Objective To assess the protective effects of a new type of leukocyte-depletion filter-1 (LD-1) on red blood cells during cardiopulmonary bypass(CPB). Methods Twelve Mongolian dogs, weight range 25-30kg, were divided into control group and leukocyte depletion group (LD group) with random number table, LD group (n=6) had our new type of leukocyte depletion filter-1 placed in venous line which was used within the first 5 minutes after onset of CPB. The control group (n=6) had no leukocyte depletion filter installed in the circuit. CPB was set up by cannulated with a venous cannula through the right atrium and with an aortic cannula after median sternotomy. Aorta was clamped at 10 minutes of CPB and released at 70 minutes of CPB. Dogs were observed for 2 hours after weaning from CPB. Blood samples were collected prior to, at 10, 40, 75 minutes, end of and 2 hours after CPB to determine circulating leukocytes, erythrocyte fragility and plasma levels of malondialdehyde(MDA), superoxide dismutase(SOD) and free hemoglobin(FHB). Results Leukocyte numbers were significantly reduced in LD group during CPB(Plt;0.01), and lower than those in control group (Plt;0.05). Plasma levels of SOD dropped after 75 minutes of CPB in control group, but those kept normal in LD group, and higher than those in control group at 2 hours after CPB (Plt;0.05, 0.01). Serum MDA and FHB levels increased sharply in two groups (Plt;0.01), but were lower in LD group than those in control group. The concentrations of NaCl when starting and complete hemolysis were also lower in LD group than those in control group at end of and 2 hours after CPB. Conclusion The new type of LD-1 used in venous line only 5 minutes after onset of CPB can decrease leukocyte counts, and reduce erythrocyte injury effectively.
In left heart disease, pulmonary artery pressure would increase due to the elevated left atrial pressure. This type of pulmonary hypertension (PH) is belonged to type Ⅱ as a passive PH (pPH) in its classification. The essential cause of pPH is excessive blood volume. Recently, we have identified another type of pPH, which is induced by vasopressors. Vasopressor-induced pPH shares similar pathophysiological manifestations with left heart disease-induced pPH. pPH would, therefore, be aggressive if vasopressors were applied in patients with left heart disease, which may be common after cardiac surgery, because heart undergoing surgical trauma may require support of vasopressors. Unfortunately, pPH after cardiac surgery is often ignored because of the difficulty in diagnosis. To improve the understanding of pPH and its effect on outcomes, here we highlight the mechanisms of interaction between vasopressor-induced and left heart failure-induced pPH, and provide insights into its therapeutic options.
Objective To observe whether additional penehycl idine hydrochloride (PHC) in mechanical ventilation produces therapeutic effect on oleic acid (OA) induced acute lung injury (ALI) in canine. Methods Seventeen male canines (weighing 12-17 kg) were divided into control group (n=5), OA group (n=6) and PHC group (n=6). ALI model was developed by central venous injection of OA in canines of OA and PHC groups. ALI model was kept steady in air, all groups received mechanical ventilation 90 minutes later. Three groups received normal sal ine 0.25 mg/kg without injection of OA(control group), normal sal ine 0.25 mg/kg after injection of OA (OA group) and PHC 0.25 mg/kg after injection of OA (PHCgroup) respectively at 0 h (90 minutes after onset time of ALI/ARDS). The heart rate (HR), mean arteial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery wedge pressure (PAWP), artery blood gas analysis, cardiac output (CO), extravascular lung water index (EVLWI), FiO2 and VT were observed respectively at basel ine, onset time of ALI/ARDS and 0 h, then again at 1 hour intervals for 6 hours. Besides the above, airway peak pressure (Ppeak), airway plat pressure (Pplat), mean airway pressure (Pmean) and positve end-expriatory pressure (Peep) were also observed each hour during 1-6 hours. Oxygenation index (OI), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), alveolar-arterial differences for O2 (AaDO2) and dynamic lung compl iance (DLC) were calculated and pulmonary tissue was collected for histopathologic investigation and dry wet weight ratio (WDR) test. Results The functional parameters of PHC group were improved when compared those of OA group, but there was no siginficant difference; WDR of independent region of three groups were 80.42% ± 3.48%, 82.67% ± 4.01% and 82.26% ± 1.43% respectively; WDR of dependent region of three groups were 80.51% ± 3.60%, 83.71% ± 1.98% and 82.57% ± 1.08% respectively. WDR of PHC group were obviously improved when compared with those of OA group, but there was no significant difference. Independent and dependent regions of PHC group were significantly improved when compared those of OA group in histopathologic scores, alveolar edema, inflammatory infiltration and over-distension (P lt; 0.01). Conclusion Additional PHC in mechanical ventilation produces obvious therapeutic effect on OA induced acute lung injury in canine.