Prevention of lung-to-lung aspiration during emergency thoracic surgery: an experimental study.

BACKGROUND: Lung separation is essential for an emergency thoracic surgery for massive hemoptysis. When using a double lumen tube (DLT), a commonly adopted lung separation device during thoracic surgery, a water-tight seal of endobronchial cuff is crucial to prevent lung-to-lung aspiration of blood. In this study, we investigated the fluid sealing characteristics of the endobronchial cuff of a DLT and examined the effect of gel lubrication on the fluid leakage beyond the endobronchial cuff of DLT. METHODS: An artificial tracheobronchial tree was intubated with a DLT. In the first phase of the study, the intra-cuff pressure of endobronchial cuff of DLT was set to 25, 50, or 100 cmH2O (n = 7, each), and the non-dependent bronchus was filled with 5 ml of water. Fluid leakage to the dependent bronchus beyond the endobronchial cuff was collected for 6 h. The time until leakage was first detected and the time until 100% leakage occurred were measured. In the second phase, the endobronchial cuff was coated with either saline (group C, n = 10) or lubricant gel (group GEL, n = 10), and the same parameters were measured. RESULTS: In the first phase of the study, the times to first leakage and 100% leakage at an intra-cuff pressure of 25 cmH2O were 21.0 (7.0 - 59.0) sec and 3.0 (2.0 - 4.0) min, respectively. Higher intra-cuff (50 and 100 cmH2O) resulted in longer time for the first leakage and 100% leakage, but the duration was not long enough for clinical purpose. In the second phase, all the DLTs in group C showed 100% fluid leakage during the 6-hour period. In contrast, in group GEL, fluid leakage beyond the endobronchial cuff was detected only in 50% of the DLTs and none of the DLT showed 100% fluid leakage during the study. Among the DLTs which exhibited fluid leakage, the time to first leakage was 252.0 (171.0-305.0) min and the leakage volume at the end of the study period was 0.3〔0.0-1.8〕ml. CONCLUSIONS: Endobronchial cuff of DLT cannot prevent fluid leakage beyond the endobronchial cuff, but lubricant gel coating on the endobronchial cuff can effectively reduce the lung-to-lung aspiration.

A peroxisome proliferator-activated receptor gamma agonist attenuates neurological deficits following spinal cord ischemia in rats.

OBJECTIVE: Neuroprotective effects of the peroxisome proliferator-activated receptor gamma (PPARγ) agonist in cerebral ischemia have been reported, but the effect of a PPARγ agonist on spinal cord ischemia has not been investigated. The objective of this study was to investigate the effect of a PPARγ agonist on spinal cord ischemia. Pioglitazone, a PPARγ agonist, was administered in a rat model of spinal cord ischemia, and the extent of neurological damage and histological alterations were assessed. METHODS: Forty-five rats were randomly enrolled into one of the three groups: (1) pioglitazone group (group PIO): rats were treated with pioglitazone 24 hours before ischemia; (2) control group (group C): rats were treated with the same volume of saline 24 hours before ischemia; and (3) sham group (group sham): rats were treated with the same volume of saline 24 hours before the sham surgery. Spinal cord ischemia was induced using a balloon-tipped catheter placed on the proximal descending aorta. Neurologic function was assessed using the motor deficit index (0 = normal, 6 = complete paralysis) during the 48 hours after reperfusion. Histological and biochemical evaluations were then performed. RESULTS: Compared with group C, group PIO presented with lower motor deficit index 48 hours after reperfusion (5.0 [4.0-6.0] vs 3.0 [2.0-3.0]; group C vs group PIO, respectively; P < .001). Group PIO presented with a higher number of normal motor neurons (10.7 [8.1-11.9] vs 14.7 [14.0-15.3]; group C vs group PIO, respectively; P = .009) and a smaller area of infarcts (48.4% [46.3%-54.0%] vs 16.8% [11.5%-18.3%]; group C vs group PIO, respectively; P = .009) when compared with group C. The degree of inflammatory reactions, assessed by microglia activities, was significantly reduced in group PIO. Oxidative stress level, assessed using malonydialdehyde assay, was significantly reduced in group PIO relative to group C (192.21% [173.5%-206.4%] of sham vs 141.1% [131.7%-152.1%] of sham; group C vs group PIO, respectively; P = .007). The sham group exhibited no abnormality upon neurological or histological examination. CONCLUSIONS: PPARγ agonist pioglitazone pretreatment significantly reduces infarct volume and attenuates neurological deficits following spinal cord ischemia. The possible mechanism of neuroprotection by PPARγ agonist may involve modulation of inflammatory reaction and oxidative stress.

Acute normovolemic hemodilution can aggravate neurological injury after spinal cord ischemia in rats.

BACKGROUND: Acute normovolemic hemodilution (ANH) is currently performed during thoracoabdominal aortic surgery. However, the effects of ANH on spinal cord ischemic injury are currently unknown. Because hemodilution below a certain level of hematocrit (Hct) aggravates the neurological damage after cerebral ischemia, we hypothesized that ANH may increase neurological damage after spinal cord ischemia. The aim of these experiments was to determine the effects of ANH on spinal cord ischemic injury. METHODS: Thirty male Sprague-Dawley rats were randomly assigned to 1 of the following 3 groups: no hemodilution (group C), target Hct level of 30% (group HD30), and target Hct level of 25% (group HD25). ANH was performed upon withdrawal of blood and simultaneous replacement with the same volume with hydroxyethyl starch. Spinal cord ischemia and reperfusion were induced by using a balloon-tipped catheter placed in the descending thoracic aorta, and changes in mean arterial blood pressure were recorded. Neurological function of the hindlimbs was evaluated for 7 days and recorded using a motor deficit score (MDS) (0 = normal; 5 = complete paraplegia). The number of motor neurons within the spinal cord was counted after final MDS evaluation. RESULTS: Group HD25 developed hypotension during the latter part of the ANH procedure. Group C and group HD30 experienced 3 minutes of reperfusion hypotension, whereas 6 minutes of hypotension was observed in group HD25. Two rats in group HD25 died during the experimental period. Seven days after reperfusion, the MDS of group C, group HD30, and group HD25 was 1.0 (0.5-2.0), 1.0 (0.5-2.0), and 4.0 (2.8-4.2) (median [95% confidence interval]), respectively. Group HD25 showed significantly higher MDS compared with group C (corrected P = 0.0018; 95% CI for median difference = 1.0-3.5). Motor neuron numbers in the anterior horns of group C, group HD30, and group HD25 were 26.5 (25.0-27.5), 23.5 (22.0-26.5), and 12.5 (8.4-16.6) (median [95% CI]), respectively. Motor neuron numbers of group HD25 were significantly lower than those of group C (corrected P < 0.0001; 95% CI for median difference = 9.0-18.0). CONCLUSION: The results of the present study indicate that intraoperative ANH to an Hct of 25%, combined with coincident hypotension, caused a delayed recovery of baseline mean arterial blood pressure during the reperfusion period and aggravated neurological outcome after spinal cord ischemia.