ABSTRACT
Objective To investigate the role of Clara cells in lung ischemia-reperfusion (I/R) injury in rabbits.Methods Twenty-four healthy 10-12 month old rabbits of either sex weighing 1.5-2.0 kg were randomly divided into 3 groups ( n = 8 each) ; group A sham operation (group S) ; group B lung I/R and group C Clara cell elimination+ lung I/R. The animals were anesthetized with iv pentobarbital 30 mg/kg , tracheostomized and mechanically ventilated. In group B and C lung I/R was induced by clamping the left hilum of lung for 60 min followed by 120 min repeffusion. In group C Clara ceils were eliminated by ventilating the lungs with 89.28 mg/m2 naphthalin vapor for 12 h before lung I/R. The animals were killed by iv KCI at the end of 120 min reperfusion after lung isehemia. The left lung was immediately removed for microscopic examination, determination of W/D lung weight ratio and serum TNF-α level and MDA content. The percentage of neutrophi] in bronchoalveolar lavage fluid (BALF) was detected as index of lung injury. The expression of Clara cell secreting protein (CCSP) in the lung was detected by immuno-histoebemistry to indicate the number and distribution of Clara cells in the lung.Results Microscopic examination showed that there were severe leukocyte infiltration in alveolar spaces, alveolar edema and destroyed alveolar structure in group B and C. The serum TNF-u leve],W/D ratio and MDA content in the left lung and neutrophil percentage and WBC counts in BALF were significantly higher in group C than in group B. Conclusion Clara cells can protect the lungs against I/R injury through inhibiting inflammatory responses.
ABSTRACT
Objective To study the expression of smad2/3 protein and the effects of flunarizine on the its expression in braln tissue following transient cerebral ischemie reperfusion in gerbils. Methods A cerebral ischemia-reperfusion model in gerbils was established by clamping both common carotids. Thirty-five gerbils were randomly divided into three groups, sham operation group, cerebral ischemia-reperfusion group and flunarizine treatment group. The expression of smad2/3 protein in brain tissue was detected by immunohistochemistry technique. Results Experimental results revealed that smad2/3 protein was expressed in neuroeyte in 35 gerbil brain. Compared with sham operation group, the expression of smad2/3 protein in neurecytes of cerebral isehemia-reperfusion group was evidently increased at the lst day, 3rd day and 7th day (P <0. 01). Compared with cerebral ischemia-reperfusion group, the expression of smad2/3 protein in neurecytes of gerbils in flunarizine treatment group was evidently decreased at these time point (P < 0.05). Condusions Smad2/3 protein was expressed in nettrcvytes of gerbils. Expression of smad2/3 protein in neuroeytes of gerbils was evidently increased following cerebral ischemic reperfusion, and its expression in flunarizine treatment group was evidently decreased.
ABSTRACT
Objective To compare the myocardial protective effect of pinacidil-induced hyperpolarized and hyperkalemic depolarized cardiac arrest on isolated rabbit heart under different temperature. Methods Forty-eight rabbits of both sexes weighing 2.0-2.5 kg were sacrificed by a knock on the head. Their hearts were excised and perfused in a Langendorff apparatus with an oxygenated Krebs-Hensleit buffer (KHB)(37℃). The study was divided into six groups: A normothermic hyperkalemic cardioplegia; B normothermic hyperkalemic blood cardioplegia; C hypothermic hyperkalemic cardioplegia; D hypothermia hyperkalemic blood cardioplegia; E normothermic hyperpolarizing blood cardioplegia; F hypothermic hyperpolarizing blood cardioplegia. Three pieces of myocardial tissue were obtained from apex of left ventricle at the end of the study for determination of myocardial adenine nucleotide and lipid peroxide content and microscopic examination. The following were recorded : (1) cardiac arrest time: the time from perfusion with cardioplegic solution to the beginning of cardiac arrest. (2) heart beat recovery time ;the time from reperfusion with KHB to the beginning of normal heart beat. (3) changes in HR, left ventricle developed pressure and myocardial contractility before and after cardiac arrest. Results The cardiac arrest time was longer and the time for the heart to restart was shorter in the two hyperpolarizing blood cardioplegia groups (group E and F) than that in the other 4 groups. No arrhythmia occurred in group E and F. Left ventricle developed pressure(LVDP) and left ventricle contractility recovered quickly after reperfusion with KHB was started and were restored to the pre-ischemia level after 20 min in group E and F. The levels of ATP, TAN and EC were higher and the MDA level was lower in group E and F than those in the other 4 groups. Myocardial structure was less injuried in group E and F. Conclusion The myocardial protection effect of hyperpolarizing blood cardioplegia with pinacidil is superior to traditional hyperkalemic depolarizing cardioplegia.