ‘n ooreenkoms tussen diafragma dikte, diafragma krag en diafragma uithouvermoë geïdentifiseer nie. 55 deelnemers is gewerf vir die primêre studie. Groepe was soortgelyk by basislyn met betrekking tot geslag, ouderdom en BMI. Die gemiddelde ouderdom van die toetsgroep was 21.16 jaar (SD=1.55), met 'n gemiddelde BMI van 25.43 kg/m2 (SD = 3.70). ‘n Middelmatige positiewe verhouding is waargeneem tussen diafragma dikte en krag (r = 0.52; r2 = 0.27; p < 0.01). Geen verhouding is gevind tussen diafragma dikte en uithouvermoë nie (r= -0.15; r2 = 0.02; p = 0.29). Daar is ook geen verhouding waargeneem tussen diafragma krag en diafragma uithouvermoë nie. (r= 0.19; r2 = 0.04; p = 0.16). Gevolgtrekking: Daar bestaan wel riglyne vir die meting van die diafragma se funksie, maar in die meerderheid van studies word dit nie nagekom nie. Studie prosedures is nie konsekwent weergegee nie en dit kan die resultate van tegnieke beinvloed in toekomende studies. ‘n Matige sterk verhouding is waargeneem tussen diafragmatiese dikte en krag. Die gebruik van ultraklank om die diafragma se dikte te meet is betroubare tegnologie en kan n redelike aanduiding gee oor die krag van die diafragma. Hierdie tegnologie kan praktisyne help om enige disfunksie van die diafragma te identifiseer en te monitor in die vroeë stadiums van toelating tot die akute omgewing.
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Reid, Wendy Darlene. "Fatigue and rest of the hamster diaphragm." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29168.
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Decreased respiratory muscle strength and/or excessive loads imposed on the respiratory muscles by disease may result in respiratory muscle fatigue and ventilatory failure. Once the respiratory muscles fatigue, the only treatment is rest by mechanical ventilation. However, no one has yet determined the best protocol of rest. The purpose of these studies was to develop an animal model in the hamster in order to examine the time course of recovery following fatigue of the diaphragm and specifically, to test whether mechanical ventilation or spontaneous unloaded breathing was a better mode for functional recovery. The studies required the initial development of an anesthetic regimen which produced minimal respiratory depression in the hamster. A new method of stimulating the diaphragm in small animals was developed by apposing plate electrodes directly against the diaphragm. The validity of this technique was examined and comparison of the mechanical and electrophysiological response to that of phrenic nerve stimulation were similar at maximal stimulation. The histological characteristics of the normal hamster diaphragm were determined for fibre type proportions and sizes, oxidative capacity and glycogen levels in the costal and crural regions of this muscle. The examination revealed three distinct areas of the diaphragm with different histological features: the abdominal surface of the crural region, the thoracic surface of the crural region and the sternal and costal region. Diaphragmatic fatigue was induced in vivo by repetitive electrical stimulation which resulted in both high and low frequency fatigue. The fatigue stimulus also produced muscle fibre damage, primarily along the abdominal surface of the diaphragm over the electrodes, and glycogen depletion in the type lib fibres. Rest by continuous mechanical ventilation resulted in recovery of high frequency fatigue in the hamster diaphragm whereas rest by spontaneous unloaded breathing resulted in no recovery. Sham fatigue groups rested by either mechanical ventilation or spontaneous breathing demonstrated progressive deterioration in transdiaphragmatic pressure throughout the rest period. Decreased muscle fibre damage but increased inflammation and glycogen depletion was demonstrated in all four fatigue/sham fatigue and rest groups compared to that demonstrated by the fatigue/sham fatigue only groups. The results suggest that passive rest by continuous mechanical ventilation promotes recovery following fatigue induced by electrical stimulation. Additional factors such as prolonged fasting, loads imposed on the diaphragm by the plate electrode apparatus, positive pressure ventilation, and cumulative effects of intraperitoneal urethane likely contributed to the progressive deterioration of diaphragmatic function demonstrated in the animals of the two sham groups rested by either spontaneous breathing or mechanical ventilation, and confounded the results shown by the two fatigue groups rested by either spontaneous breathing or mechanical ventilation.Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Beck, Jennifer 1968. "Measurement of diaphragm myoelectric activity in humans." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=34912.
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This thesis is about the development and evaluation of a standardized method to measure the crural diaphragm electromyogram (EMG) in humans, with an esophageal electrode. In order for the diaphragm EMG to be physiologically relevant, its measurement and analysis require objective control of the disturbances and filter effects which can influence the sigma. One issue of importance is the maintenance of diaphragm-to-electrode positioning throughout the inspiration. In the present work, we describe a cross-correlation algorithm by which the position of the diaphragm along a multiple army esophageal electrode can be determined at any instant during a breath, and a second algorithm, the "double subtraction technique", which further minimizes the detrimental effects of diaphragm movement. The double subtraction technique also results in the improvement of the diaphragm EMG signal to noise ratio by 2 dB. By implementing these algorithms, we demonstrate in healthy subjects that there is no artifactual influence of lung volume/chest wall configuration on the diaphragm EMG frequency content nor on the diaphragm EMG signal strength during voluntary isometric contractions of the diaphragm. This is in contrast to the electrically elicited diaphragm compound muscle action potentials which are severely influenced by changes in lung volume. We also show that the volume-activation relationship of the diaphragm (required change in activation for changes in lung volume at a given tension) is directly related to the length-tension properties of the muscle. During dynamic, voluntary breathing maneuvers, we could find no evidence for an increase in diaphragm EMG signal strength when inspirations from functional residual capacity to total lung capacity (TLC) were performed at increasing inspiratory flow rates (velocities of shortening) up to 1.4 l/s. To account for anatomical and physiological differences between subjects, we demonstrate that the diaphragm EMG signal strength can be no
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Gauthier, Alain P. "Structure and function of the fresh and fatigued diaphragm." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41596.
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This thesis examines the importance of the length-force relationship and the three-dimensional shape of the diaphragm with regard to its inspiratory function. As well as it reports on the manner in which fatigue and aminophylline affect the length-force properties of the diaphragm. First, I studied the effect of fatigue on diaphragm contractility as a function of sarcomere length using an in vitro rat diaphragm strips. Results indicated that fatigue resulted in disproportionately greater reduction of tetanic force at short sarcomere lengths. Second, I reconstructed the three-dimensional shape of the diaphragm to determine if in vitro results are physiologically relevant in humans. I estimated the changes in fibre length and shape that occurs with lung inflation from residual volume to total lung capacity in normal subjects. Results suggested that the inspiratory function of the human diaphragm can be entirely attributed to its length-force relationship rather than changes in shape under conditions of twitch phrenic nerve stimulations. Finally, I confirmed that fatigue caused a greater percent reduction of transdiaphragmatic pressure at high lung volume in response to single supramaximal shocks delivered bilaterally to the phrenic nerves at high lung volume; and demonstrated that aminophylline potentiated human diaphragm contractility more at high than at low lung volumes, both under fresh and fatigue conditions. I propose an explanation for the effect of fatigue and aminophylline on diaphragm contractility at different sarcomere lengths based on known actions of these factors and muscle shortening on excitation-contraction coupling mechanisms of skeletal muscles.
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Ward, Michael Edward. "Mechanical, neural and vascular determinants of diaphragm function." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28549.
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The respiratory muscles play a role in respiratory failure when the efficient performance of the work of ventilation and/or their supply of metabolic substrates is disrupted. In this report a model of inspiratory muscle action is presented. The inflationary pressure applied to the lungs and the lung apposed rib cage is partitioned into two parts. One component is attributable to the action of rib cage muscles and the other is due to the interaction between upper and lower rib cage compartments. These contributions were found to be equal.The role of afferent impulses travelling in the phrenic nerve in the control of respiratory muscle activity was investigated by electrical stimulation of its central cut end. Activation of these fibres exerts a non-uniform effect on the activities of the upper airway, rib cage and abdominal muscles and may influence respiratory muscle recruitment.
The roles of blood flow and oxygen delivery in determining diaphragm function was investigated. The rate at which diaphragmatic fatigue develops is diminished at high rates of blood flow and this effect is not related to the associated increase in oxygen delivery. The critical oxygen delivery at which oxygen consumption becomes supply dependent is the same for the resting diaphragm as for the rest of the body tissues. Activation of the diaphragm results in a higher critical oxygen delivery, however, this effect is mitigated by an increase in the critical oxygen extraction ratio.
The role of nitric oxide in regulating diaphragmatic blood flow and oxygen uptake was investigated by infusion of N$ sp{G}$-nitro-L-arginine. This treatment increased diaphragmatic vascular resistance, reduced the duration and magnitude of reactive vasodilation and increased the oxygen consumption and critical extraction ratio in the contracting diaphragm.
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Labbé, Katherine. "The role of monocyte chemoattractant protein-1 in diaphragm dysfunction during sepsis /." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101595.
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Sepsis-induced diaphragmatic force loss and failure are associated with an increased exposure to proinflammatory mediators. The septic diaphragm has recently been reported to overexpresse chemokines, including the CC chemokine MCP-1 (monocyte chemoattractant protein-1). This thesis seeks to address the significance of MCP-1 overproduction in diaphragm proinflammatory mediator expression and skeletal muscle contractile function. Neutralization of endogenous MCP-1, produced following administration of LPS, decreased transcription of iNOS, IL-6, IL-1alpha, IL-1beta and MCP-1 in the diaphragm and prevented a decrease in diaphragm force production. Furthermore, exogenous MCP-1 stimulated IL-6 and MCP-1 transcription in primary diaphragm myotubes, and injection of MCP-1 in the healthy EDL muscle led to contractile weakness. Taken together, these results suggest that increased MCP-1 production in the septic diaphragm stimulates proinflammatory mediator production by diaphragm myocytes, contributing to the muscle's contractile dysfunction.
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Singh, Bhajan. "The function of the human diaphragm as a volume pump and measurement of its efficiency." University of Western Australia. School of Biomedical and Chemical Sciences, 2004. http://theses.library.uwa.edu.au/adt-WU2004.0029.
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[Truncated abstract] The function of the diaphragm as a volume pump has not been adequately evaluated because there are no accurate methods to measure the volume displaced by diaphragm motion (ΔVdi). As a consequence, the work done, power output and efficiency of the diaphragm have not been measured. Efficiency of the diaphragm could be measured by relating the power output of the diaphragm to its neural activation. The aims of this thesis were to (a) develop a new biplanar radiographic method to measure ΔVdi and use this to evaluate the effect of costophrenic fibrosis and emphysema on ΔVdi, (b) develop a new fluoroscopic method to enable breath-by-breath measurements of ΔVdi, (c) evaluate a method for quantifying neural activation of the diaphragm, and (d) combine measurements of transdiaphragmatic pressure, ΔVdi, inspiratory duration and neural activation of the diaphragm to quantify the neuromechanical efficiency of the diaphragm
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Easton, Paul A. "Differential function of costal and crural diaphragm in the awake canine." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41004.
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These investigations examined the relative function of costal and crural diaphragm segments. This work produced the first direct measurements of length and electromyogram (EMG) of the diaphragm in an awake, intact animal.Examination of diaphragm function following laparotomy revealed a consistent pattern of postoperative segmental recovery, and showed the inadequacy of EMG alone as an indicator of diaphragm activity. Segmental contraction during airway occlusion was confirmed to be non-isometric and different per segment. The basic relation between segmental velocity of shortening and mean inspiratory flow, was confirmed for diaphragm but not for intercostal musculature. Anesthesia produced a distinctive alteration in the resting length of crural compared to costal segment, suggesting a difference in inherent segmental tonic activity. Costal and crural activity during hypoxic and hypercapnic stimulated breathing revealed different, stimulant-specific activities of the segments; hypoxia elicited prominent crural post inspiratory activity (PIIA). During thermal panting, peak crural shortening was out of phase with costal shortening and inspiratory airflow. This unique segmental asynchrony may represent a natural analog to high frequency ventilation.
We conclude that costal and crural diaphragm segments can function as individual segment-muscles, exhibiting distinctive, differential activities under certain conditions of respiration.
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Brown, Jacob D. "Liver Kinase B1/AMP-Activated Protein Kinase Signaling in the Diaphragm." BYU ScholarsArchive, 2010. https://scholarsarchive.byu.edu/etd/2543.
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The Liver Kinase B1 (LKB1)/AMP-Activated Protein Kinase (AMPK) signaling pathway is a major regulator of skeletal muscle metabolic processes. During exercise, LKB1-mediated phosphorylation of AMPK leads to its activation, promoting mitochondrial biogenesis and glucose transport, among other effects. The roles of LKB1 and AMPK have not been fully characterized in the diaphragm. Two methods of AMPK activation were used to characterize LKB1/AMPK signaling in diaphragms from muscle-specific LKB1 knockout (KO) and littermate control (C) mice: (1) acute injection of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) and (2) 5-min direct electrical stimulation (ES) of the diaphragm. Diaphragms were excised 60 minutes post-AICAR injection and immediately after ES. AMPK phosphorylation increased with AICAR and ES in C but not KO mice. Acetyl CoA carboxylase (ACC) phosphorylation increased with AICAR in C but not KO mice, but increased in both genotypes with ES. While the majority of mitochondrial enzyme levels were lower in KO diaphragms, uncoupling protein 3 (UCP-3) levels were not different between genotypes. A IIx to IIb fiber type switch was observed in KO diaphragms. While in vitro peak force generation was similar between genotypes, KO diaphragms fatigued more quickly and had an impaired ability to recover. In conclusion, LKB1 regulates AMPK phosphorylation, mitochondrial enzyme expression, fiber type distribution, as well as recovery of the diaphragm from fatigue.
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Faltus, Robert E. "The changes in the force-frequency and length-tension relationship of rat diaphragm in vitro following repetitive stimulation /." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61880.
Full textBooks on the topic "Diaphragm – Physiology"
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Criswell, David S. Mechanisms of contractile dysfunction in the senescent rat diaphragm. 1994.
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Mechanisms of contractile dysfunction in the senescent rat diaphragm. 1994.
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Mechanisms of contractile dysfunction in the senescent rat diaphragm. 1994.
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Mechanisms of contractile dysfunction in the senescent rat diaphragm. 1994.
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Breslin, Eileen Hanafin. DIAPHRAGM AND PARASTERNAL MUSCLE RECRUITMENT, THORACOABDOMINAL MOTION, AND DYSPNEA RESPONSES TO UPPER EXTREMITY EXERCISE WITH NORMAL BREATHING AND INSPIRATORY RESISTANCE BREATHING. 1989.
Find full textBook chapters on the topic "Diaphragm – Physiology"
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Goligher, Ewan C. "Diaphragm Ultrasound: Physiology and Applications." In Cardiopulmonary Monitoring, 521–32. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73387-2_35.
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Macklem, P. T. "Inspiratory muscle physiology, with particular regard to the diaphragm." In Respiratory Muscles in Chronic Obstructive Pulmonary Disease, 23–34. London: Springer London, 1988. http://dx.doi.org/10.1007/978-1-4471-3850-1_2.
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Vassilakopoulos, Theodoros. "Ventilator-induced diaphragm dysfunction: the clinical relevance of animal models." In Applied Physiology in Intensive Care Medicine, 327–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01769-8_48.
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Vassilakopoulos, Theodoros. "Ventilator-induced diaphragm dysfunction: the clinical relevance of animal models." In Applied Physiology in Intensive Care Medicine 2, 197–206. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28233-1_20.
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Shaher, Abdulaziz. "Thoracoabdominal Compartment Syndrome." In A Comprehensive Review of Compartment Syndrome [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97307.
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As we advance our knowledge in understanding abdominal compartment syndrome, it is worth going back to revisit our basic embryologic development of the main determinant of the abdominal and thoracic cavities, i.e., the diaphragm. The abdominal and thoracic cavities used to be one cavity at some stage of the embryonic life — “intraembryonic coelom” — before the “septum transversum” — diaphragmatic origin — divided it into two cavities. Therefore, if a condition develops that will impair the diaphragm from separating the cavities, leading to the possibility of pressures to transmit from one cavity to another, this becomes relevant as abdominal compartment syndrome. Diaphragmatic eventration is a congenital developmental defect in the muscular portion of the diaphragm with preserved attachments to the sternum, ribs, and dorsolumbar spine, leading to a semi-membranous diaphragm that anatomically separates the two cavities, but not physiologically. In the case of high abdominal pressure, the pressure will transmit to the thoracic cavity, causing derangement in both the anatomy and physiology. This was reported and named “Thoracoabdominal Compartment Syndrome”.
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Davies, Jamie A. "6. From thought to action." In Human Physiology: A Very Short Introduction, 89–103. Oxford University Press, 2021. http://dx.doi.org/10.1093/actrade/9780198869887.003.0006.
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This chapter addresses muscles. The ultimate result of sensation and thought is usually some kind of action, be it moving the whole body; manipulating an object with the hand; or moving diaphragm, mouth, tongue, and voice-box to speak. All of these depend on muscles which, in their various forms, provide a nearly universal means for the nervous system to control the body and the world. Muscle cells are highly adapted for turning chemical energy into mechanical force. The chapter then looks at skeletal muscle and the musculoskeletal system. Some muscles are arranged circumferentially around a cavity. Two examples of this are the heart and the gut.
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Harrison, Dr Mark. "Endocrine physiology." In Revision Notes for MCEM Part A, 329–39. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199583836.003.0037.
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6.1 Pituitary function, 330 6.2 Adrenal function, 333 6.3 Endocrine pancreas, 335 6.4 Thyroid physiology, 337 6.5 Calcium and bone physiology, 338 • The pituitary sits in the sella turcica (pituitary fossa, part of the sphenoid bone). See Figure C.6.1. ▪ Separated from the brain by the diaphragma sellae (a reflection of dura mater)....
Conference papers on the topic "Diaphragm – Physiology"
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Arun, C. P. "The Covenant of NOA: Neighbouring Organ Assistance (NOA) to Soft Tissue Structures." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-42731.
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Soft tissues hollow structures are capable of collapsing not only under their own power but also able to employ movements of their neighbors to aid their function of propelling content. An intensive study of collapsible hollow structures is a recent development and no general law recognising this convenient coupling of the dynamics of neighboring organs is available in the literature. The literature on whole organ physiology was analysed and examples of neighboring organs providing assistance to soft tissue structures was collected. We offer the title Covenant of NOA to the arrangement that soft tissue structures have with their neighbors. The calf muscle pump and parturition are obvious examples of NOA. From examining videocystometric recordings, we are able to offer, as the latest to a long list of known NOAs, the assistance of the pelvic diaphragm to the urinary bladder that aids the latter in emptying completely. The modeling of soft tissue hollow organs as functioning somewhat in isolation must be considered antediluvian. Very often, soft tissue structures come in pairs to implement NOA: it is time we too hearkened to the Covenant of NOA.
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Rice, Brenda L., Loutfi S. Aboussouan, and Rendell W. Ashton. "Clinical And Physiologic Characteristics Of Patients With Diaphragm Dysfunction Due To Neuralgic Amyotrophy: A Case Series." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5050.
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