ABSTRACT
Hyperthyroidism is a clinically common endocrine disease. It often has no specific clinical symptoms in the early stage and is easily overlooked. The long-term effects of excessive thyroid hormones in the body can alter cardiovascular hemodynamics, which may lead to heart enlargement, atrial fibrillation, and heart failure. Cardiovascular disease is one of the common complications of hyperthyroidism, but it is the main cause of death. This article focuses on the related cardiovascular diseases of hyperthyroidism, and summarizes the molecular mechanism of thyroid hormone on the heart, the mechanism of hyperthyroidism induced heart failure, atrial fibrillation, pulmonary hypertension, and the treatment and prognosis of hyperthyroidism. In addition, we also analyzed the association between subclinical hyperthyroidism and the occurrence of cardiovascular disease. When combined with risk factors, subclinical hyperthyroidism patients need early treatment. It should be noted that long-term use of amiodarone can cause secondary hyperthyroidism, which should be used with caution in clinical use.
ABSTRACT
Hyperthyroidism is a clinically common endocrine disease.It often has no specific clinical symptoms in the early stage and is easily overlooked.The long-term effects of excessive thyroid hormones in the body can alter cardiovascular hemodynamics,which may lead to heart enlargement,atrial fibrillation,and heart failure.Cardiovascular disease is one of the common complications of hyperthyroidism,but it is the main cause of death.This article focuses on the related cardiovascular diseases of hyperthyroidism,and summarizes the molecular mechanism of thyroid hormone on the heart,the mechanism of hyperthyroidism induced heart failure,atrial fibrillation,pulmonary hypertension,and the treatment and prognosis of hyperthyroidism.In addition,we also analyzed the association between subclinical hyperthyroidism and the occurrence of cardiovascular disease.When combined with risk factors,subclinical hyperthyroidism patients need early treatment.It should be noted that long-term use of amiodarone can cause secondary hyperthyroidism,which should be used with caution in clinical use.
ABSTRACT
Objective To investigate the effects of propofol on the development of spatial learning and memory and neuron proliferation of neonatal rats at different doses. Methods 60 neonatal rats were divided into four groups among per litter by using a randomized block design. Three different doses of propofol group were induced with propofol 10 mg/kg( group P10) ,50 mg/kg( group P50) or 50 mg/kg twice( group P50D) by subcutaneous injection respectively. Neuron proliferation at dentate gyrus was detected by using BrdU marker 3 days later.Morris water maze test was carried out on postnatal day 28. Escape latency,time in probe quadrant were recorded.Results Compared to the control group,neuron marked with BrdU at dentate gyrus in group P50D was significantly decreased( (840±76) vs (225 ±66), P＜0.05) ,group P10 was significantly increased( (840 ±76) vs ( 1225± 154), P＜0.05). Compared to the control group,latency of group P50D was significantly increased( ( 15.12 ±3.43 ) s vs (42.68 ± 6. 18 ) s, P ＜ 0. 05 ), time in probe quadrant of group P50D were significantly decreased ( ( 55.66 ± 8.57 ) s vs (32. 18 ± 5. 38 ) s, P＜ 0. 05 ). Compared to the control group, there was no significant difference between group P50 and group P10. Conclusion Propofol given to seven-day-old rats with 50 mg/kg twice by subcutaneous injection suppresses neuron proliferation and impairs development of memory and learning in neonatal rats,but propofol given with 10 mg/kg once promotes neuron proliferation.
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Objective To investigate the effects of different concentrations of isoflurane on the caspase-3 expression in the hippocampus and S100β level of plasma in fetal rats. Methods 18 pregnant rats at gestational day 21 were divided into control group, 1. 3% isoflurane group,3% isoflurane group. Rats in the control group spontaneously breathed 100% oxygen for 1 h. Rats in the treatment groups breathed 1.3% or 3% isoflurane in 100% oxygen through an endotracheal tube, with mechanical ventilation for 1 h. Rat pups were delivered by cesarean section 6 h after treatment, and fetal blood was sampled from the left ventricle of each fetal heart and evaluated for S100β. Fetal brains were then evaluated for apoptosis, using caspase-3 immunohistochemistry in the CA1 region of the hippocampus. Results Compared to the control group ((1. 48 ± 0. 08) μg/L) and the 1. 3% isoflurane group( (1.53 ±0. 12)μg/L) ,the 3% isoflurane group showed significantly higher level of S100β( (3. 12 ±0. 15) μg/L, P＜0.05) . There was no differences in densities of caspase-3-positive cells between the control ((33 ±4) cell/mm ) and 1.3% isoflurane groups((31 ±5)cell/mm2). Compared to 1.3% isoflurane,isoflurane at a concentration of 3%((75 ± 7) cell/mm2, P＜0.05) for lh increased neurodegeneration in the hippocampal CA1 area in the developing brain of fetal rats. Conclusion Isoflurane can dose-dependently induce brain damage. Isoflurane at a concentration of 3% for lh can induce apoptosis in the hippocampal CA1 area and increase S100β levels of fetal rats.
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Objective To investigate the effect of propofol pretreatment on the expression of phosphorylated c-Jun N-terminal kinase (p-JNK), matrix metalloproteinase-9 (MMP-9) and aquaporin-4 (AQP-4) during focal cerebral ischemia-reperfusion (I/R) in rats. Methods Seventy-two healthy male SD rats weighing 250-280 g were randomly divided into 4 groups (n = 18 each): sham operation group (group S), I/R group and propofol pretreatment group (P1 and P2). In group I/R, P1 and P2, focal cerebral I/R was induced by occlusion of middle cerebralartery for 2 h followed by 24 h of reperfusion. In group P1 and P2, intraperitioneal 0.5 % and 1% propofol 10 ml/kg were injected 30 rmin before ischemia respectively. In group I/R, normal saline 10 ml/kg was given instead of propofol 30 min before ischemia. Neurological deficit score (NDS) was assessed after consciousness was recovered. 2% Evans blue (EB) 3 ml/kg was injected intravenously 1 h before the animals were sacrificed at 24 h of reperfusion. The brain tissues were taken for determination of the brain water content, EB content and expression of p-JNK, MMP-9 and AQP-4. Results Compared with group S, the NDS and content of water and EB were significantly increased and the expression of p-JNK, MMP-9 and AQP-4 was up-regulated in group I/R, P1 and P2(P ＜ 0.05). Compared with group I/R, the NDS and content of water and EB were significantly decreased and the expression of p-JNK, MMP-9 and AQP-4 was down-regulated in group P1 and P2 (P ＜ 0.05). Compared with group P1 , the expression of p-JNK and MMP-9 was down-regulated (P ＜ 0.05), but no significant difference was found in the NDS, water and EB content and the expression of AQP-4 in group P2 (P ＞ 0.05). Conclusion Propofol pretreatment can reduce focal cerebral I/R injury by inhibiting the activation of JNK signal pathway and up-regulation of MMP-9 and AQP-4 expression.
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OBJECTIVE:To evaluate the effect of Stronger Neo-Mioniphagen C(SNMC)on liver function of the patients with hepatocarcinoma associated with cirrhosis.METHODS:55patients with hepatocarcinoma associated with cirrhosis were allocated to2groups randomly,group A:before operation SNMC(1ml/kg)was dripped intravenously to the patients,group B:before surgery NS(1ml/kg)was administered.On the1st、3rd、6th postoperative day,the index of liver function of the perive?nous blood were analyzed statistically.RESULTS:On the1st、3rd postoperative day,all the value of liver function in both group is higher than the basic,and the value in group A is lower than that in group B(P