We surveyed the incidence of blood pump diaphragm damage (rupture or crack) in the NIPRO-ventricular assist device (VAD). In the cases in which rupture or suspected blood pump crack was detected, we disassembled the pumps to visually check the condition of the diaphragm after replacement or use. Of 366 blood pumps surveyed, diaphragm damage was observed in 2.7 %. The duration of use of the blood pumps with diaphragm damage was significantly longer than that of pumps without damage. The incidence of diaphragm damage increased with longer duration of use. On the basis of these findings, blood pump diaphragm damage in the NIPRO-VAD may be associated with duration of use. However, some blood pumps were used for prolonged periods without diaphragm damage. All blood pumps with damage had a crack in the diaphragm on the air chamber side near the diaphragm-housing (D-H) junction. Cracks were not found in any specific part of the diaphragm. In blood pumps with diaphragm rupture, the crack had a through-hole reaching the blood-contacting surface. Although we were unable to identify the causes of the cracks, it is suggested that when a crack appears in the diaphragm it will gradually expand and eventually lead to rupture. If a crack is detected in a blood pump, we advocate replacing the pump before it grows. When the NIPRO-VAD is used, it is necessary to keep in mind that blood pump diaphragm damage may occur.
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http://dx.doi.org/10.1007/s10047-012-0657-1 | DOI Listing |
Anesthesiology
January 2025
Department of Anesthesiology and Critical Care Medicine B (DAR B), Saint-Eloi Hospital, University Teaching Hospital of Montpellier, 80 avenue Augustin Fliche, 34295 Montpellier, France.
Background: Long-term controlled mechanical ventilation (CMV) in intensive care unit (ICU) induces ventilatory-induced-diaphragm-dysfunction (VIDD). The transition from CMV to assisted mechanical ventilation is a challenge that requires clinicians to balance over-assistance and under-assistance. While the effects of over-assistance on the diaphragm are well known, we aimed to assess the impact of under-assistance on diaphragm function and structure in piglet model with pre-existing VIDD (after long-term CMV) or without VIDD (short-term CMV).
View Article and Find Full Text PDFMuscle Nerve
January 2025
Department of Anatomy, Federal University of Alfenas (UNIFAL-MG), Alfenas, Brazil.
Introduction/aims: Duchenne muscular dystrophy (DMD) is caused by pathogenic variants in the DMD gene, making muscle fibers susceptible to contraction-induced membrane damage. Given the potential beneficial action of cannabidiol (CBD), we evaluated the in vitro effect of full-spectrum CBD oil on the viability of dystrophic muscle fibers and the in vivo effect on myopathy of the mdx mouse, a DMD model.
Methods: In vitro, dystrophic cells from the mdx mouse were treated with full-spectrum CBD oil and assessed with cell viability and cytotoxic analyses.
Life Sci
January 2025
Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address:
The pandemic due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in over 7 million global fatalities and billions of individuals diagnosed with COVID-19. Acute and chronic muscle impairment associated with SARS-CoV-2 infection affected a substantial number of patients, leading to the development of symptoms such as fatigue, muscle pain, and exercise intolerance. Our study introduces an animal model to improve understanding of the pathogenicity caused by SARS-CoV-2 in human skeletal muscle.
View Article and Find Full Text PDFEur J Ophthalmol
January 2025
Dept of Vitreoretinal Diseases, Sankara Nethralaya, Chennai, India.
J Cachexia Sarcopenia Muscle
February 2025
Sprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Canada.
Background: Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting that leads to diminished lifespan. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells (MuSC) significantly contributes to disease progression.
Methods: Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and MuSC function in dystrophin-deficient skeletal muscle using immunohistology, isometric force measurements, transcriptomic analysis and transplantation assays.
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