不同亚低温治疗时间对缺氧缺血性脑病新生患儿疗效的影响

目的:比较不同亚低温治疗时间对缺氧缺血性脑病患儿疗效及预后的影响,探讨亚低温治疗的最优时间,并且观察此治疗对新生儿有无不良影响。方法:选取我院收治的80例缺氧缺血性脑病(HIE)新生儿作为研究对象,将患儿随机分亚低温治疗48 h组、72 h组、96 h组和常规治疗组,每组20例患儿。所有患儿均给予常规治疗,亚低温组患儿在上述治疗基础上,在出生后6 h内加用选择性头部亚低温治疗。四组患儿生后28 d时进行神经测定(NBNA)评分,出生18月时进行Bayley评分。患儿接受治疗7天后统计血小板减少、电解质紊乱以及血糖紊乱的发生例数。结果:72 h组和96 h组患儿生后NBNA评分、Bayley评分比48 h组和常规治疗组高(P0.05),有统计学差异;72 h组和96 h组的NBNA评分、Bayley评分均没有统计学差异(P0.05),48 h组和常规组的评分也没有统计学差异(P0.05)。亚低温治疗96 h组患儿中,发生血小板减少、电解质紊乱及血糖紊乱等不良反应的比例较48 h组和72 h组明显增多(P0.05),有统计学差异;对比48 h组和72 h组不良反应的患儿比例,没有显著统计学差异(P0.05)。结论:亚低温治疗72 h对HIE患儿的治疗效果优于48 h,产生的副作用小于治疗96 h,建议临床亚低温治疗时间采用72 h以取得最佳治疗效果,产生最小不良反应。     

A clinical trial of the Bentley BOS-5 pediatric oxygenator

The performance of the Bentley BOS-5 pediatric oxygenator was evaluated on the basis of its response to maintain arterial pH between 7.35 and 7.45, arterial pO(2) between 100 and 200 mm Hg, and arterial pCO(2) between 35 and 45 mm Hg (Texas Heart Institute perfusion protocol). The oxygenator was found to be efficient at all flow rates employed; however, the pO(2) parameter could not be consistently maintained within protocol limits, but could be improved when a mixture of 5% carbon dioxide/95% oxygen was used for the duration of a case.     

局部亚低温联合硫酸镁对局灶性脑缺血大鼠的保护作用

目的:探讨联合应用局部亚低温(32-35℃)及硫酸镁对局灶性脑缺血大鼠的保护作用及其可能机制。方法:通过线栓法建立大鼠大脑中动脉阻塞(MCAO)模型,将40只雄性Wistar大鼠随机分为假手术组、常温组、亚低温组、硫酸镁组、亚低温+硫酸镁组,每组8例,采用Longa神经功能评分、TTC染色、TUNEL技术,检测和比较各组脑缺血后大鼠的神经功能、脑梗死体积、凋亡细胞数。结果:与常温组相比,亚低温组与亚低温+硫酸镁组的梗死体积、神经功能评分、凋亡细胞数均明显降低,差异有显著意义(P0.05);而与亚低温组相比,亚低温+硫酸镁组局灶脑缺血大鼠的脑梗死体积、神经功能评分、凋亡细胞数均显著减少,差异有显著意义(P0.05)。结论:与单独应用亚低温相比,局部亚低温与硫酸镁联合应用,对局灶性脑缺血大鼠可发挥更有效的脑保护作用,其机制可能与抑制脑缺血后凋亡有关。     

Mild hypothermia attenuates mitochondrial oxidative stress by protecting respiratory enzymes and upregulating MnSOD in a pig model of cardiac arrest

Mild hypothermia is the only effective treatment confirmed clinically to improve neurological outcomes for comatose patients with cardiac arrest. However, the underlying mechanism is not fully elucidated. In this study, our aim was to determine the effect of mild hypothermia on mitochondrial oxidative stress in the cerebral cortex. We intravascularly induced mild hypothermia (33°C), maintained this temperature for 12 h, and actively rewarmed in the inbred Chinese Wuzhishan minipigs successfully resuscitated after 8 min of untreated ventricular fibrillation. Cerebral samples were collected at 24 and 72 h following return of spontaneous circulation (ROSC). We found that mitochondrial malondialdehyde and protein carbonyl levels were significantly increased in the cerebral cortex in normothermic pigs even at 24 h after ROSC, whereas mild hypothermia attenuated this increase. Moreover, mild hypothermia attenuated the decrease in Complex I and Complex III (i.e., major sites of reactive oxygen species production) activities of the mitochondrial respiratory chain and increased antioxidant enzyme manganese superoxide dismutase (MnSOD) activity. This increase in MnSOD activity was consistent with the upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA and protein expressions, and with the increase of Nrf2 nuclear translocation in normothermic pigs at 24 and 72 h following ROSC, whereas mild hypothermia enhanced these tendencies. Thus, our findings indicate that mild hypothermia attenuates mitochondrial oxidative stress in the cerebral cortex, which may be associated with reduced impairment of mitochondrial respiratory chain enzymes, and enhancement of MnSOD activity and expression via Nrf2 activation.     

Influence of Plasma and Cerebrospinal Fluid Levels of Endothelin-1 and No in Reducing Cerebral Vasospasm after Subarachnoid Hemorrhage During Treatment with Mild Hypothermia,in a Dog Model

Using vascular heat-exchange controller implemented mild hypothermia treatment, the authors established the cerebral vasospasm model in which blood was injected twice into dog’s foramen magnum; and it was discussed the influence of the concentration of endothelin-1 and NO in blood plasma and cerebrospinal fluid through continuing treatment of mild hypothermia at different times in secondary brain vasospasm model after subarachnoid hemorrhage. Thirty healthy mongrel dogs were randomly divided into five groups; artificial cerebrospinal fluid group (group A), normal temperature control group (group C), mild hypothermia 8 h group (group H1), mild hypothermia 16 h group (group H2), and mild hypothermia 32 h group (group H3). The authors injected the artificial CSF into dog’s foramen magnum in group A while the other four groups were injected with autologous arterial blood. The normal group’s temperature maintained 38.5°C. The authors set the temperature at 33.5°C in mild hypothermia groups and this was maintained for 8, 16, and 32 h, respectively. ET-1 and NO levels in the cerebrospinal fluid and plasma were assayed in each group on days 0, 7, 14, and 21. Then the changes of the diameter of blood vessels of cerebral basilar artery and overall performance categories score in each group through application of CT angiography were recorded. In the cerebral vasospasm model which was constructed by injecting the blood to dog twice, mild hypothermia treatment, through the application of vascular heat-exchange controller, could reduce cerebral vasospasm. It was observed that the duration of the mild hypothermia is directly proportional to the longer duration of the relieving of cerebral vasospasm. The reciprocal changes observed in the levels of ET-1 and NO in cerebrospinal fluid and plasma revealed that it might be possible to reduce the cerebral vasospasm by regulating the rising amplitude of ET-1 and the decrease in NO in CSF and plasma.     

Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model

The aim of this study was to evaluate the effect of mild hypothermia on the coagulation-fibrinolysis system and physiological anticoagulants after cardiopulmonary resuscitation (CPR). A total of 20 male Wuzhishan miniature pigs underwent 8 min of untreated ventricular fibrillation and CPR. Of these, 16 were successfully resuscitated and were randomized into the mild hypothermia group (MH, n = 8) or the control normothermia group (CN, n = 8). Mild hypothermia (33°C) was induced intravascularly, and this temperature was maintained for 12 h before pigs were actively rewarmed. The CN group received normothermic post-cardiac arrest (CA) care for 72 h. Four animals were in the sham operation group (SO). Blood samples were taken at baseline, and 0.5, 6, 12, 24, and 72 h after ROSC. Whole-body mild hypothermia impaired blood coagulation during cooling, but attenuated blood coagulation impairment at 72 h after ROSC. Mild hypothermia also increased serum levels of physiological anticoagulants, such as PRO C and AT-III during cooling and after rewarming, decreased EPCR and TFPI levels during cooling but not after rewarming, and inhibited fibrinolysis and platelet activation during cooling and after rewarming. Finally, mild hypothermia did not affect coagulation-fibrinolysis, physiological anticoagulants, or platelet activation during rewarming. Thus, our findings indicate that mild hypothermia exerted an anticoagulant effect during cooling, which may have inhibitory effects on microthrombus formation. Furthermore, mild hypothermia inhibited fibrinolysis and platelet activation during cooling and attenuated blood coagulation impairment after rewarming. Slow rewarming had no obvious adverse effects on blood coagulation.     

Therapeutic hypothermia in the management of acute liver failure

A large body of experimental data and preliminary clinical studies point to the induction of mild hypothermia (32-35 °C) as a valuable approach to control the development of brain edema and intracranial hypertension in acute liver failure (ALF). The ability of hypothermia to affect multiple processes probably explains its efficacy to prevent these cerebral complications. Remarkably, mild hypothermia has been shown to prevent or attenuate most of the major alterations involved in the pathogenesis of the cerebral complications of ALF, including the accumulation of ammonia in the brain and the circulation, the alterations of brain glucose metabolism, the brain osmotic disturbances, the accumulation of glutamate and lactate in brain extracellular space, the development of inflammation and oxidative/nitrosative stress, and others. Limited information suggests that the systemic effects of hypothermia may also be beneficial for some peripheral complications of ALF. Translation of the beneficial effects of therapeutic hypothermia into standard clinical practice, however, needs to be confirmed in adequately designed clinical trials. Such trials will be important to determine the safety of therapeutic hypothermia, to identify which patients might benefit from it, and to provide the optimal guidelines for its use in patients with ALF.     

亚低温联合镁剂对脑缺血再灌注大鼠保护作用的研究

目的:rt-PA溶栓为缺血性卒中最有效的治疗方法,脑血流再通后挽救濒临死亡的神经细胞同时,也可能发生更为严重而持久的脑缺血再灌注损伤。本研究探讨联合应用局部亚低温(32-35℃)及硫酸镁对局灶性脑缺血再灌注大鼠的保护作用及其可能机制。方法:通过线栓法建立大鼠大脑中动脉阻塞(MCAO)及再通模型,将50只雄性Wistar大鼠随机分为假手术组、常温组、亚低温组、硫酸镁组、亚低温+硫酸镁组,每组10例,采用Longa神经功能评分、TTC染色、干湿重法、TUNEL技术,检测和比较各组脑缺血再灌注后大鼠的神经功能、脑梗死体积、脑组织含水量及凋亡细胞数。结果:与常温组相比,亚低温组与亚低温+硫酸镁组的梗死体积、神经功能评分、脑组织含水量、凋亡细胞数均明显降低,差异有显著意义(P0.05);而与亚低温组相比,亚低温+硫酸镁组局灶脑缺血大鼠的脑梗死体积、神经功能评分、脑组织含水量、凋亡细胞数均显著减少,差异有显著意义(P0.05)。结论:与单独应用亚低温相比,局部亚低温与硫酸镁联合应用,对局灶性脑缺血再灌注大鼠可发挥更有效的脑保护作用。其机制可能与抑制脑缺血再灌注后凋亡及减轻脑水肿有关。二者联用可能为缺血性卒中患者提供一种减轻溶栓后再灌注损伤的有效脑保护方法。     

亚低温对脊髓损伤后反应性星形胶质细胞增生的影响

目的：观察在不同温度条件下脊髓星形胶质细胞划痕损伤活化后的形态和活性改变,以探讨亚低温对脊髓损伤后反应性星形胶质细胞增生的影响。方法：体外原代培养新生SD大鼠脊髓星形胶质细胞,以划痕实验制备反应性星形胶质细胞。亚低温选择33℃,细胞培养48 h。实验分为对照组、划痕组、亚低温组和划痕+亚低温组。各组在相应的时间点观察细胞形态,采用免疫荧光染色方法检测Nestin阳性率,MTT比色法观察细胞活性,PI染色方法观察细胞凋亡程度。结果：与对照组和亚低温组相比,划痕组和划痕+亚低温组细胞胞体肥大,周围突起增多、延展以及胞浆丰富,细胞生长率明显升高。与划痕组相比,划痕+亚低温组细胞变化减慢,周围突起减少,细胞长入划痕处所需时间增加,细胞Nestin阳性率、PI阳性率和细胞生长率明显降低,各结果差异显著（P<0.01）。结论：划痕损伤后星形胶质细胞活化为反应性星形胶质细胞并会增生,亚低温明显抑制脊髓反应性星形胶质细胞的活化增生,并可以抑制星形胶质细胞的凋亡。     

亚低温治疗对重型颅脑损伤患者颅内压、脑血流及氧代谢的影响

目的:探讨亚低温治疗对重症颅脑损伤(sTBI)患者颅内压(ICP)、脑血流及氧代谢的影响。方法:收集50例sTBI患者随机分为实验组和对照组,每组25例,均给予常规治疗,观察组在常规治疗基础上给予亚低温辅助治疗,检测患者治疗前、治疗第3、5、7天ICP动态变化以及治疗前和治疗7天后脑血流和氧代谢等指标变化。结果:治疗第3、5、7天ICP组间差异均具有统计学意义(P0.05),随着治疗时间增加两组ICP均逐渐降低,差异具有统计学意义(P0.05);治疗前Qmean、Vmean、Wv、DR等组间差异无统计学意义(P0.05),治疗7天后Qmean、Vmean均升高,Wv、DR均降低,差异具有统计学意义(P0.05);治疗前SjvO_2、CjvO_2、CaO_2、CERO_2组间差异无统计学意义(P0.05),治疗7天后SjvO_2、CjvO_2、CERO_2均升高,CaO_2降低,差异具有统计学意义(P0.05)。结论:亚低温治疗可以显著降低患者颅内压,改善脑血流和氧代谢水平。     

Risk of hypothermia in elderly patients with diabetes.

The incidence of admissions of patients with hypothermia was determined to examine whether hypothermia was more common in elderly patients with diabetes than in the general population after diabetic metabolic emergency cases had been excluded. A prospective survey of three accident and emergency departments identified 134 cases of hypothermia admitted from a catchment population of almost 157,000 aged 65 or over during the winters of 1981-2 to 1983-4. The predicted number of patients with diabetes in the population was nearly 5600 (3.5%). Twenty three admissions for hypothermia (17%) occurred in 20 patients with previously diagnosed diabetes. Women made up 87% of the diabetic admissions; the ratio of diabetic to non-diabetic admission rates in women was 7.9 (95% confidence interval 5.3 to 12.0). After excluding diabetic metabolic emergency admissions the ratio was 6.4. The ratio in men was 2.4, but the small number of admissions produced wide confidence intervals. Ten of the admissions with diabetes (43%) had pathological disorders that are associated with an increased risk of hypothermia. The frequency of these conditions is higher in patients with diabetes than in the general population and partly explains the increased risk of hypothermia in these patients.     

Cold‐inducible protein RBM3 mediates hypothermic neuroprotection against neurotoxin rotenone via inhibition on MAPK signalling

Mild hypothermia and its key product, cold‐inducible protein RBM3, possess robust neuroprotective effects against various neurotoxins. However, we previously showed that mild hypothermia fails to attenuate the neurotoxicity from MPP⁺, one of typical neurotoxins related to the increasing risk of Parkinson disease (PD). To better understand the role of mild hypothermia and RBM3 in PD progression, another known PD‐related neurotoxin, rotenone (ROT) was utilized in this study. Using immunoblotting, cell viability assays and TUNEL staining, we revealed that mild hypothermia (32°C) significantly reduced the apoptosis induced by ROT in human neuroblastoma SH‐SY5Y cells, when compared to normothermia (37°C). Meanwhile, the overexpression of RBM3 in SH‐SY5Y cells mimicked the neuroprotective effects of mild hypothermia on ROT‐induced cytotoxicity. Upon ROT stimulation, MAPK signalling like p38, JNK and ERK, and AMPK and GSK‐3β signalling were activated. When RBM3 was overexpressed, only the activation of p38, JNK and ERK signalling was inhibited, leaving AMPK and GSK‐3β signalling unaffected. Similarly, mild hypothermia also inhibited the activation of MAPKs induced by ROT. Lastly, it was demonstrated that the MAPK (especially p38 and ERK) inhibition by their individual inhibitors significantly decreased the neurotoxicity of ROT in SH‐SY5Y cells. In conclusion, these data demonstrate that RBM3 mediates mild hypothermia‐related neuroprotection against ROT by inhibiting the MAPK signalling of p38, JNK and ERK.     

Nitrotyrosine and nitrate/nitrite levels in cardiac arrest survivors treated with endovascular hypothermia

The protective effect of therapeutic hypothermia in cardiac arrest survivors (CAS) has been previously well documented. Animal studies have indicated that attenuation of tissue oxidative stress (OS) may be involved in the mechanisms that lead to the beneficial effect of hypothermia. The extent of OS and nitric oxide (NO) production in adult CAS treated with endovascular hypothermia is, however, unknown. A total of 11 adult patients who experienced cardiac arrest out of hospital were included in the present study, and all were treated with mild hypothermia using the Thermogard XP (Alsius, USA) endovascular system. A target core temperature of 33 °C was maintained for 24 hours, with a subsequent rewarming rate of 0.15 °C per hour, followed by normothermia at 36.8 °C. Blood samples for the measurement of nitrotyrosine and nitrate/nitrite levels were drawn at admission and every 6 hours thereafter for two days. During the hypothermic period, the levels of nitrotyrosine and nitrates/nitrites were comparable with baseline values. During the rewarming period, serum levels of both parameters gradually increased and, during the normothermic period, the levels were significantly higher compared with hypothermic levels (nitrotyrosine, P<0.001; nitrates/nitrites, P<0.05). In our study, significantly lower levels of nitrotyrosine and nitrates/nitrites were demonstrated during hypothermia compared with levels during the normothermic period in adult CAS. These data suggest that attenuation of OS and NO production may be involved in the protective effect of hypothermia in adult CAS.     

Mild hypothermia protects against postischemic hepatic endothelial injury and decreases the formation of reactive oxygen species

The ability of mild hypothermia (MH; 34 degrees C) to protect against postischemic endothelial injury and decrease reactive oxygen species' (ROS) formation was studied using lucigenin and luminol enhanced chemiluminescence (CL). Lucigenin CL is largely specific for superoxide, while luminol reacts with many ROS. Isolated rat livers perfused under constant flow in a non-recirculating system were exposed to 2.5 h of ischemia after 0.5 h perfusion with Krebs-Henseleit buffer at either normothermia (38 degrees C) or mild hypothermia (34 degrees C) (n = 5, all groups). CL (cps), vascular resistance (Woods units), O2 consumption, and potassium efflux were measured at the end of perfusion, and at 0 min reperfusion, and every 30 min during reperfusion. For both the lucigenin and luminol groups, CL and vascular resistance increased significantly (repeat measures ANOVA, P <0.05) for normothermia (NT, 38 degrees C) but not mild hypothermia. Potassium efflux did not change significantly for the mild hypothermia groups. In the luminol enhanced group, oxygen consumption was greater in the mildly hypothermic group at 1 h and 1.5 h of reperfusion. Mild hypothermia decreased postischemic ROS production. Increased vascular resistance in the normothermia group may indicate an endothelial injury. Mild hypothermia appears to protect against this injury.     

Acute Renal Failure and Open Heart Surgery

A retrospective study of 428 open heart operations showed the incidence of mild and severe renal failure to be 26% and 4·7% respectively. The mortality rate was 38% in the mild cases and 70% in the severe cases. Only half of the patients whose death was associated with renal failure showed macroscopic or microscopic renal lesions at necropsy. The patients who developed renal impairment had significantly higher mean preoperative blood urea (40 mg/100 ml) than the non-renal-failure cases (33 mg/100 ml). Periods of perfusion over 60 minutes, mean perfusion pressures below 80 mm Hg, and multiple valve replacement operations also increased the incidence of renal failure. There was no statistical correlation between the age of individual patients, the degree of cooling, and postoperative blood urea values. There was no evidence to suggest that frusemide or mannitol separately or together influenced the development of renal failure. Peritoneal dialysis was preferred for initial treatment of patients with severe renal failure, and haemodialysis was required only in special cases.     

亚低温联合手术治疗对重型颅脑损伤患者血清ET-1、Ang-1、G-CSF及预后的影响

目的:研究亚低温联合手术治疗对重型颅脑损伤患者血清内皮素-1(endothelin-1,ET-1)、血管生成素-1(Angiopoietin-1,Ang-1)、粒细胞集落刺激因子(Granulocyte-colony stimulating factor,G-CSF)及预后的影响。方法:选取我院收治的118例重型颅脑损伤患者,按照抛硬币法分为治疗组和对照组,每组各59例。两组患者入院后均进行手术治疗,治疗组则在术后进行亚低温治疗。观察并比较两组患者临床治疗效果、治疗前后血清ET-1、Ang-1、G-CSF水平变化情况、不良反应发生情况以及预后情况。结果:治疗后,治疗组第1、3、7、14天的颅内压均显著低于对照组,两组组间比较差异显著(P0.05)。两组患者血清ET-1、Ang-1、G-CSF较治疗前显著下降,且治疗组血清各指标水平改善情况显著优于对照组(P0.05)。两组患者均发生脑梗死、脑积水、癫痫、肺部感染、切口脑脊液瘘以及应激性溃疡出血等并发症,但两组差异无统计学意义(P0.05)。治疗组患者的预后良好率达到49.15%,显著高于对照组的13.56%;而治疗组的死亡率(5.08%)则明显低于对照组(13.56%),两组差异显著(P0.05)。结论:亚低温联合手术治疗较单纯手术治疗可以更好的改善患者血清ET-1、Ang-1以及G-CSF水平,其不良反应发生率也更低,从而可以更好的改善患者的预后情况,值得在临床上推广应用。     

Full recovery of a patient after oxygenator replacement during open-heart surgery

During an open-heart procedure in a 69-year-old man, a damaged mitral valve was being examined when suddenly the venous return line from the oxygenator of the heart-lung machine became filled with gas. After the venous line had been flushed and cardiopulmonary bypass had been reinstated, the line again filled with gas, and the aortic line also had to be clamped to prevent a massive air embolism. The oxygenator was immediately exchanged, bypass was resumed after 7 to 8 minutes, and the surgical procedures were completed. The patient survived, and a year and a half later continues in good health. His survival was attributed to three factors: intraaortic balloon support, hypothermia to 28 degrees C, and the prompt exchange of oxygenators.     

Hypothermia: a complication of diabetic ketoacidosis.

During 1969-77, 20 episodes of severe hypothermia occurred in 19 diabetic patients in Nottingham. Thirteen were associated with ketotic hyperosmolar coma, two with lactic acidosis, and one with hypoglycaemia, while in four there was no loss of diabetic control. Ketoacidosis accounted for 11.8% of all admissions for severe accidental hypothermia and was a commoner cause than hypothyroidism (8%). Patients with ketoacidosis were younger and developed hypothermia as often during the summer as during the winter. The metabolic disturbance was characteristic, with severe acidosis (mean pH 7.04), a high blood glucose concentration (mean 56.6 mmol/l; 1020 mg/100 ml), and high plasma osmolality (mean 379.7 mmol (mosmol)/kg). Eight of the 13 episodes proved fatal. Hypothermia may aggravate ketoacidosis and complicate treatment and should be sought in all patients with severe diabetic coma.     

Mild hypothermia protects against postischemic hepatic endothelial injury and decreases the formation of reactive oxygen species

Abstract

The ability of mild hypothermia (MH; 34°C) to protect against postischemic endothelial injury and decrease reactive oxygen species' (ROS) formation was studied using lucigenin and luminol enhanced chemiluminescence (CL). Lucigenin CL is largely specific for superoxide, while luminol reacts with many ROS.

Isolated rat livers perfused under constant flow in a non-recirculating system were exposed to 2.5 h of ischemia after 0.5 h perfusion with Krebs-Henseleit buffer at either normothermia (38°C) or mild hypothermia (34°C) (n = 5, all groups). CL (cps), vascular resistance (Woods units), O₂ consumption, and potassium efflux were measured at the end of perfusion, and at 0 min reperfusion, and every 30 min during reperfusion.

For both the lucigenin and luminol groups, CL and vascular resistance increased significantly (repeat measures ANOVA, P <0.05) for normothermia (NT, 38°C) but not mild hypothermia. Potassium efflux did not change significantly for the mild hypothermia groups. In the luminol enhanced group, oxygen consumption was greater in the mildly hypothermic group at 1 h and 1.5 h of reperfusion.

Mild hypothermia decreased postischemic ROS production. Increased vascular resistance in the normothermia group may indicate an endothelial injury. Mild hypothermia appears to protect against this injury.     

血清尿酸水平与老年轻度高血压患者的内皮功能相关性分析

目的:探讨血清尿酸水平与老年轻度高血压患者的内皮功能相关性。方法:选取我院2020年1月到2020年12月共收治的200例老年轻度高血压患者作为研究对象,所有患者均为未使用过降压药物治疗,将其分为轻度高血压组。另选取同期收治的200例高血压常规药物治疗患者作为重度高血压组与200名健康者作为对照组,对比三组患者血清尿酸水平与血管内皮功能。对观察组所有患者依照血清尿酸水平进行分组,将血清尿酸水平208-360μmol/L的患者分为低尿酸组,共计136例,将血清尿酸水平≥360μmol/L的患者分为高尿酸组,共计64例。对比两组患者的一般临床指标、血管内皮功能与氧化应激指标,并分析血清尿酸水平与老年轻度高血压患者的内皮功能相关性。结果:重度、轻度高血压组与对照组患者NO、ET-1、SUA水平对比差异显著,具有统计学意义(P<0.05);高尿酸组与低尿酸组患者TG、TC、DBP、SBP水平对比无明显差异(P>0.05),高尿酸组患者Cr水平高于低尿酸组,组间对比,差异具有统计学意义(P<0.05);高尿酸组与低尿酸组患者T-AOC、GSH-Px、LHP、MDA、NO、ET-1水平对比差异显著,高尿酸组患者LHP、MDA和ET-1水平明显高于低尿酸组,高尿酸组患者T-AOC、GSH-Px、NO水平明显低于低尿酸组,组间对比,差异具有统计学意义(P>0.05);Spearman相关分析结果显示:TG、TC、Cr、DBP、SBP与血尿酸水平无明显相关性(P>0.05),T-AOC、GSH-Px、NO与血清尿酸水平呈负相关(P<0.05),LHP、MDA、ET-1与血清尿酸水平呈正相关(P<0.05)。结论:血清尿酸水平与老年轻度高血压患者的内皮功能具有明显相关性,而且证明血尿酸水平的升高可能由患者氧化应激导致,因此氧化应激水平也是引起血管内皮功能障碍的一种潜在机制,希望本研究结果能够为高血压患者的疾病控制提供参考意见。