ABSTRACT
Objective To determine whether the extent of airflow obstruction is associated with left ventricular function in mild-to-moderate chronic obstructive pulmonary disease (COPD) patients.Methods Left ventricle end diastolic volume ( LVEDV ),left ventricle end systolic volume ( LVESV ),left ventricle stroke volume( LVSV),left ventricle ejection fraction( LVEF),heart rate ( HR),cardiac output ( CO) and cardiac index (CI) were measured by ultrasonic cardiogram.Thirty-one patients with chronic bronchitis,42 mild-to-moderate COPD patients and 16 controls with normal lung function were recruited.The relations between the extent of airflow obstruction and the impairment of left ventricular function were analyzed.Results There were no significant differences of LVEDV,LVESV,LVSV,HR,CO or CI between the control and chronic bronchitis groups.LVEDV,LVESV,LVSV,CO and CI of chronic bronchitis group were significantly higher than those of mild-to-moderate COPD group while HR was lower.LVEDV,LVESV,LVSV,CO and CI had a positive correlation with forced expiratory volume in 1 second ( FEV1 ),forced vital capacity (FVC) and FEV1/FVC ratio.And HR had a negative correlation with FEV1 and FEV1/FVC.LVEF was positively correlated with FVC,but not with FEV1 and FEV1/FVC.LVEDV,LVESV,LVSV,HR,CO and CI were linearly related with FEV1.Conclusions Left ventricular function is maintained in chronic bronchitis patients. Left ventricular function,especially left ventricular end diastolic filling,deteriorates among the mild-to-moderate COPD patients.The extent of airflow obstruction may reflect the impairment of left ventricular function in COPD patients.
ABSTRACT
Background Visual electrophysiology is a sensitive index for the evaluation of visual function.It has an important value in the assessment of traumatic optic neuropathy.Rabbit is an ideal animal model of traumatic optic neuropathy,and it is simple for the record of flash visual evoked potential(F-VEP)in rabbits.ObjectiveThe present study is to establish the animal model of traumatic optic neuropathy with or without lens injury and observe the repairing procedure using F-VEP. MethodsModels of traumatic optic neuropathy associated with lens injury were established in the right eyes and only traumatic optic neuropathy were created in the left eyes of 64 healthy SPF Chinese white rabbits using fluid percussion brain injury device(FPI).F-VEP was recorded based on the Proposal of International Visual Electrophysiology on 1,2,4,7,10,14,21,28 days after injury of optic nerves.Experimental animals were sacrificed in above time points for the histopathological examination.Macrophages were labeled by ED-1 antibody and survival retinal ganglion cells (RGCs)were stained by Nissl method.Results At the first day after injury,the latencies of P_(100) in both group were longer,and the amplitudes of P_(100) in both group were lower than before injury,showing statistically significant differences among different time points(P<0.05),but no significant difference was seen between the two groups(P>0.05).The duration of latency in traumatic optic neuropathy associated with lens injury group was shorter than that in only traumatic optic neuropathy group(P<0.05).The restore of latency in traumatic optic neuropathy associated with lens injury group was much faster than that in only traumatic optic neuropathy group(P<0.05).The numbers of macrophages were significantly increased and numbers of survival RGCs were considerably decreased with lapse of injury time (P<0.05).The abnormalities of VEP P_(100) and RGCs were obviously improved in 28 days after injury in both groups. ConclusionThis animal model can be established successfully by FPI.The result of retinal histopathological examination confirms F-VEP findings in this model.
ABSTRACT
Objective Previous study showed that the histopathological basis of visual function damage caused by optical nerve injury is apoptosis of retinal ganglion cells(RGCs). This procedure is regulated by P53, bax and caspase 3 genes. Present study aimed to observe the expression of bax, P53 and caspase 3 mRNA in RGCs after traumatic optic nerve damage in the rats by SYBR green I fluorescence quantitative PCR method. Methods The animal model of optic nerve injury was established in the right eyes of 56 adult Wistar rats by a fluid percussion brain injury device (FPI) . Animal were killed on days 1, 3, 5, 7, 9, 14, 28 days separately after injury. Other 16 Wistar rats were divided into normal control group and sham operation group. The total RNA was isolated from rat fresh retina tissue by Trizol method and was treated by reverse transcription to cDNA using 01igo(dt) 18 as primer and then amplified. The target fragments of bax, P53 and caspase 3 cDNA were linked with carrier pTZ57 R/T to construct recombined plasmids which were transformated to E. Coli DH5α by T/A clone method. Recombined plasmids were extracted with alkaline lysis method and the plasmids were selected in white colonies by ampicillin screening, EcoR I restrictive enzyme analysis, and their specificity was evaluated using DNA sequencing. The standard curves were created by plasmid DNA and the precise expression level of target genes in samples were determined using software. The results were expressed as the ratios of target gene mRNA to GAPDH mRNA. Results The standard curve drawn by pTZ57R/T and target gene presented a good linear tendency with the higher sensitivity and specificity. The expression of P53 and bax mRNA began to increase on the third day after the injury of optic nerve and peaked on the fifth day and started to decline on the seventh day. The expression of caspase 3 mRNA increased from the fifth day through the ninth days after injury and declined on the fourteenth day. The significant differences were found in the expression of P53, bax and caspase 3 between model group and control group (P ＜ 0. 05) . Conclusion The pro-apoptotic protein P53, bax and caspase 3 play an important role in RGCs apoptosis.