Documento de consenso SEDAR/SECCE sobre el manejo de ECMO

ECMO is an extracorporeal cardiorespiratory support system whose use has been increased in the last decade. Respiratory failure, postcardiotomy shock, and lung or heart primary graft failure may require the use of cardiorespiratory mechanical assistance. In this scenario perioperative medical and surgical management is crucial.Despite the evolution of technology in the area of extracorporeal support, morbidity and mortality of these patients continues to be high, and therefore the indication as well as the ECMO removal should be established within a multidisciplinary team with expertise in the area.This consensus document aims to unify medical knowledge and provides recommendations based on both the recent bibliography and the main national ECMO implantation centers experience with the goal of improving comprehensive patient care.     

Pulse wave reflection at the collapsed segment of an artery in Riva-Rocci's method

Summary The contours of pressure and flow of a pulse wave arriving at the entrance of a collapsed segment of an elastic tube can be described by application of the basic laws of reflection. The collapsed segment acts like a valve. It is opened by the pressure of the pulse wave when the pressure within the tube becomes higher than the collapse pressure, i.e. the pressure exerted on the segment from outside. This opening of the collapsed segment suddenly changes the sign of the pulse wave reflection from positive to negative; thus a typical contour change of the pulse proximal to the segment is observed. The most obvious effect is a reduction of the pulse pressure. The extent of this reduction is a function of the collapse pressure.A typical example of this phenomenon can be observed in an artery proximal to the segment which is collapsed due to the pressure exerted by an inflated Riva-Rocci cuff. The effect is explained by the assumption that the sign of reflection changes when the pressure of the pulse wave crosses the level of the cuff pressure. This explanation is supported by the results of model experiments.     

Caspase inhibitor Z-VAD-FMK potentiates heat shock-induced apoptosis and HSP70 synthesis in macrophages

Caspase inhibitor Z-VAD-FMK potentiated heat shock-induced apoptosis in macrophages. Z-VAD-FMK did not activate HSP70 synthesis, but significantly increased the intensity of this process during heat shock. It cannot be excluded that caspases abolish HSP70 accumulation under these conditions. The HSP70 synthesis inhibitor quercetin potentiated DNA fragmentation in macrophages cocultured with Z-VAD-FMK after heat shock. HSP70 play an important role in the protection of macrophages from caspase-independent apoptosis.Translated from Byulleten Eksperimentalnoi Biologii i Meditsiny, Vol. 138, No. 9, pp. 261–263, September, 2004     

Unpredictable and uncontrollable stress impairs neuronal plasticity in the rat hippocampus

Almost by definition, learning and the effect of stress on learning represent modifications of existing neuronal circuitry. Under some circumstances, this modification can be measured electrophysiologically. One such measure of plasticity is long-term potentiation (LTP), a long-lasting increase in synaptic efficacy following brief exposure to tetanic stimulation. In 1987, Foy et al. reported that hippocampal LTP was impaired by exposure to inescapable shock. We have recent evidence that the impairment in LTP can be prevented by allowing the animal to learn to escape the shock (Shors et al., 1989), indicating that the stress effect is to some extent mediated by "psychological" variables. Regardless of LTP's putative role in learning and memory processes, such a stress-induced decrease in neuronal plasticity is likely to have profound effects on the behaving organism.     

31P and23Na nuclear magnetic resonance study on forebrain ischemia in rats with shift reagent Dy(TTHA)

³¹P and ²³Na nuclear magnetic resonance (NMR) spectroscopy was employed to study the dynamic changes in intracellular high-energy phosphates and sodium during 15min of forebrain ischemia and recirculation in in vivo rat brain. In the presence of the shift reagent Dysprosium triethylenetetramine-N,N,N,N,N,N-hexaacetic and [Dy(TTHA)], the sodium peak separated into two peaks, unshifted and shifted. During 15min of ischemia, the unshifted sodium peak decreased and the shifted sodium peak increased. With recirculation, the unshifted and the shifted sodium peaks returned to the preischemia level within 10min, but the shifted one increased during 30–60min. Intracellular high-energy phosphates and intracellular pH (pHi) decreased during 15min of ischemia and returned to the preischemia levels within 20min of recirculation. We conclude that the decrease in unshifted sodium peak during ischemia is due to the decrease in subarachnoid sodium and the cellular influx of interstitial sodium would be minimum. The increase in shifted sodium peak during ischemia is considered to be due to the dilatation of cerebral blood vessels and the increase in interstitial sodium which was transported from subarachnoid space.(Kurata M: ³¹P and ²³Na nuclear magnetic resonance study on forebrain ischemia in rats with shift reagent Dy(TTHA). J Anesth 7: 325–333, 1993)     

Septischer Schock und multiples Organversagen in der chirurgischen Intensivmedizin

Zusammenfassung Beschrieben wird ein tierexperimentelles Sepsismodell, das der Problematik chirurgischer Intensivpatienten entspricht. Nach rezidivierender Applikation von E.-coli-Endotoxin W0111:134 unter standardisierten Bedingungen konnten spezifische hämodynamische, biochemische (TNF, TXA₂, PG I₂, IL-6, PAF) und morphologische Veränderungen (pulmonales Endothel) nachgewiesen werden. Die sepsisinduzierten ARDS-Veränderungen werden mit einer Hochfrequenzdruck-und-flowmessung mit 385 Meßpunkten fiber einem Atemzyklus analysiert. Die Rolle des Darms in der Sepsis wurde mit ionenselektivem Kaliummonitoring vergleichend auf der Mukosa and Serosa untersucht. Jede Endotoxingabe wurde vom Dünndarm mit selektiven Anstiegen der Kaliumaktivität als Ausdruck einer Endotoxin-induzierten relativen Ischämie beantwortet. Das Profil der Oberflächenkaliumwerte korreliert sowohl mit dem cardiaco output als auch mit den Prostazyklinspiegeln. Die während der Versuchsdauer kontinuierlich abnehmende Mukosa-Serosa-Kaliumdifferenz kann als Nachweis einer die Sepsis katalysierenden intestinalen Permeabilitätsstörung interpretiert werden.

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Septic shock and multiple organ failure during surgical intensive care. Evaluation of pulmonary and intestinal dysfunction assessment in a porcine model

The study deals with an animal model for the problems of surgical intensive care patients. Following repeated applications of E. coli endotoxin W0111:134 under standard conditions, specific hemodynamic and biochemical (TNF, TXA₂, PGI₂, IL-6, PAF) and morphological (endothelium of the lung) alterations were detected. ARDS patterns induced by the sepsis were analyzed by high-frequency measurement of pressure and flow (385 measurements per breathing cycle). The role of the intestine in sepsis was investigated by ion-selective monitoring of surface potassium activity comparing mucosa and serosa. Every injection of endotoxin was followed by a selective increase of the potassium activity revealing relative ischemia induced by the endotoxin. The profile of the potassium levels on the surface correlates both with the cardiac output and with the prostacyclin levels. The continuous narrowing of the difference between mucosa and serosa, potassium during the period of investigation can be regarded as evidence for pathologic change in permeability fostering the septic course.

     

人体胆结石高能震波碎石的动物实验

目的　研究人体 3种胆结石在一定能量下 ,冲击次数和能量的关系 ,确定不损伤胆囊和小肠内膜的能量安全阈值 .方法　犬胆囊和小肠内放入固醇石、混合石和色素石 ,在不同的输出电压下 ,放电碎石 .结果　固醇石、混合石和色素石破碎所需的能量不同 ,在同样电压下 ,固醇石所需的次数最少 ,混合石次之 ,色素石最多 ;病理检查表明 ,在电压 <15 k V时 ,胆囊和小肠粘膜处 ,细胞膜轻度充血 ,出现小出血点 .当电压 >15 k V后 ,粘膜有脱落 ,膜下组织水肿 .结论　电压具有依赖性 ;该仪器临床应用的冲击电压应小于 15 k V     

压力波对豚鼠耳蜗血管纹、毛细胞心钠素免疫活性改变的研究

目的为探讨压力波的致聋机理,对豚鼠耳蜗血管纹(SV)、毛细胞(HC)中心钠素免疫活性(ANP-IR)的改变及与听阈阈移的相关性进行研究。方法采用免疫细胞化学(ABC法)法、图像分析听性脑干反应测听技术(ABR)对压力波暴露后不同时间分组的豚鼠耳蜗SV、HC中ANP-IR产物进行检测。结果压力波暴露后6、12、24h和48h组SV组织中ANP-IR光密度值较对照组均有明显的差异(P<0．05),其中24h组最高;冲击波暴露后6、12、24h组内毛细胞(IHC)中ANP-IR阳性产物的光密度值较对照组明显增高(P<0．05),其中以12h组最高。二者的变化均与听阈阈移有明显的正相关性(r1=0．8175,P＞0．05;r2=0．9185,P＞0．05)。而外毛细胞(OHC)中ANP-IR阳性产物变化不明显。结论压力波暴露后,SV组织中ANP的增高可能是内耳的一种代偿机制;IHC和OHC中ANP-IR的变化可能是冲击波对其损伤机制的不同表现。