纯氧与空气复苏对窒息新生大鼠肺泡超微结构的对比观察

目的研究纯氧和空气复苏窒息新生大鼠后,肺泡超微结构的变化。方法选用清洁级7d龄SD大鼠（n=30）,随机分为正常对照组、实验组（空气组和纯氧组）,将实验组建立缺氧模型后,分别给与空气和纯氧复苏,每组又分为24h、72h两个亚组（n=5）。制作常规电镜标本,在透射电镜下观察。结果1.与正常组比较,实验组出现AECⅠ局部肿胀、胞质脱落,AECⅡ线粒体肿胀、板层小体失去正常结构及数目减少、游离面微绒毛稀少,间质细胞水肿及染色体淡染等超微病理学改变,但空气组的病理改变较纯氧组轻微;2.无论空气组还是纯氧组,其各自的72h组与24h组两个亚组比较,超微病理学改变并无明显差异。结论与空气复苏比较,采用纯氧复苏窒息新生大鼠对于肺组织超微结构损伤严重。     

The relationship between the cardiac contractile function,adenine nucleotides and amino acids of cardiac tissue and mitochondria at acute respiratory hypoxia

The effect of asphyxia and subsequent resumption of respiration on the content of adenine nucleotides and some amino acids in heart tissue and mitochondria, as well as respiration of heart mitochondria was studied in rats. The depression of cardiac contractile function during asphyxia showed a better correlation with losses in mitochondrial adenine nucleotides (ATP+ADP+AMP) than those in cardiac tissue. The decrease in the heart work index was accompanied by a decrease in state 3 respiration with glutamate and malate as well as uncoupled respiration with these substrates. This did not occur with succinate. Nonphosphorylating (state 4) respiratory rates and ADP/O ratios were slightly affected by asphyxia, when respiratory substrates of both types were used. The decreased level of glutamic acid in the tissue and mitochondria of asphyxic hearts was simultaneously observed with a significant increase of alanine in cardiac tissue and of aspartic acid in the mitochondria. The losses of intramitochondrial ATP and respiratory activity with NAD-dependent substrates during asphyxia were associated with a reduction of glutamic acid level in mitochondria. The recovery of cardiac function during resumption of respiration was related to the restoration of mitochondrial respiration supported by glutamate and malate, as well as to the restoration of mitochondrial adenine nucleotides and glutamic acid. The results suggest that the depression of cardiac function caused by acute respiratory hypoxia may be attributed to impairment of electron transport, particularly in complex I of the respiratory chain and changes in metabolism of glutamic acid.     

Hypoxia and hypercapnia in asphyctic differentiation of regional sympathetic activity in the anesthetized rabbit

Summary The contributions of hypoxia and of hypercapnia to the differentiated changes of regional sympathetic activity during asphyxia were investigated in anesthetized, paralyzed rabbits. Under artificial ventilation with gas mixtures of various O₂ and CO₂ contents, the discharges of a postganglionic nerve twig accompanying the retroauricular artery (cutaneous sympathetic) and of a splanchnic nerve branch (visceral sympathetic) were recorded. PaO₂, PaCO₂, pH, arterial pressure, and heart rate were measured.Moderate hypoxia (PaO₂ 27.2 Torr) induced a differentiated response of regional sympathetic activity similar to that observed during moderate asphyxia, i.e. increase of visceral and decrease of cutaneous sympathetic activity. During severe hypoxia (PaO₂ 16.4 Torr) both visceral and cutaneous sympathetic activity increased, the latter after a temporary decrease.—During hypercapnia (PaCO₂ 59.3 Torr) only a slight increase of visceral sympathetic activity was observed, while cutaneous sympathetic activity did not change.—It is concluded that the differentiated responses of the sympathetic nervous system during asphyxia are caused mainly by hypoxia.     

Immunohistochemical investigation of a pulmonary surfactant in fatal mechanical asphyxia

We evaluated the usefulness of pulmonary surfactant protein A (SP-A) as a practical diagnostic marker of fatal mechanical asphyxia in forensic autopsy cases. A total of 27 cases of asphyxia were examined histologically and immunohistochemically and compared with a control group consisting of 16 cases of poisoning (n = 9) and peracute death (n = 7). Both groups showed histological findings of local atelectasis and local emphysema, congestion, intra-alveolar and interstitial edema in most cases and pulmonary hemorrhages in some cases. The mechanical asphyxia group showed a significantly increased intensity of SP-A staining in the intra-alveolar space accompanied by many massive aggregates in approximately 60% of cases, which was not found in the control group. These structures may be interpreted as aggregates of pulmonary surfactant released from the alveolar wall due to enhanced secretion caused by strong forced breathing or over-excitement of the autonomic nervous system by mechanical asphyxia. The results of our investigation suggest the practical usefulness of the immunohistochemical detection of SP-A in distinguishing mechanical asphyxia from other types of hypoxia.     

Newer concepts and approaches to neonatal brain asphyxia

The asphyxial injury to neonate brain seems to be mediated through a cascade of biochemical events during ischaemia—reperfusion which includes excitatory amino acids, free radicals and accelerated programmed cell death (Apoptosis). The diagnosis of asphyxia requires rigorous approach based on background clinical information, certain diagnostic tests and exclusion of alternative diagnosis which may have similar clinical presentation. The treatment currently employed for the management of birth asphyxia controversial and requires critical appraisal. The future strategies for management include a number of approaches based on putative mechanism for asphyxial brain injury but they are still being evaluated as research and should not be used for clinical purposes in human newborns as yet.     

Effect of allopurinol on NMDA receptor modification following recurrent asphyxia in newborn piglets

The present study tests the hypothesis that repeated episodes of asphyxia will lead to alterations in the characteristics of the N-methyl-d-aspartate (NMDA) receptor in the brain cell membrane of newborn piglets and that pre-treatment with allopurinol, a xanthine oxidase inhibitor, will prevent these modifications. Eighteen newborn piglets were studied. Six untreated and six allopurinol treated animals were subjected to eight asphyxial episodes and compared to six normoxic, normocapneic controls. Brain cell membrane Na⁺,K⁺-ATPase activity was determined to assess membrane function. Na⁺,K⁺-ATPase activity was decreased from control following asphyxia in both the untreated and treated animals (47.7±3.2 vs. 43.0±2.2 and 41.0±5.3 μmol Pi/mg protein/h, p<0.05, respectively). ³H-MK-801 binding studies were performed to measure NMDA receptor binding characteristics. The receptor density (B_max) in the untreated asphyxia group was decreased compared to control animals (0.80±0.11 vs. 1.13±0.33, p<0.05); furthermore, the dissociation constant (K_d) was also decreased (3.8±0.7 vs. 9.2±2.2, p<0.05), indicating an increase in receptor affinity. In contrast, B_max in the allopurinol treated asphyxia group was similar to control (1.06±0.37); and K_d was higher (lower affinity) than in the untreated group (6.5±1.4, p<0.05). The data indicate that recurrent asphyxial episodes lead to alterations in NMDA receptor characteristics; and that despite cell membrane dysfunction as seen by a decrease in Na⁺,K⁺-ATPase activity, allopurinol prevents modification of NMDA receptor–ion channel binding characteristics induced by repeated episodes of asphyxia.     

Nonoliguric and oliguric acute renal failure in asphyxiated term neonates

The purpose of this study was to determine the prevalence and types of acute renal failure in asphyxiated full-term neonates and to evaluate the accuracy of an asphyxia morbidity score in predicting acute renal failure. Neonates admitted to one institution from 1990 through 1993 with a gestational age 36 weeks and 5-min Apgar score 6, without congenital malformations or sepsis, were studied retrospectively for acute renal failure in the 1st week of life. Acute renal failure was defined as serum creatinine >1.5 mg/dl (133 mol/l) with normal maternal renal function. Nonoliguric renal failure was defined as renal failure with urine output >1 ml/kg per hour after the 1st day. An asphyxia morbidity scoring system was used to distinguish severe from moderate asphyxia. The score ranged from 0 to 9 and was based upon fetal heart rate, Apgar score at 5 min, and base deficit in the 1st h of life. The score for severe asphyxia was defined as 6–9 and for moderate asphyxia as 1–5. Sixty-six neonates fulfilled study criteria. Acute renal failure was present in 20 of 33 (61%) infants with severe asphyxia scores and 0 of 33 with moderate asphyxia scores (P<0.0001). Acute renal failure was nonoliguric in 12 of 20 (60%), oliguric in 5 of 20 (25%) and anuric in 3 of 20 (15%). In conclusion 1) acute renal failure occurred in 61% of infants with severe asphyxia, 2) acute renal failure associated with severe asphyxia was predominantly nonoliguric and 3) an asphyxia morbidity score, which can be determined at 1 h of age, predicted acute renal failure in full-term infants with 100% sensitivity and 72% specificity.     

29例颈脊髓损伤高位截瘫患者不同时段并发窒息的原因分析与护理干预

探讨29例颈脊髓损伤高位截瘫患者在不同时段并发窒息的原因与护理干预方法.回顾性分析、总结108例颈脊髓损伤高位截瘫患者的临床资料,进行数据分析.有29例患者并发了窒息,呼吸中枢受损、呼吸肌麻痹、术区血肿压迫、食物返流、喉头水肿、植骨块脱落、肺部感染是其发生的主要原因,而且在不同时段各有突出.分阶段、针对性地实施护理干预,能有效预防和减少窒息的发生,提高护理质量.     

新产程标准中第二产程时长对产妇和新生儿结局的影响研究

目的 探讨新产程标准管理下第二产程时长对产妇和新生儿结局的影响。 方法 选取新产程标准试行以来于 2015 年 4 月至 2016 年 4 月在医院分娩且第二产程时长 ≥2 h 的单胎足月头先露初产妇 281 例作为观察组 （ A 组）, 依据第二产程时长不同将观察组细分成A1 、 A2 、 A3 组,其中 A1 组（ 183 例）第二产程时长 ≥2 h 且 ＜2.5 h , A2 组（ 62 例）第二产程时长 ≥2.5 h 且 ＜3 h , A3 组（ 36 例）第二产程时长 ≥3 h 。 随机抽取 280 例同期在我院分娩且第二产程时长 ＜2 h 的初产妇作为对照组（ B 组）。 对以上两组产妇和新生儿结局临床资料进行回顾性分析。 结果 A1 组与对照组比较,中转剖宫产率、产钳助产率、产后出血率、会阴侧切率、切口不良愈合率、新生儿窒息发生率、新生儿住院率差异均无统计学意义（ P>0.05 ）;但 A2 组和 A3 组的中转剖宫产率、产钳助产率、会阴侧切率均显著高于对照组（ P＜0.05 ）, A2 组和 A3 组的新生儿窒息率、新生儿住院率和对照组相比差异无统计学意义（ P>0.05 ）。 结论 随着新产程标准中第二产程时限的延长,新生儿窒息率及住院率未见增加;而产妇在第二产程时长超过 2.5 h 后其不良分娩结局的发生比例会明显增加。     

亚低温治疗及选择时机对窒息大鼠心肺复苏后的脑保护作用

【目的】探讨亚低温治疗及选择时机对窒息大鼠心肺复苏后的脑保护作用。【方法】36只成年 SD 大鼠随机分为假手术组(6只,A 组)、常温组(6只,B 组)和亚低温治疗组(24只,C 组),C 组随机分为 C1、C2、C3和 C4组四个亚组,每组6只。A 组仅进行麻醉、气管切开及血管穿刺操作,不进行心肺复苏;B 组不行低温治疗;C1~4组分别于心脏骤停后2、4、6、8 min 立即实施心肺复苏。统计各组复苏成功率;免疫组化法检测皮质及海马组织 Nrf2及 HO-1蛋白表达;按 Elliott 法计算脑组织百分水含量。【结果】C 组皮质、海马组织 Nrf2及 HO-1蛋白表达水平均显著高于 A 组和 B 组(P <0.05);C1、C2、C3和 C4四个亚组比较差异无统计学意义(P >0.05)。B 组和 C 组脑组织含水量均显著高于 A 组(P <0.05),但 B 组和 C 组比较差异无统计学意义(P >0.05),C1、C2、C3和 C4四个亚组比较差异也无统计学意义(P >0.05)。【结论】亚低温干预对心肺复苏大鼠的脑保护作用可能是通过激活 Nrf2-ARE 信号通路,上调 Nrf2及其下游基因 HO-1表达实现的,对窒息性心脏骤停心肺复苏后应早期进行亚低温治疗以减轻脑损伤,提高心肺复苏的成功率。