Regional distribution of blood flow within the diaphragm

Brancatisano, A.; Amis, Terence C.; Tully, A.; Kelly, W. T.; Engel, L. A.

doi:10.1152/jappl.1991.71.2.583

Cited by 34 publications

(28 citation statements)

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“…Reductions in vascular conductance (i.e., blood flow÷ MAP) paralleled changes in blood flow with the duration MV (Figure 1B). Consistent with what others have found (29, 30) there was a marked heterogeneity in regional distribution of blood flow within the diaphragm, with all regions demonstrating a reduced blood flow (Figure 2) and vascular conductance (supplemental Figure 2) after 6 hrs of MV versus both spontaneous breathing and 30 min of MV. Blood flow and vascular conductance to the intercostal muscles, which would be subject to similar alterations in intrathoracic pressures as the diaphragm, did not change across the measurement period (Figure 3A &B).…”

Section: Resultssupporting

confidence: 90%

Mechanical ventilation reduces rat diaphragm blood flow and impairs oxygen delivery and uptake*

Davis

Bruells

Stabley

et al. 2012

Critical Care Medicine

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Objectives Although mechanical ventilation (MV) is a life-saving intervention in patients suffering from respiratory failure, prolonged MV is often associated with numerous complications including problematic weaning. In contracting skeletal muscle, inadequate O2 supply can limit oxidative phosphorylation resulting in muscular fatigue. However, whether prolonged MV results in decreased diaphragmatic blood and induces an O2 supply-demand imbalance in the diaphragm remains unknown. Design We tested the hypothesis that prolonged controlled MV results in a time-dependent reduction in rat diaphragmatic blood flow and microvascular PO2 and that prolonged MV would diminish the diaphragm’s ability to increase blood flow in response to muscular contractions. Measurements and Main Results Compared to 30 min of MV, 6 hrs of MV resulted in a 75% reduction in diaphragm blood flow (via radiolabeled microspheres), which did not occur in the intercostal muscle or high-oxidative hindlimb muscle (e.g., soleus). There was also a time-dependent decline in diaphragm microvascular PO2 (via phosphorescence quenching). Further, when contrasted to 30 min of MV, 6 hrs of MV significantly compromised the diaphragm’s ability to increase blood flow during electrically-induced contractions which resulted in a ~80% reduction in diaphragm O2 uptake. In contrast, 6 hrs of spontaneous breathing in anesthetized animals did not alter diaphragm blood flow or the ability to augment flow during electrically-induced contractions. Conclusions These new and important findings reveal that prolonged MV results in a time-dependent decrease in the ability of the diaphragm to augment blood flow to match O2 demand in response to contractile activity and could be a key contributing factor to difficult weaning. Although additional experiments are required to confirm, it is tempting to speculate that this ventilator-induced decline in diaphragmatic oxygenation could promote a hypoxia-induced generation of reactive oxygen species in diaphragm muscle fibers and contribute to ventilator-induced diaphragmatic atrophy and contractile dysfunction.

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Section: Resultssupporting

confidence: 90%

Mechanical ventilation reduces rat diaphragm blood flow and impairs oxygen delivery and uptake*

Davis

Bruells

Stabley

et al. 2012

Critical Care Medicine

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“…Trend of arterial pH, arterial PCO2 (PaCO 2 ), and bicarbonate (HCO3 Ϫ ) in control animals and animals subjected to 0 cmH2O continuous positive airway pressure (CPAP) for 1 day (1d-CPAP) and 3 days (3d-CPAP) and controlled mechanical ventilation (CMV) for 1 day (1d-CMV) and 3 days (3d-CMV). Values are means Ϯ SE; n ϭ 6 animals.…”

mentioning

confidence: 99%

Altered diaphragm contractile properties with controlled mechanical ventilation

Sassoon

Caiozzo

Mańka

et al. 2002

Journal of Applied Physiology

253

236

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This study shows that, over time, diaphragm inactivity with controlled mechanical ventilation (CMV) decreases diaphragm force and produces myofibril damage contributing to the reduced force. We measured in vivo and in vitro diaphragm contractile and morphological properties in 30 sedated rabbits grouped (n = 6) as follows: 1 or 3 days of CMV, 1 or 3 days of 0 cmH(2)O continuous positive airway pressure, and control. The CMV rate was set sufficient to suppress diaphragm electrical activity. Compared with the control group, phrenic-stimulated maximum transdiaphragmatic pressure did not decrease with continuous positive airway pressure but decreased to 63% after 1 day of CMV and to 49% after 3 days of CMV. The in vitro tetanic force decreased to 86% after 1 day of CMV and to 44% after 3 days of CMV. After 3 days of CMV, significant myofibril damage occurred in the diaphragm but not in the soleus. The decrease in tetanic force correlated with the volume density of abnormal myofibrils. We conclude that CMV had a detrimental effect on diaphragm contractile properties.

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“…Regional blood flow in the diaphragm is heterogeneous and is greatest in the medial aspects and lowest in the most dorsal and ventral regions [30]. As we created the defect and implanted the SIS material in the central region of the left hemidiaphragm, it is tempting to speculate that this may be an area where insufficient blood flow impedes the proper vascularization and maintenance of implant growth.…”

Section: Discussionmentioning

confidence: 99%