Ultrastructural changes in the human lung following cardiopulmonary bypass

Abstract

In order to assess the degree of the pathological changes presenting in the lungs of patients after elective cardiac operations in cardiopulmonary bypass and to determine their prognosis, lung biopsies were taken from the right lower lobe of 36 patients after extracorporeal circulation and studied ultrastructurally. Prepump biopsies from the same presenting anterior portion of the lower lobe of the lung served as controls. Perivascular and interstitial edema featured prominently. Intraalveolar edema and extravasated corpuscular blood elements were observed, too. Damages to the mitochondria and to the lamellar bodies and swelling of the endothelial and alveolar cells were major observations following cardiopulmonary bypass lasting more than 60 minutes. These changes were also prominent in those lungs presenting with severe edema and fibrosis. Many intact type-II pneumocytes presented with enhanced metabolic and secretory activities. Merocrine and apocrine secretions were observed after extracorporeal circulation. The alveoli of the postpump lungs contained numerous detached normal appearing type-II pneumocytes, in contrast to the paucity of such cells in the alveoli of the control biopsies. The prognosis for the patients depends on any one or combination of any of the following factors: the pathological changes present in the lungs prior to the extracorporeal circulation, the duration of the cardiopulmonary bypass, the rate of the elimination of the surfactant and finally the ability of the undamaged type-II pneumocytes to step up the synthesis and secretion of the surface acting agent.

Use of inhaled nitric oxide and acetylcholine in the evaluation of pulmonary hypertension and endothelial function after cardiopulmonary bypass.

“…Abnormalities in pulmonary vascular endothelial structure have been described in children with congenital heart disease.2'3'27'43'47 Alterations in preoperative endothelial structure and function may predispose this population to postoperative abnormalities of the regulatory mechanisms mediated by the endothelium. 27,48,49 Evidence is also accumulating that the abnormal pulmonary endothelium is further damaged when its normal blood supply via the pulmonary artery is removed by instituting total CPB.31,32,4850 Pulmonary endothelial blood supply from the vasovasorum via the bronchial circulation may not be adequate on CPB; ischemic damage to the endothelium has been described after CPB.2748 Postoperative pulmonary hypertensive crises promoted by an injured endothelium may be analogous to vasospasm in the coronary circulation resulting from supersensitivity to circulating catecholamines occurring in the context of endothelium damaged by atherosclerotic disease.22'51 Elevation in endogenous catecholamines and sensitivity of the pulmonary circulation to stimuli are common postoperative profiles in children with congenital heart disease.52,53 Endothelial dysfunction after a transient ischemic event has been demonstrated in other organ systems and may be further affected by ischemic reperfusion injury.54 Thus, prior data would suggest that preoperative conditioning of the pulmonary bed, perioperative vasospastic stimuli, and increased postoperative adrenergic tone may conspire with the pulmonary endothelium, damaged by intraoperative ischemia, to increase PVR after CPB.…”

Peripheral bypass-induced pulmonary and coronary vascular injury. Association with increased levels of tumor necrosis factor.

“…[9][10][11][12][13][14][15] Since blood flow to the heart and the lungs is markedly reduced during conventional bypass with cardiopulmonary blood flow diversion, subsequent cardiac and pulmonary dysfunction may reflect direct effects of flow diversion, organ ischemia, and reperfusion.1-3 However, associated cerebral,5 renal,4 and splanchnic16 dysfunction suggests that mechanisms other than local ischemia may play a role. Although vascular injury may play a role in postbypass organ dysfunction, previous studies using predominantly indirect methods of assessing vascular injury have produced conflicting results regarding its occurrence after bypass.…”

“…Although vascular injury may play a role in postbypass organ dysfunction, previous studies using predominantly indirect methods of assessing vascular injury have produced conflicting results regarding its occurrence after bypass. [9][10][11][12][13][14][15][16][17] In addition, prior studies of pulmonary and coronary vascular injury have not distinguished between the roles of local flow diversion and Complement activation that occurs with bypass could mediate bypass-induced organ dysfunction and vascular injury.2,3'7'8 However, several recent studies suggest that complement activation alone is not sufficient to cause vascular injury and that other factors, including local ischemia and neutrophil priming by other mediators, are necessary.18-20 A role for endotoxin in bypassinduced vascular injury seems possible, because several features of the "postperfusion" syndrome, including multiorgan dysfunction, circulating neutropenia with tissue neutrophil sequestration, eicosanoid production, lipid peroxidation, and complement activation, have been observed in sepsis or after the administration of endotoxin. 21,22 In addition, Rocke et a123 and Kharazmi and coworkers24 reported increases in circulating endotoxin levels in patients undergoing bypass.…”

Aortic Valve Replacement in a Patient With Myelodysplastic Syndrome and Interstitial Pneumonia

“…Generally, cardiac surgery using ECC causes a systemic inflammatory response, resulting in deterioration of lung function. [11][12][13] It has been reported that various cytokines, such as interleukin 6 and tumor necrosis factor, play important roles in the blood -surface interaction. To prevent progression of the lung disease, we administered ulinastatin during surgery.…”