共查询到20条相似文献,搜索用时 8 毫秒
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Elliott Shang-shun Li Po-Yin Cheung Megan O'Reilly Joseph LaBossiere Tze-Fun Lee Shaun Cowan David L. Bigam Georg Marcus Schm?lzer 《PloS one》2016,11(1)
Background
End-tidal CO2 (ETCO2), partial pressure of exhaled CO2 (PECO2), and volume of expired CO2 (VCO2) can be continuously monitored non-invasively to reflect pulmonary ventilation and perfusion status. Although ETCO2 ≥14mmHg has been shown to be associated with return of an adequate heart rate in neonatal resuscitation and quantifying the PECO2 has the potential to serve as an indicator of resuscitation quality, there is little information regarding capnometric measurement of PECO2 and ETCO2 in detecting return of spontaneous circulation (ROSC) and survivability in asphyxiated neonates receiving cardiopulmonary resuscitation (CPR).Methods
Seventeen newborn piglets were anesthetized, intubated, instrumented, and exposed to 45-minute normocapnic hypoxia followed by apnea to induce asphyxia. Protocolized resuscitation was initiated when heart rate decreased to 25% of baseline. Respiratory and hemodynamic parameters including ETCO2, PECO2, VCO2, heart rate, cardiac output, and carotid artery flow were continuously measured and analyzed.Results
There were no differences in respiratory and hemodynamic parameters between surviving and non-surviving piglets prior to CPR. Surviving piglets had significantly higher ETCO2, PECO2, VCO2, cardiac index, and carotid artery flow values during CPR compared to non-surviving piglets.Conclusion
Surviving piglets had significantly better respiratory and hemodynamic parameters during resuscitation compared to non-surviving piglets. In addition to optimizing resuscitation efforts, capnometry can assist by predicting outcomes of newborns requiring chest compressions. 相似文献3.
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J. Selwyn Crawford 《BMJ (Clinical research ed.)》1963,1(5347):1739-1740
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Kasper J. Kyng Torjus Skajaa Sigrid Kerrn-Jespersen Christer S. Andreassen Kristine Bennedsgaard Tine B. Henriksen 《Journal of visualized experiments : JoVE》2015,(99)
Birth asphyxia, which causes hypoxic-ischemic encephalopathy (HIE), accounts for 0.66 million deaths worldwide each year, about a quarter of the world’s 2.9 million neonatal deaths. Animal models of HIE have contributed to the understanding of the pathophysiology in HIE, and have highlighted the dynamic process that occur in brain injury due to perinatal asphyxia. Thus, animal studies have suggested a time-window for post-insult treatment strategies. Hypothermia has been tested as a treatment for HIE in pdiglet models and subsequently proven effective in clinical trials. Variations of the model have been applied in the study of adjunctive neuroprotective methods and piglet studies of xenon and melatonin have led to clinical phase I and II trials1,2. The piglet HIE model is further used for neonatal resuscitation- and hemodynamic studies as well as in investigations of cerebral hypoxia on a cellular level. However, it is a technically challenging model and variations in the protocol may result in either too mild or too severe brain injury. In this article, we demonstrate the technical procedures necessary for establishing a stable piglet model of neonatal HIE. First, the newborn piglet (< 24 hr old, median weight 1500 g) is anesthetized, intubated, and monitored in a setup comparable to that found in a neonatal intensive care unit. Global hypoxia-ischemia is induced by lowering the inspiratory oxygen fraction to achieve global hypoxia, ischemia through hypotension and a flat trace amplitude integrated EEG (aEEG) indicative of cerebral hypoxia. Survival is promoted by adjusting oxygenation according to the aEEG response and blood pressure. Brain injury is quantified by histopathology and magnetic resonance imaging after 72 hr. 相似文献
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Qunying Mao Yiping Wang Rong Gao Jie Shao Xin Yao Shuhui Lang Chao Wang Panyong Mao Zhenglun Liang Junzhi Wang 《Journal of virology》2012,86(22):11967-11976
To evaluate vaccine efficacy in protecting against coxsackievirus A16 (CA16), which causes human hand, foot, and mouth disease (HFMD), we established the first neonatal mouse model. In this article, we report data concerning CA16-induced pathological changes, and we demonstrate that anti-CA16 antibody can protect mice against lethal challenge and that the neonatal mouse model could be used to evaluate vaccine efficacy. To establish a mouse model, a BJCA08/CA16 strain (at 260 50% lethal doses [LD50]) was isolated from a patient and used to intracerebrally (i.c.) inoculate neonatal mice. The infection resulted in wasting, hind-limb paralysis, and even death. Pathological examination and immunohistochemistry (IHC) staining indicated that BJCA08 had a strong tropism to muscle and caused severe necrosis in skeletal and cardiac muscles. We then found that BJCA08 pretreated with goat anti-G10/CA16 serum could significantly lose its lethal effect in neonatal mice. When the anti-G10 serum was intraperitoneally (i.p.) injected into the neonatal mice and, within 1 h, the same mice were intracerebrally inoculated with BJCA08, there was significant passive immunization protection. In a separate experiment, female mice were immunized with formaldehyde-inactivated G10/CA16 and BJCA08/CA16 and then allowed to mate 1 h after the first immunization. We found that there was significant protection against BJCA08 for neonatal mice born to the immunized dams. These data demonstrated that anti-CA16 antibody may block virus invasion and protect mice against lethal challenge, and that the neonatal mouse model was a viable tool for evaluating vaccine efficacy. 相似文献
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Yin Zhichao Wu Yuanyuan Zhu Rui Xu Longfa Lin Yu Yang Hongwei Fu Wenkun Huang Qiongzi Zhang Dongqing Wang Jue Wang Wei Wang Yingbin Cheng Tong Xia Ningshao 《中国病毒学》2021,36(6):1575-1584
Virologica Sinica - Coxsackievirus B1 (CVB1) is a leading causative agent of severe infectious diseases in humans and has been reported to be associated with outbreaks of aseptic meningitis,... 相似文献
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Robert W. Arnold 《The Yale journal of biology and medicine》1984,57(4):715-716
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Francisco Jose Alvarez Miren Revuelta Francisco Santaolalla Antonia Alvarez Hector Lafuente Olatz Arteaga Daniel Alonso-Alconada Ana Sanchez-del-Rey Enrique Hilario Agustin Martinez-Ibargüen 《PloS one》2015,10(5)
IntroductionHypoxia–ischemia (HI) is a major perinatal problem that results in severe damage to the brain impairing the normal development of the auditory system. The purpose of the present study is to study the effect of perinatal asphyxia on the auditory pathway by recording auditory brain responses in a novel animal experimentation model in newborn piglets.MethodHypoxia-ischemia was induced to 1.3 day-old piglets by clamping 30 minutes both carotid arteries by vascular occluders and lowering the fraction of inspired oxygen. We compared the Auditory Brain Responses (ABRs) of newborn piglets exposed to acute hypoxia/ischemia (n = 6) and a control group with no such exposure (n = 10). ABRs were recorded for both ears before the start of the experiment (baseline), after 30 minutes of HI injury, and every 30 minutes during 6 h after the HI injury.ResultsAuditory brain responses were altered during the hypoxic-ischemic insult but recovered 30-60 minutes later. Hypoxia/ischemia seemed to induce auditory functional damage by increasing I-V latencies and decreasing wave I, III and V amplitudes, although differences were not significant.ConclusionThe described experimental model of hypoxia-ischemia in newborn piglets may be useful for studying the effect of perinatal asphyxia on the impairment of the auditory pathway. 相似文献
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