Ultrastructural changes in pneumocyte type II cells following traumatic brain injury in rats

Abstract

The data suggested that ultrastructural damage is obvious at 2 h and deteriorates with time. The electron microscopic scoring model worked well in depicting the traumatic changes, which were supported by lipid peroxidation. Further experiments are needed to determine the exact outcome after brain death model.

Pulmonary Complications in Patients with Brain Injury

“…All of this would make lungs more susceptible to secondary damage ("double lesion model") that could result from initial trauma, respiratory strategy, infection, transfusion, etc. [19][20][21][22][23] These experimental and clinical data support the hypothesis that after severe brain injury eventually leading to brain death, preclinical lung injury occurs. The catecholamine storm and the systemic production of inflammatory mediators create a systemic inflammatory environment where the lung is more susceptible to further injurious stimuli, such as ventilatory settings, infections, and transfusions.…”

“…Such inflammatory processes could in turn worsen the initial brain damage, harm distant organs and cause multiorgan dysfunction. [19][20][21][22][23] After severe brain injury, respiratory failure is the commonest associated dysfunction. In such cases, pathophysiological processes to be considered are: preclinical lung injury, altered capillary permeability with activated neutrophils and macrophages migrating into the airways and alveolar spaces, increased concentrations of pro-inflammatory cytokines in bronchoalveolar lavage and damage to type II pneumocytes -characterized by intense cell vacuolation and lipid peroxidation of lung tissue that causes lysis of the cell membranes.…”

Respiratory mechanics in brain injury: A review

“…Ultrastructural changes in type Ⅱ pneumocytes along with an inflammatory response in the lung, similar to that induced by high tidal volume ventilation, have been observed in animals within the first hours of traumatic brain injury [7] . Similarly, alterations in lung architecture, such as alveolar hemorrhage, proteinaceous debris and neutrophilic infiltration were detected by Weber et al [8] in experimental traumatic brain damage.…”

“…A "double hit" model could explain the development of organ failure associated hypertension [10] . Finally, atelectasis, associated with anesthesia and paralysis or with impaired production/function of pulmonary surfactant as a result of brain damage, as well as alterations in chest wall mechanics, may be additional potential explanations for the increased Est,rs in this setting [7,47,48,52,53] .…”

“…Mascia et al [60] found that BD patients who subsequently developed ARDS had at baseline an abnormal PaO2/ FiO2 ratio (< 300 mmHg), and that hypoxemia was the strongest independent predictor of ARDS development. Ventilation/perfusion (V/Q) mismatch and shunt, the main pathophysiological mechanisms of hypoxemia [61] ensuing from airway closure and atelectasis due to lung surfactant depletion [7,53] and/or increased extravascular lung water [10,47] might explain oxygenation impairment.…”