A long-term ventricular assist device utilizing a magnetic bearing system and implantable physiologic controller.
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Cardiac Output, Low↗
Biomedical subjects
C G Tribble
Publications and source records attributed to C G Tribble.
A technique for the treatment of sternal infections using the Vacuum Assisted Closure device.
BACKGROUND: Sternal infections after median sternotomy remain a serious cause of postoperative morbidity and mortality. The treatment of sternal infections has evolved over the past few decades, and now aggressive surgical debridement with rotational muscle flap closure has provided an acceptable means of managing this complication. However, there are several disadvantages with this approach, mainly related to the morbidity associated with serial debridements with dressing changes and open packing until the wound is closed. Other disadvantages include potential morbidity and mortality associated with the shearing forces between the beating heart and the debrided sternal edges, and the need to paralyze the patient during the period after debridement. METHODS: Our method of managing sternal infections is based on the triad of prompt surgical debridement, serial quantitative wound cultures, and the use of the Vacuum Assisted Closure (VAC) device (KCI International, San Antonio, TX). Following debridement and irrigation, a biopsy of the healthy appearing bone is sent for quantitative culture. If culture results are favorable, the wound is then fitted with the VAC device, which consists of a non-collapsible, open-cell, polyurethane sponge with embedded vacuum tubing, a vacuum pump, and transparent adhesive dressing. When systemic signs of infection and quantitative cultures indicate the resolution of the local infection, regional muscle flap or primary wound closure is performed. CONCLUSIONS: The VAC serves as a bridge to sternal wound closure and is a safe and effective therapeutic strategy for patients with impaired physiologic reserve and/or highly contaminated wounds. We feel that it is also reasonable to consider the VAC as a preventive strategy against right ventricular rupture. Furthermore, because the firmness of the vacuum sponge apparatus acts as an impressive sternal stabilizer, post-debridement extubation is possible, reducing the need for prolonged paralysis and mechanical ventilation. This stabilization also allows early postoperative ambulation with the VAC in place. In summary, we believe that the VAC device offers an effective means of managing patients with sternal infections.
Debridement↗
Retrograde perfusion with a sodium channel antagonist provides ischemic spinal cord protection.
BACKGROUND: Neuronal voltage-dependent sodium channel antagonists have been shown to provide neuroprotection in focal and global cerebral ischemic models. We hypothesized that retrograde spinal cord venous perfusion with phenytoin, a neuronal voltage-dependent sodium channel antagonist, would provide protection during prolonged spinal cord ischemia. METHODS: In a rabbit model, spinal cord ischemia was induced for 45 minutes. Six groups of animals were studied. Controls (group I, n = 8) received no intervention during aortic cross-clamping. Group II (n = 8) received systemic phenytoin (100 mg). Group III (n = 4) received systemic phenytoin (200 mg). Group IV (n = 8) received retrograde infusion of room temperature saline (22 degrees C) only. Group V (n = 8) and group VI (n = 9) received retrograde infusion of 50 mg and 100 mg of phenytoin, respectively, (infusion rate: 0.8 mL x kg(-1) x min(-1) during the ischemic period). Mean arterial blood pressure was monitored continuously. Animals were allowed to recover for 24 hours before assessment of neurologic function using the Tarlov scale. RESULTS: Tarlov scores (0 = complete paraplegia, 1 = slight lower limb movement, 2 = sits with assistance, 3 = sits alone, 4 = weak hop, 5 = normal hop) were as follows (mean +/- SEM): group I, 0.50 +/- 0.50; group II, 0.25 +/- 0.46; group IV, 1.63 +/- 0.56; group V, 4.13 +/- 0.23; and group VI, 4.22 +/- 0.22 (p < 0.0001 V, VI versus I, II, IV by analysis of variance). No differences in mean arterial blood pressure were observed. All animals in group III became profoundly hypotensive and died before the conclusion of the 45-minute ischemic time. CONCLUSIONS: Retrograde venous perfusion of the spinal cord with phenytoin, a voltage-sensitive sodium channel blocker, is safe and provides significant protection during prolonged spinal cord ischemia.
Animals↗
Reperfusion injury significantly impacts clinical outcome after pulmonary transplantation.
BACKGROUND: Reperfusion injury after pulmonary transplantation can contribute significantly to postoperative pulmonary dysfunction. We hypothesized that posttransplantation reperfusion injury would result in an increase in both in-hospital mortality and morbidity. We also hypothesized that the incidence of reperfusion injury would be dependent upon the cause of recipient lung disease and the interval of donor allograft ischemia. METHODS: We performed a retrospective study of all lung transplant recipients at our institution from June 1990 until June 1998. One hundred patients received 120 organs during this time period. We compared two groups of patients in this study: those experiencing a significant reperfusion injury (22%) and those who did not (78%). RESULTS: In-hospital mortality was significantly greater in patients experiencing reperfusion injury (40.9% versus 11.7%, p < 0.02). Posttransplantation reperfusion injury also resulted in prolonged ventilation (393.5 versus 56.8 hours, p < 0.001) and an increased length of stay in both the intensive care unit (22.2 versus 10.5 days, p < 0.01) and in the hospital (48.8 versus 25.6 days, p < 0.03). The incidence of reperfusion injury could not be attributed to length of donor organ ischemia (221.5 versus 252.9 minutes, p < 0.20). The clinical impact of reperfusion injury was significantly greater in patients undergoing transplantation for preexisting pulmonary hypertension (6/14) than those with chronic obstructive pulmonary disease or emphysema alone (6/54) (42.9% versus 11.1%, p < 0.012). CONCLUSIONS: Clinically significant pulmonary reperfusion injury increased in-hospital mortality and morbidity resulting in prolonged ventilation, length of stay in the intensive care unit, and cost of hospitalization. The incidence of reperfusion injury was not dependent upon the duration of donor organ ischemia but increased with the presence of preoperative pulmonary hypertension. These findings suggest that recipient pathophysiology and donor allograft quality may play important roles in determining the incidence of reperfusion injury.
Female↗
Aprotinin improves pulmonary function during reperfusion in an isolated lung model.
BACKGROUND: We hypothesized that the use of aprotinin would ameliorate the reperfusion injury observed after lung transplantation because of a reduction in the inflammatory response. METHODS: We used an isolated, whole blood-perfused, ventilated rabbit lung model to study the effects of aprotinin during reperfusion. The control animals (group A, n = 8) underwent lung harvest after pulmonary arterial prostaglandin E1 injection and Euro-Collins preservation flush before saline storage for 18 hours at 4 degrees C. The experimental groups received either a low dose (3,000 KIU/mL; group B, n = 8) or a high dose (10,000 KIU/mL; group C, n = 8) of aprotinin added to the pulmonary flush before storage. Each lung was reperfused at 37 degrees C at a rate of 60 mL/min. RESULTS: The arterial partial pressure of oxygen values of group B (low-dose aprotinin) were significantly higher than those of group A (control) after 10 minutes of reperfusion (69.19 +/- 5.69 mm Hg versus 264.30 +/- 48.59 mm Hg, respectively, p = 0.001). Similar results were recorded at 20 and at 30 minutes of reperfusion. Similarly, after 10 minutes of reperfusion, the differences between groups A and C were 69.19 +/- 5.69 mm Hg versus 235.91 +/- 28.63 mm Hg, respectively (p = 0.001). CONCLUSIONS: The addition of aprotinin to the Euro-Collins pulmonary flush significantly improves arterial oxygenation in the early reperfusion period. The enhanced oxygenation suggests that aprotinin may offer protection against early reperfusion injury.
Animals↗
Sodium nitroprusside mitigates oleic acid-induced acute lung injury.
BACKGROUND: Acute lung injury (ALI) is associated with pulmonary hypertension, intrapulmonary shunting, and increased microvascular permeability, leading to altered oxygenation capacity. Oleic acid (OA) creates a significant ALI that physiologically mimics human adult respiratory distress syndrome (ARDS). It has been hypothesized that pulmonary vasodilatation may improve ALI. Studies in our laboratory using this model and nitric oxide (NO) have shown that NO inhalation is detrimental and worsens the effects of OA. We studied the effect of pretreatment with a potent vasodilator, sodium nitroprusside (SNP), on ALI induced by OA in an isolated lung model. We hypothesized that pretreatment with SNP will worsen pulmonary hypertension and oxygenation in OA-induced ALI, similar to the effects seen with inhaled NO in this model. METHODS: Rabbit heart lung blocks were isolated, flushed in vivo, harvested, immediately perfused with whole blood, and ventilated with 50% oxygen. Pulmonary artery pressure was determined every 15 seconds for 90 minutes of perfusion. Oxygenation was determined by blood gas analysis of pulmonary venous effluent at 0, 20, 40, 60, and 90 minutes after initiation of OA infusion. Four groups were studied: saline control (SC), oleic acid control (OAC; 20-minute infusion of 50% OA/ethanol into pulmonary circulation), SNP control (NPC; 10 microg/ kg/min SNP infused without subsequent OA infusion), and SNP treatment (NPRx); 10 microg/kg/min SNP infused before OA/ethanol. Pulmonary artery pressure (PAP), oxygenation (arterio-venous oxygen difference [AVO2], compliance (CPL), and wet/dry lung weight were determined. RESULTS: No significant differences were found between the NPRx group and SC. Pretreatment with SNP eliminated the detrimental effects of OA infusion. CONCLUSIONS: Contrary to our hypothesis, pretreatment with SNP eliminates the decrease in oxygenation and increase in lung weight, and ameliorates pulmonary hypertension in our isolated lung model of OA-induced ALI.
Animals↗
Hypothermic retrograde venous perfusion with adenosine cools the spinal cord and reduces the risk of paraplegia after thoracic aortic clamping.
OBJECTIVE: We evaluated the utility of retrograde venous perfusion to cool the spinal cord and protect neurologic function during aortic clamping. We hypothesized that hypothermic adenosine would preserve the spinal cord during ischemia. METHODS: Six swine (group I) underwent thoracic aortic occlusion for 30 minutes at normothermia. Group II animals underwent spinal cooling by retrograde perfusion of the paravertebral veins with hypothermic (4 degrees C) saline solution during aortic occlusion. The spinal cords of group III animals were cooled with a hypothermic adenosine solution in a similar fashion. Intrathecal temperature was monitored and somatosensory evoked potentials assessed the functional status of spinal pathways. RESULTS: Spinal cooling without systemic hypothermia significantly improved neurologic Tarlov scores in group III (4.8 +/- 0.2) and group II (3.8 +/- 0.4) when compared with group I scores (1.3 +/- 0.6) (P <.001). Furthermore, 5 of the 6 animals in group III displayed completely normal neurologic function, whereas only one animal in group II and no animals in group I did (P =.005). Somatosensory evoked potentials were lost 10.6 +/- 1.4 minutes after ischemia in group I. In contrast, spinal cooling caused rapid cessation of neural transmission with loss of somatosensory evoked potentials at 6.9 +/- 1.2 minutes in group II and 7.0 +/- 0.8 minutes in group III (P =.06). Somatosensory evoked potential amplitudes returned to 85% of baseline in group III and 90% of baseline in group II compared with only 10% of baseline in group I (P =.01). CONCLUSIONS: We conclude that retrograde cooling of the spinal cord is possible and protects against ischemic injury and that adenosine enhances this effect. The efficacy of this method may be at least partly attributed to a more rapid reduction in metabolic and electrical activity of the spinal cord during ischemia.
Adenosine↗
The safety of combined cardiac and vascular operations: how much is too much?
OBJECTIVE: The purpose of this study was to identify factors correlating with a poor outcome following combined cardiac and vascular procedures. METHODS: We reviewed 45 consecutive patients undergoing combined cardiac and vascular operations. These included cardiac/CEA (n=27), cardiac/AAA (n=13), cardiac/AAA/one other vascular reconstruction (n=4), and cardiac/renal artery bypass (n=1). Group I included all patients with no morbidity or mortality (n=41) and Group II included patients who died or suffered significant morbidity (stroke, renal failure) (n=4). RESULTS: Overall mortality was 4.4% (2/45). These two patients underwent cardiac surgery combined with two additional vascular procedures (cardiac/AAA/other). In patients undergoing cardiac/CEA or cardiac/AAA, there were no deaths and one stroke (contralateral to CEA). Group II had significantly decreased ejection fraction (39%+/-6% vs 52%+/-1%) and an increased number of procedures (2.75 vs 2.04). CONCLUSIONS: Combined cardiac surgery and vascular reconstruction can be performed safely. However, multiple vascular reconstructions or the presence of decreased ejection fraction increased operative risk.
Aged↗
Intensive care is cost-effective in carotid endarterectomy.
The purpose of this study was to analyze the utilization, cost profile, and predictors of intensive care unit (ICU) services after carotid endarterectomy. A retrospective medical record review of all patients undergoing isolated carotid endarterectomy by a vascular surgery service at one university hospital during a 12-month period was performed. Eighty-four patients undergoing 91 carotid endarterectomies were identified for review. All carotid endarterectomy patients at the authors' institution were routinely admitted to an ICU postoperatively. Sixty-five of the 91 patients (71.4%) required ICU interventions, the majority of which were intravenous antihypertensive therapy. There were no deaths in the group. There was one non-fatal stroke (1.1%), and one non-fatal myocardial infarction (1.1%). There were three reoperations (3.3%): two for hematoma and one for a change in neurological status. One patient required reintubation. Five of the six major adverse events after carotid endarterectomy occurred within 12 hours postoperatively. No preoperative factors predicted a significant risk for complications following carotid endarterectomy. There is no reliable predictor that carotid endarterectomy patients will require postoperative interventions or develop adverse outcomes. Mandatory intensive care immediately after carotid endarterectomy upholds high safety standards, avoids the uncertainty of preoperative ICU planning, and avoids the high cost of a recovery room stay to determine the need for intensive care. In addition, costs may be further reduced as the ICU length of stay may be decreased if there are no necessary interventions or complications after 12 hours of intensive care.
Aged↗
Early carotid endarterectomy after stroke.
The authors sought to determine if patients with stroke and a high-grade carotid stenosis benefited from a delay before carotid endarterectomy. A retrospective study of 45 patients undergoing carotid endarterectomy after stroke is presented. The patients were divided into two groups: group I (early group, n = 20), composed of patients who had carotid endarterectomy less than 6 weeks after stroke, and group II (late group, n = 25), comprised of patients who had carotid endarterectomy more than 6 weeks after stroke. As assessed by cerebral angiography, 100% of patients in group I and 64% of patients in group II had carotid artery stenoses > 76% (P < 0.001). The median interval from stroke to carotid endarterectomy was 14 days in group I and 129 days in group II. There was no mortality in either group. No patients in either group demonstrated any neurological deterioration. The authors conclude that, in select patients, carotid endarterectomy may be done safely less than 6 weeks after stroke in order to avoid new events or carotid occlusion while awaiting surgery.
Aged↗
Epidermal growth factor augments postpneumonectomy lung growth.
OBJECTIVE: Epidermal growth factor has been shown to play an important role in prenatal and postnatal lung development, but little is known about its effects on adult lung growth. We hypothesized that postpneumonectomy compensatory lung growth can be augmented by the administration of epidermal growth factor. METHODS: Adult Sprague-Dawley rats were divided into 3 groups. Sham left thoracotomy was performed in the first group (group C), left pneumonectomy in the second group (group P), and left pneumonectomy with administration of epidermal growth factor (0.2 microgram/g body weight intraperitoneally, at 72-hour intervals) in the third group (group E). The right lung growth was studied in each group 1, 3, 5, 10, and 21 days after the operation. Lung weights (in grams) and volumes (in milliliters) were expressed as a ratio to the total body weight (in kilograms) (lung weight and volume indices). Epidermal growth factor receptor was quantitated by using Western blotting. RESULTS: Using analysis of variance and contrast analysis, we noted a significant increase in lung weight index in group E versus group P rats at 3 days (3.08 vs 2.75; P =.034) and 21 days (4.62 vs 3.61; P =.006). Lung volume index was significantly increased in group E versus group P rats at 5 (16.98 vs 15.09), 10 (24.48 vs 18.81), and 21 (28.54 vs 21.01) days (P <.001). Epidermal growth factor receptor was noted to be up-regulated in the lungs of animals that received exogenous epidermal growth factor. CONCLUSIONS: This study demonstrates that administration of exogenous epidermal growth factor has a significant effect on postpneumonectomy lung growth. This process may be mediated by an up-regulation of growth factor receptor expression in the contralateral lung.
Analysis of Variance↗
Retrograde venous perfusion with hypothermic saline and adenosine for protection of the ischemic spinal cord.
PURPOSE: Spinal cord injury and the resultant postoperative paraplegia are devastating complications of thoracic aortic surgery, for which no widely accepted protective interventions exist. We hypothesized that retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution would protect it from ischemic injury caused by thoracic aortic occlusion. METHODS: Adult domestic swine of either sex (weight range, 20 to 30 kg) were intubated and ventilated. A left thoracotomy was performed. The accessory hemiazygous vein was divided, and a catheter was inserted distally. The aorta was clamped at the left subclavian artery. The venous catheter was not used in the animals in the control group (n = 7); in the animals in the experimental group (n = 7), a cold (4 degrees C) saline and adenosine solution was infused into the accessory hemiazygous vein. After 30 minutes, the clamp and catheter were removed, and the chest was closed. A blinded observer evaluated the animals' hind-leg motor activity 24 hours later. The Tarlov scale was used: 0, complete paralysis; 1, minimal movement; 2, stands with assistance; 3, stands alone; 4, weak walk; 5, normal gait. The animals' rectal temperatures were measured at the end of the experiment, and blood pressure was measured throughout. Two other groups were studied to assess the effect of the intervention on spinal cord temperature. RESULTS: The animals in the control group had a mean Tarlov score of 1.7 +/- 0.6; the animals in the experimental group had a mean Tarlov score of 4.9 +/- 0.1 (P <.01). The animals in the experimental group had a significantly greater drop in spinal cord temperature than those in the control group (4. 05 +/- 0.6 degrees C vs 0.58 +/- 0.12 degrees C; P <.01). No significant difference in rectal temperatures was found, nor did any arrhythmias or hypotensive episodes occur in either group. Perfusion of the spinal cord was confirmed with angiography by using this approach. CONCLUSION: Retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution protects the cord from ischemic injury caused by clamping of the thoracic aorta.
Adenosine↗
Does the additive risk of mitral valve repair in patients with ischemic cardiomyopathy prohibit surgical intervention?
OBJECTIVE: To assess the surgical risk of additional mitral valve repairs in patients with ischemic cardiomyopathy. SUMMARY BACKGROUND DATA: Severe mitral regurgitation in patients with ischemic cardiomyopathy increases the death rate and symptomatic status. The 1-year survival rate for medical therapy in this subset of patients is less than 20%. Transplantation is usually not feasible because of donor shortage and death while on the waiting list. METHODS: To assess additive risk, a retrospective chart review from 1993 to 1998 was performed comparing patients with ischemic cardiomyopathy (ejection fraction [EF] <25%) and severe mitral regurgitation undergoing mitral valve repair and coronary artery bypass graft operations with patients with an EF of <25% undergoing coronary artery bypass graft alone. These groups were also compared with 140 patients receiving heart transplants since 1993 (group 3). RESULTS: The overall hospital death rate for group 1 was 6.3%. The one death occurred 2 weeks after surgery secondary to sepsis. This was not significantly different from the death rate of 4.1% in group 2. In group 1, there were two deaths at 1 year (87% survival rate), one related to heart failure. One patient was New York Heart Association (NYHA) class IV at 1 year; the remainder of patients were NYHA class I-II. These results were not significantly different than the 8% death rate noted with transplantation. There was no change in EF and minimal residual mitral regurgitation in group 1 based on postoperative transesophageal echocardiography, whereas group 2 had an average 11.7% improvement in EF. CONCLUSIONS: Previously, severe mitral regurgitation in the setting of ischemic cardiomyopathy has been associated with poor survival. In these authors' experience, repairing the mitral valve along with coronary artery bypass grafting does not increase the surgical risk, yields improvement in symptomatic status, and compares favorably to coronary artery bypass grafting alone and cardiac transplantation. However, the lack of change in EF in these patients probably represents an overestimation of the EF before surgery secondary to severe mitral regurgitation.
Cardiomyopathy, Dilated↗
Attenuation of lung reperfusion injury after transplantation using an inhibitor of nuclear factor-kappaB.
A central role for nuclear factor-kappaB (NF-kappaB) in the induction of lung inflammatory injury is emerging. We hypothesized that NF-kappaB is a critical early regulator of the inflammatory response in lung ischemia-reperfusion injury, and inhibition of NF-kappaB activation reduces this injury and improves pulmonary graft function. With use of a porcine transplantation model, left lungs were harvested and stored in cold Euro-Collins preservation solution for 6 h before transplantation. Activation of NF-kappaB occurred 30 min and 1 h after transplant and declined to near baseline levels after 4 h. Pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of NF-kappaB, given to the lung graft during organ preservation (40 mmol/l) effectively inhibited NF-kappaB activation and significantly improved lung function. Compared with control lungs 4 h after transplant, PDTC-treated lungs displayed significantly higher oxygenation, lower PCO(2), reduced mean pulmonary arterial pressure, and reduced edema and cellular infiltration. These results demonstrate that NF-kappaB is rapidly activated and is associated with poor pulmonary graft function in transplant reperfusion injury, and targeting of NF-kappaB may be a promising therapy to reduce this injury and improve lung function.
Animals↗
Does a focal neurologic deficit contraindicate operation in a patient with endocarditis?
BACKGROUND: As many as 40% of patients with left-sided bacterial endocarditis will sustain a neurologic insult. The importance of a neurologic change as an indication or a contraindication for valve replacement remains controversial. METHODS: We performed a retrospective analysis of the records of 33 patients admitted to the University of Virginia Health Sciences Center between January 1, 1978, and June 30, 1996, with a diagnosis of endocarditis and a neurologic change. RESULTS: All 33 patients had echocardiographic or pathologic evidence of left-sided endocarditis; 23 were seen with focal neurologic findings and had a mortality rate of 22% (5 of 23), and 10 patients were seen with nonfocal, diffuse encephalopathy and had a mortality rate of 60% (6 of 10) (p<0.05). Of the 33 patients, 14 underwent operation and 19 were treated medically. The mortality rate was 21.4% (3 of 14) in the surgical group and 42.1% (8 of 19) in the medical group (p = not significant). In 71% (10 of 14) of the surgical patients, the operation was done within 1 week of the neurologic event. Additional neurologic deterioration occurred in 18.2% (2 of 11) of survivors in the surgical group and 9.1% (1 of 11) in the medical group (p = not significant). CONCLUSIONS: Choosing therapy for a patient with endocarditis and a neurologic change remains a difficult challenge. Initial findings of nonfocal, global dysfunction on examination are a predictor of a poor outcome. By comparing surgical and medical groups derived from the same series of patients, it is clear that patients with bacterial endocarditis and central nervous system changes face substantial mortality regardless of intervention. However, these data demonstrate that when compared with a similar group of medical patients, surgical patients who require and receive operation early in the course of their illness do comparatively well. Improving outcomes by delaying surgical intervention may serve to "select out" hardier patients but will lead to the death of patients who might benefit from such intervention.
Adult↗
Membranous tracheobronchial injury repaired with gastric serosal patch.
This unusual case involves pharyngolaryngoesophagectomy complicated by injury to the membranous trachea and right bronchus. Repair was possible after partial sternal split and elevation of the tracheostoma through the anterior mediastinum, pulling the stomach to the neck, and using the stomach as a patch to repair the injury to the membranous portion of the airway.
Bronchi↗
Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation.
BACKGROUND: There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. METHODS: Using an isolated, whole blood-perfused, ventilated rabbit lung model, we sought to characterize the pattern of reperfusion injury and investigate the contribution of neutrophils to this injury. Donor rabbits underwent lung harvest after pulmonary arterial prostaglandin E1 injection and Euro-Collins preservation solution flush. Group I lungs (n = 8) were immediately reperfused without ischemic storage. Group II lungs (n = 8) were stored for 18 h at 4 degrees C before reperfusion. Group III lungs (n = 10) underwent 18 h of ischemic storage and were reperfused with whole blood that was first passed through a leukocyte-depleting filter. All lungs were reperfused for 2 h. RESULTS: Arterial oxygenation in group III progressively improved, and was significantly higher than that of group II after 2 h of reperfusion (272.58+/-58.97 vs 53.58+/-5.34 mm Hg, p = 0.01). Both pulmonary artery pressure and pulmonary vascular resistance were significantly reduced in group III when compared with group II (27.85+/-1.45 vs 44.15+/-4.77 mm Hg, p = 0.002; and 30,867+/-2,323 vs 52,775+/-6,386 dynes x sec x cm(-5), p = 0.003, respectively). Microvascular permeability in group III lungs was reduced to 73.98+/-6.15 compared with 117.16+/-12.78 ng Evans blue dye/g tissue in group II (p = 0.005). Group III myeloperoxidase activity was 56.92+/-6.31 deltaOD/g/min compared with 102.84+/-10.41 delta0d/g/min in group II (p = 0.002). CONCLUSIONS: Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.
Animals↗