By H. Schmid-Schönbein (auth.), H. Schmid-Schönbein, P. Teitel (eds.)
The touch among the human blood and overseas technical gear (circulatory) and breathing support units, arti ficial kidneys) results in adjustments within the plasmatic and cel lular elements of the blood, that have frequently merely been taken as indicators of gross yet passive blood destruction. there's a lot facts to aid this inspiration in components (mechanical cellolysis of erythrocytes and thrombocytes), even if, those adjustments must be noticeable in a broader bio logical context as an organ-specific response of the blood. it really is an unjustified oversimplification to easily deal with the blood as delivery organ for respiration gases (02 and CO ) and metabolites. The blood is very additionally an organ 2 method for particular and unspecific safety mechanisms, di rected opposed to the dangers of mechanical, microbiological and toxicological hazards posed to multicellular macro-orga nisms in an atmosphere during which trauma and different distur bances of the actual integrity are universal. the 2 safety platforms of the blood are in response to humural and mobile elements; the latter must be regarded as "excitable cells", able to responding in a predictable and automated type to enough stimuli. The reaction of the mobile components in managed and coordinated by means of chemical mediators. The immunological examine of the final century has exclusive separate protection structures of the blood: I. The hugely particular safeguard approach (immune procedure sen sustrictori) that's phylogenetically new and is ontogenetically learned.
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Additional info for Basic Aspects of Blood Trauma: A Workshop Symposium on Basic Aspects of Blood Trauma in Extracorporeal Oxygenation held at Stolberg near Aachen, Federal Republic of Germany, November 21–23, 1978
Have previously been shown to be essential for the completion of a "release reaction" triggered by chemical stimuli. , HUNG et al. and ANDERSON have presented evidence of such "activation" following prolonged shearing of whole blood and platelet rich plasma. The present work attempts to quantify possible platelet "activation" by short exposure times, such as they might occur in artificial organs. To this end, heparinized and citrated platelet rich plasma was perfused with varying wall shear stresses through stainless steel tubes of varying lengths.
Int. Organs, 20A:35, 1974. : Improved platelet economy using filler-free sil icone rubber in long term membrane lung perfusion. Trans. Amer. Soc. Artif. Int. :587, 1975. : Platelet pharmacology in relation to thrombosis. Adv. , ~: 161, 1970. C. : Adenosine analogs and human Platelets: Effects on nucleotide pools and the aggregation phenomenon. Biochem. Pharmacol. 3i:2239, 1975. C. : Formation of platelet aggregate embol i in a prototype hollow fiber membrane oxygenator. J. Biomed. Mater. Res. ~:163, 1974.
A proteolysis, or whether the thrombocytes cause the activation. It is interesting that you can't find activation Born: because other people have done so. As far as I know, there is no other explanation for the temporary disappearance of the platelets. I do know that granulocytes disappear in the same way and that too is due to complement activation. Wildevuur: Indeed, PMN's showed an identical initial dip as described for platelets (1). About the location of trapping of these blood elements MIELKE (2) described that the platelets are mainly trapped in the liver, at least in splenectomized dogs.
Basic Aspects of Blood Trauma: A Workshop Symposium on Basic Aspects of Blood Trauma in Extracorporeal Oxygenation held at Stolberg near Aachen, Federal Republic of Germany, November 21–23, 1978 by H. Schmid-Schönbein (auth.), H. Schmid-Schönbein, P. Teitel (eds.)