Negative Pressure Ventilation and Positive Pressure Ventilation Promote Comparable Levels of Ventilator-induced Diaphragmatic Dysfunction in Rats

2013 ◽  
Vol 119 (3) ◽  
pp. 652-662 ◽  
Author(s):  
Christian S. Bruells ◽  
Ashley J. Smuder ◽  
Lucy K. Reiss ◽  
Matthew B. Hudson ◽  
William Bradley Nelson ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Negative Pressure ◽  
Positive Pressure Ventilation ◽  
Cross Sectional Area ◽  
Contractile Properties ◽  
Positive Pressure ◽  
Sectional Area ◽  
Diaphragmatic Dysfunction ◽  
Cross Sectional ◽  
Negative Pressure Ventilation

Abstract Background: Mechanical ventilation is a life-saving intervention for patients with respiratory failure. Unfortunately, a major complication associated with prolonged mechanical ventilation is ventilator-induced diaphragmatic atrophy and contractile dysfunction, termed ventilator-induced diaphragmatic dysfunction (VIDD). Emerging evidence suggests that positive pressure ventilation (PPV) promotes lung damage (ventilator-induced lung injury [VILI]), resulting in the release of signaling molecules that foster atrophic signaling in the diaphragm and the resultant VIDD. Although a recent report suggests that negative pressure ventilation (NPV) results in less VILI than PPV, it is unknown whether NPV can protect against VIDD. Therefore, the authors tested the hypothesis that compared with PPV, NPV will result in a lower level of VIDD. Methods: Adult rats were randomly assigned to one of three experimental groups (n = 8 each): (1) acutely anesthetized control (CON), (2) 12 h of PPV, and (3) 12 h of NPV. Dependent measures included indices of VILI, diaphragmatic muscle fiber cross-sectional area, diaphragm contractile properties, and the activity of key proteases in the diaphragm. Results: Our results reveal that no differences existed in the degree of VILI between PPV and NPV animals as evidenced by VILI histological scores (CON = 0.082 ± 0.001; PPV = 0.22 ± 0.04; NPV = 0.25 ± 0.02; mean ± SEM). Both PPV and NPV resulted in VIDD. Importantly, no differences existed between PPV and NPV animals in diaphragmatic fiber cross-sectional area, contractile properties, and the activation of proteases. Conclusion: These results demonstrate that NPV and PPV result in similar levels of VILI and that NPV and PPV promote comparable levels of VIDD in rats.

scholarly journals Effects of Various Modes of Mechanical Ventilation in Normal Rats

2014 ◽  
Vol 120 (4) ◽  
pp. 943-950 ◽  
Author(s):  
Matteo Pecchiari ◽  
Ario Monaco ◽  
Antonia Koutsoukou ◽  
Patrizia Della Valle ◽  
Guendalina Gentile ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Negative Pressure ◽  
Positive Pressure Ventilation ◽  
Lung Mechanics ◽  
Whole Body ◽  
Positive Pressure ◽  
Negative Pressure Ventilation ◽  
Cytokine Levels

Abstract Background: Recent studies in healthy mice and rats have reported that positive pressure ventilation delivered with physiological tidal volumes at normal end-expiratory volume worsens lung mechanics and induces cytokine release, thus suggesting that detrimental effects are due to positive pressure ventilation per se. The aim of this study in healthy animals is to assess whether these adverse outcomes depend on the mode of mechanical ventilation. Methods: Rats were subjected to 4 h of spontaneous, positive pressure, and whole-body or thorax-only negative pressure ventilation (N = 8 per group). In all instances the ventilatory pattern was that of spontaneous breathing. Lung mechanics, cytokines concentration in serum and broncho–alveolar lavage fluid, lung wet-to-dry ratio, and histology were assessed. Values from eight animals euthanized shortly after anesthesia served as control. Results: No evidence of mechanical ventilation–dependent lung injury was found in terms of lung mechanics, histology, or wet-to-dry ratio. Relative to control, cytokine levels and recruitment of polymorphonuclear leucocytes increased slightly, and to the same extent with spontaneous, positive pressure, and whole-body negative pressure ventilation. Thorax-only negative pressure ventilation caused marked chest and lung distortion, reversible increase of lung elastance, and higher polymorphonuclear leucocyte count and cytokine levels. Conclusion: Both positive and negative pressure ventilation performed with tidal volumes and timing of spontaneous, quiet breathing neither elicit an inflammatory response nor cause morpho-functional alterations in normal animals, thus supporting the notion of the presence of a critical volume threshold above which acute lung injury ensues. Distortion of lung parenchyma can induce an inflammatory response, even in the absence of volotrauma.

scholarly journals Assessment of Internal Diameter and Cross-sectional Area of Right Internal Jugular Vein Pre-induction and Post-intubation

2005 ◽  
Vol 33 (3) ◽  
pp. 381-383 ◽  
Author(s):  
S. Manikappa ◽  
C. Cokis
Keyword(s):  
Internal Jugular Vein ◽  
Positive Pressure Ventilation ◽  
Jugular Vein ◽  
Cross Sectional Area ◽  
Positive Pressure ◽  
Internal Diameter ◽  
Operating Table ◽  
Sectional Area ◽  
Cross Sectional ◽  
Post Intubation

This prospective observational study compared the internal diameter and cross-sectional area of the right internal jugular vein pre-induction and post-initiation of positive pressure ventilation. Twenty patients undergoing coronary artery bypass surgery were studied. Measurements were taken with the operating table tipped to 30° head down and the head turned 10° away from the side of cannulation. There was a statistically significant increase in both measurements post-intubation. This study suggests that it may be easier and safer to perform cannulation of RIJV after institution of intermittent positive pressure ventilation in patients in the modified Trendelenburg position.

scholarly journals Neurally adjusted ventilatory assist mitigates ventilator-induced diaphragm injury in rabbits

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Tatsutoshi Shimatani ◽  
Nobuaki Shime ◽  
Tomohiko Nakamura ◽  
Shinichiro Ohshimo ◽  
Justin Hotz ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Caspase 3 ◽  
Cross Sectional Area ◽  
Neurally Adjusted Ventilatory Assist ◽  
Sectional Area ◽  
Diaphragmatic Dysfunction ◽  
Cross Sectional ◽  
Ventilatory Assist ◽  
The Cross

Abstract Background Ventilator-induced diaphragmatic dysfunction is a serious complication associated with higher ICU mortality, prolonged mechanical ventilation, and unsuccessful withdrawal from mechanical ventilation. Although neurally adjusted ventilatory assist (NAVA) could be associated with lower patient-ventilator asynchrony compared with conventional ventilation, its effects on diaphragmatic dysfunction have not yet been well elucidated. Methods Twenty Japanese white rabbits were randomly divided into four groups, (1) no ventilation, (2) controlled mechanical ventilation (CMV) with continuous neuromuscular blockade, (3) NAVA, and (4) pressure support ventilation (PSV). Ventilated rabbits had lung injury induced, and mechanical ventilation was continued for 12 h. Respiratory waveforms were continuously recorded, and the asynchronous events measured. Subsequently, the animals were euthanized, and diaphragm and lung tissue were removed, and stained with Hematoxylin-Eosin to evaluate the extent of lung injury. The myofiber cross-sectional area of the diaphragm was evaluated under the adenosine triphosphatase staining, sarcomere disruptions by electron microscopy, apoptotic cell numbers by the TUNEL method, and quantitative analysis of Caspase-3 mRNA expression by real-time polymerase chain reaction. Results Physiological index, respiratory parameters, and histologic lung injury were not significantly different among the CMV, NAVA, and PSV. NAVA had lower asynchronous events than PSV (median [interquartile range], NAVA, 1.1 [0–2.2], PSV, 6.8 [3.8–10.0], p = 0.023). No differences were seen in the cross-sectional areas of myofibers between NAVA and PSV, but those of Type 1, 2A, and 2B fibers were lower in CMV compared with NAVA. The area fraction of sarcomere disruptions was lower in NAVA than PSV (NAVA vs PSV; 1.6 [1.5–2.8] vs 3.6 [2.7–4.3], p < 0.001). The proportion of apoptotic cells was lower in NAVA group than in PSV (NAVA vs PSV; 3.5 [2.5–6.4] vs 12.1 [8.9–18.1], p < 0.001). There was a tendency in the decreased expression levels of Caspase-3 mRNA in NAVA groups. Asynchrony Index was a mediator in the relationship between NAVA and sarcomere disruptions. Conclusions Preservation of spontaneous breathing using either PSV or NAVA can preserve the cross sectional area of the diaphragm to prevent atrophy. However, NAVA may be superior to PSV in preventing sarcomere injury and apoptosis of myofibrotic cells of the diaphragm, and this effect may be mediated by patient-ventilator asynchrony.

scholarly journals PROLONGED INVASIVE MECHANICAL VENTILATION IS ASSOCIATED WITH REDUCTION IN RESPIRATORY MUSCLE CROSS-SECTIONAL AREA

CHEST Journal ◽  
2020 ◽  
Vol 158 (4) ◽  
pp. A579
Author(s):  
Connor Wakefield ◽  
Emily Hejna ◽  
Sarah Jochum ◽  
Sarah Peterson ◽  
Palmi Shah ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Muscle ◽  
Invasive Mechanical Ventilation ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Cross Sectional ◽  
Muscle Cross Sectional Area

Contractile properties of rat, rhesus monkey, and human type I muscle fibers

1997 ◽  
Vol 272 (1) ◽  
pp. R34-R42 ◽  
Author(s):  
J. J. Widrick ◽  
J. G. Romatowski ◽  
M. Karhanek ◽  
R. H. Fitts
Keyword(s):  
Rhesus Monkey ◽  
Body Mass ◽  
Fiber Length ◽  
Peak Power ◽  
Cross Sectional Area ◽  
Contractile Properties ◽  
Type I ◽  
Sectional Area ◽  
Shortening Velocity ◽  
Cross Sectional

It is well known that skeletal muscle intrinsic maximal shortening velocity is inversely related to species body mass. However, there is uncertainty regarding the relationship between the contractile properties of muscle fibers obtained from commonly studied laboratory animals and those obtained from humans. In this study we determined the contractile properties of single chemically skinned fibers prepared from rat, rhesus monkey, and human soleus and gastrocnemius muscle samples under identical experimental conditions. All fibers used for analysis expressed type I myosin heavy chain as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Allometric coefficients for type I fibers from each muscle indicated that there was little change in peak tension (force/fiber cross-sectional area) across species. In contrast, both soleus and gastrocnemius type I fiber maximal unloaded shortening velocity (Vo), the y-intercept of the force-velocity relationship (Vmax), peak power per unit fiber length, and peak power normalized for fiber length and cross-sectional area were all inversely related to species body mass. The present allometric coefficients for soleus fiber Vo (-0.18) and Vmax (-0.11) are in good agreement with published values for soleus fibers obtained from common laboratory and domesticated mammals. Taken together, these observations suggest that the Vo of slow fibers from quadrupeds and humans scale similarly and can be described by the same quantitative relationships. These findings have implications in the design and interpretation of experiments, especially those that use small laboratory mammals as a model of human muscle function.

Changes in the human muscle force-velocity relationship in response to resistance training and subsequent detraining

2005 ◽  
Vol 99 (1) ◽  
pp. 87-94 ◽  
Author(s):  
Lars L. Andersen ◽  
Jesper L. Andersen ◽  
S. Peter Magnusson ◽  
Charlotte Suetta ◽  
Jørgen L. Madsen ◽  
...  
Keyword(s):  
Resistance Training ◽  
Knee Extension ◽  
Limb Movement ◽  
Cross Sectional Area ◽  
Contractile Properties ◽  
Type I ◽  
Maximal Velocity ◽  
Sectional Area ◽  
Cross Sectional ◽  
Muscle Cross Sectional Area

Previous studies show that cessation of resistance training, commonly known as “detraining,” is associated with strength loss, decreased neural drive, and muscular atrophy. Detraining may also increase the expression of fast muscle myosin heavy chain (MHC) isoforms. The present study examined the effect of detraining subsequent to resistance training on contractile performance during slow-to-medium velocity isokinetic muscle contraction vs. performance of maximal velocity “unloaded” limb movement (i.e., no external loading of the limb). Maximal knee extensor strength was measured in an isokinetic dynamometer at 30 and 240°/s, and performance of maximal velocity limb movement was measured with a goniometer during maximal unloaded knee extension. Muscle cross-sectional area was determined with MRI. Electromyographic signals were measured in the quadriceps and hamstring muscles. Twitch contractions were evoked in the passive vastus lateralis muscle. MHC isoform composition was determined with SDS-PAGE. Isokinetic muscle strength increased 18% ( P < 0.01) and 10% ( P < 0.05) at slow and medium velocities, respectively, along with gains in muscle cross-sectional area and increased electromyogram in response to 3 mo of resistance training. After 3 mo of detraining these gains were lost, whereas in contrast maximal unloaded knee extension velocity and power increased 14% ( P < 0.05) and 44% ( P < 0.05), respectively. Additionally, faster muscle twitch contractile properties along with an increased and decreased amount of MHC type II and MHC type I isoforms, respectively, were observed. In conclusion, detraining subsequent to resistance training increases maximal unloaded movement speed and power in previously untrained subjects. A phenotypic shift toward faster muscle MHC isoforms (I → IIA → IIX) and faster electrically evoked muscle contractile properties in response to detraining may explain the present results.

scholarly journals Lower-body negative pressure decreases noninvasively measured intracranial pressure and internal jugular vein cross-sectional area during head-down tilt

2017 ◽  
Vol 123 (1) ◽  
pp. 260-266 ◽  
Author(s):  
William Watkins ◽  
Alan R. Hargens ◽  
Shannon Seidl ◽  
Erika Marie Clary ◽  
Brandon R. Macias
Keyword(s):  
Intracranial Pressure ◽  
Tympanic Membrane ◽  
Internal Jugular Vein ◽  
Negative Pressure ◽  
Jugular Vein ◽  
Lower Body Negative Pressure ◽  
Cross Sectional Area ◽  
Lower Body ◽  
Sectional Area ◽  
Cross Sectional

Long-term spaceflight induces a near visual acuity change in ~50% of astronauts. In some crew members, postflight cerebrospinal fluid (CSF) opening pressures by lumbar puncture are as high as 20.9 mmHg; these members demonstrated optic disc edema. CSF communicates through the cochlear aqueduct to affect perilymphatic pressure and tympanic membrane motion. We hypothesized that 50 mmHg of lower-body negative pressure (LBNP) during 15° head-down tilt (HDT) would mitigate elevations in internal jugular vein cross-sectional area (IJV CSA) and intracranial pressure (ICP). Fifteen healthy adult volunteers were positioned in sitting (5 min), supine (5 min), 15° HDT (5 min), and 15° HDT with LBNP (10 min) postures for data collection. Evoked tympanic membrane displacements (TMD) quantified ICP noninvasively. IJV CSA was measured using standard ultrasound techniques. ICP and IJV CSA increased significantly from the seated upright to the 15° HDT posture ( P < 0.05), and LBNP mitigated these increases. LBNP at 25 mmHg reduced ICP during HDT (TMD of 322.13 ± 419.17 nl) to 232.38 ± 445.85 nl, and at 50 mmHg ICP was reduced further to TMD of 199.76 ± 429.69 nl. In addition, 50 mmHg LBNP significantly reduced IJV CSA (1.50 ± 0.33 cm2) during 15° HDT to 0.83 ± 0.42 cm2. LBNP counteracts the headward fluid shift elevation of ICP and IJV CSA experienced during microgravity as simulated by15° HDT. These data provide quantitative evidence that LBNP shifts cephalic fluid to the lower body, reducing IJV CSA and ICP. NEW & NOTEWORTHY The current study provides new evidence that 25 or 50 mmHg of lower body negative pressure reduces jugular venous pooling and intracranial pressure during simulated microgravity. Therefore, spaceflight countermeasures that sequester fluid to the lower body may mitigate cephalic venous congestion and vision impairment.

scholarly journals Effects of high- and low-velocity resistance training on the contractile properties of skeletal muscle fibers from young and older humans

2011 ◽  
Vol 111 (4) ◽  
pp. 1021-1030 ◽  
Author(s):  
Dennis R. Claflin ◽  
Lisa M. Larkin ◽  
Paul S. Cederna ◽  
Jeffrey F. Horowitz ◽  
Neil B. Alexander ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Cross Sectional Area ◽  
Contractile Properties ◽  
Sectional Area ◽  
Low Velocity ◽  
Cross Sectional ◽  
Men And Women ◽  
The Cross

A two-arm, prospective, randomized, controlled trial study was conducted to investigate the effects of movement velocity during progressive resistance training (PRT) on the size and contractile properties of individual fibers from human vastus lateralis muscles. The effects of age and sex were examined by a design that included 63 subjects organized into four groups: young (20–30 yr) men and women, and older (65–80 yr) men and women. In each group, one-half of the subjects underwent a traditional PRT protocol that involved shortening contractions at low velocities against high loads, while the other half performed a modified PRT protocol that involved contractions at 3.5 times higher velocity against reduced loads. Muscles were sampled by needle biopsy before and after the 14-wk PRT program, and functional tests were performed on permeabilized individual fiber segments isolated from the biopsies. We tested the hypothesis that, compared with low-velocity PRT, high-velocity PRT results in a greater increase in the cross-sectional area, force, and power of type 2 fibers. Both types of PRT increased the cross-sectional area, force, and power of type 2 fibers by 8–12%, independent of the sex or age of the subject. Contrary to our hypothesis, the velocity at which the PRT was performed did not affect the fiber-level outcomes substantially. We conclude that, compared with low-velocity PRT, resistance training performed at velocities up to 3.5 times higher against reduced loads is equally effective for eliciting an adaptive response in type 2 fibers from human skeletal muscle.

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