Dog Platelets Research Articles

The role of complement in endotoxin shock and disseminated intravascular coagulation: experimental observations in the dog.

Summary.The endotoxin shock response of Beagle dogs, characterized by profound hypotension and progressive fatal disseminated intravascular coagulation (DIC) was compared in anaesthetized normal dogs and in dogs previously decomplemented with purified cobra venom factor. The hypotension and the early thrombocytopenia were abolished in the decomplemented group, while the subsequent DIC was greatly ameliorated. Factor VII was apparently activated in decomplemented dogs but consumed in normal dogs. An observation as yet to be defined in relation to the shock syndrome was that dog platelets lost their collagen aggregation throughout the period of total decomplementation. It is suggested that complement activation is a major requirement for the full expression of fatally progressive DIC in endotoxin shock and that the activation of the coagulation system occurs, at least in part, via the extrinsic pathway.

Density distribution of 51CR-labelled platelets within the circulating dog platelet population

The density distribution of 51Cr-labelled platelets was studied in a linear colloidal silica-polyvinylpyrrolidone density gradient and compared with the density distribution of the circulating platelet population. Twenty-four, 48 and 72 hours after labelling of the platelets close correspondence was found between the density distribution of the label and the platelets, These results seem to justify the use of 51Cr-labelled platelets for turnover studies and for quantitation of platelet deposition in various organs as well as in experimental thrombi.

The Effects of Brinolase (Fibrinolytic Enzyme from Aspergillus Oryzae) on Platelet Aggregation of Dog and Man

SummaryInhibition of blood platelet aggregation by brinolase (fibrinolytic enzyme from Aspergillus oryzae) has been demonstrated with human platelets in vitro and with dog platelets in vivo and in vitro, using both ADP and collagen as aggregating stimuli. It is suggested that the optimal inhibitory effects of brinolase occur indirectly through the generation of plasma fibrinogen degradation products, without compromising platelet viability, rather than by direct proteolysis of platelet structures.

The induction of vascular renal allograft rejection by leukocyte sensitizatin.

Abstract Human renal allograft rejection occurring within the first 2 months after surgery is frequently a vascular phenomenon, characterized by fibrinoid necrosis and endothelial cell proliferation of small vessels and plugging of glomerular capillaries with platelets and fibrin. This contrasts with interstitial edema and mononuclear cell infiltration, and only minimal vascular involvement, usually seen in renal allograft rejection in animals but also seen in man. To investigate this difference, 18 dogs were administered intravenous donor buffy coat prior to transplantation. These were compared to 7 dogs similarly treated except that buffy coat was not administered. Three autografts served as controls. All dogs received azathioprine daily (3 mg. per kilogram) beginning on the day of the operation. Daily assays of renal function, dog survival time, platelet counts, platelet survival times, and repeated biopsy specimens were compared. A marked difference between the immunized and nonimmunized groups was apparent morphologically. In the immunized group, vascular wall necrosis, platelet and fibrin plugging of glomerular capillaries, and endothelial cell proliferation were striking features of the rejection process. The over-all appearance was similar to that often seen in severe early (but not hyperacute) rejection in man. No significant difference in dog survival times or platelet studies was demonstrable between the groups. It is suggested that in man, the morphologic changes seen in early vascular rejection are a result of prior sensitization to transplantation antigen. Drug trials in animal transplantation aimed at studying reversal of the vascular aspects of rejection should be performed on animals exposed preoperatively to donor antigen.

Vasoactivity of adenine nucleotides released in vitro from blood cells by thrombin.

AbstractSmall amounts of thrombin infused into the Cenioral artery of dogs decrease the peripheral vascular resistance, due to release of adenine nucleotides from blood cells.The present study was designed to determine the source of vasoactive adenine nucleotides released from blood cells by thrombin. Washed human platelcts, red cells and white cells were incubated with thrombin and the resulting supernatant was tested for vasoactivity. Dog platelet rich plasma and platelet poor plasma incubated with thrombin was also assayed for vasoactivity, as well as hemolysed red cells. Supernatants from incubated platelets showed strong vasocativity which disappeared after exposure to ADP‐ase and ATP‐ase (Apyrase). Supernatants from red cells and white cells were not vasoactive. Platelet rich plasma incubated with thrombin was highly vasoactive in contrast to platelet poor plasma treated similarly. Hemolysed red cells were highly vasoactive and this vasoactivity also disappeared after treatment with Apyrase. It is concluded that small amounts of thrombin release adenine nucleotides from the platelets. This does not occur when red cells or white cells are acted upon by thrombin although the major supply of the nucleotides is to be found in the red cells.

Comparative aspects of sugar penetration into blood platelets

1. 1. The relative rates of penetration of pentoses and hexoses into blood platelets of dog ( Canis familiaris) and sheep ( Ovis aries) were studied with a photoelectric densimeter. 2. 2. In both species of platelets D-ribose and L-sorbose penetrated more rapidly than D-xylose. No penetration of D-glucose into these cells was detected by the methods employed. 3. 3. It was shown also that dog platelets are more permeable to some sugars than sheep platelets.

Studies of Platelets

Abstract : A technique was devised for obtaining a cohort of tagged young platelets in dogs. These studies reveal that dog platelets are randomly destroyed by the process of continuous in vivo coagulation. This process results in a half-life of 1.5 days. Dog platelets begin to die by aging when they reach 8 days, and no platelets survive beyond 12 days of age. However, in the normal dog less than two percent of the platelets survive theANDOM PROCESS OF DESTRUCTION FOR 8 DAYS SO THAT AGING PLAYS A NEGLIGIBLE ROLE IN DETERMINING PLATELET SURVIVAL. Neither warfarin nor heparin is able completely to stop the process of in vivo coagulation. Of the two, however, heparin appears to be more effective in dogs. A comparable study in humans reveals a similar random process of platelets destruction by continuous in vivo coagulation. The half-life of this process is 2.8 days. Senescence for human platelets begins on day 10 and is complete by day 15. Less than 3% of human platelets survive to day 10 and senescence. Heparin slows the random process of platelet destruction from the normal half-life of 2.8 days to a half-life of 7 days. (Author)

Platelet Aggregation in Mammalians (Human, Rat, Rabbit, Guinea-Pig, Horse, Dog) A Comparative Study

SummaryA comparative study of mammalian (human, rat, rabbit, guinea-pig, horse, dog) platelet aggregation was done using phase contrast microscopy and photometric method and gave us the following results :1. The animal platelets do not spread spontaneously onto glass in contrast to human ones (in their own plasma).2. They do not aggregate in presence of adrenalin, noradrenalin, 5-HT but these amines increase the sensitivity of the platelets towards ADP.3. Although all the platelets aggregate in presence of ADP, bovine thrombin, collagen or thimerosal, there exists some quantitative differences from one species to another.4. Adenosine and AMP are inhibitors of ADP-induced aggregation for human, rabbit and dog platelets and not for guinea-pig and horse. As for the rat, if adenosine is not inhibitor, AMP can be inhibitor if used at strong doses.5. There exist great differences in the ability of the various platelet-poor plasmas studied to inactivate the aggregating property of ADP, as for instance the weakest being the human one and the strongest the rat one.6. The authors insist on the importance of ADP-inhibition by AMP and adenosine, and the ADP-inactivation by the plasmas for the mammalian platelet aggregation and almost disaggregation.

Binding of serotonin and other amines by blood platelets

1. 1. Platelets have been found to be able to bind a variety of amines both in vitro and in vivo. 2. 2. Factors influencing the in vitro binding of serotonin by dog platelets have been studied. 3. 3. It is suggested that platelets may have the function of rapidly binding circulating amines, so as to render them physiologically inactive.

Absorption of serotonin (5-hydroxytryptamine) by canine and human platelets.

Serotonin absorption was studied by incubating platelets for 5 or 10 minutes at room temperature with synthetic serotonin in a concentration of 0.2–4 µg/ml. Serotonin disappeared from the supernatant in two experiments with canine platelet-rich plasma, seven experiments with human platelet-rich plasma and three out of four experiments with native whole human blood. It did not disappear in four out of nine experiments using washed dog platelets suspended in saline and in none of five experiments with washed human platelets. Assay of the platelets in two experiments with human platelet-rich plasma demonstrated that much or all of the serotonin could be recovered in the platelets. The ability of the platelets to absorb serotonin could be correlated with their morphological appearance. Normal disc-shaped platelets absorbed serotonin, whereas spiny spherical platelets often seen in shed blood did not. The quantity of serotonin absorbed by washed dog platelets or by human platelets in platelet-rich plasma from a solution of 0.2 µg/ml was about 0.38 µg/109 platelets, and virtually all of the serotonin was taken up. When the initial concentration was 2 µg/ml, human platelets absorbed up to 2.8 µg/109 platelets, and appreciable quantities of serotonin were left in the supernatant.

Absorption of serotonin (5-hydroxytryptamine) and histamine by dog platelets.

The Journal of PhysiologyVolume 124, Issue 2 p. 300-304 ArticleFree Access Absorption of serotonin (5-hydroxytryptamine) and histamine by dog platelets J. H. Humphrey, J. H. HumphreySearch for more papers by this authorC. C. Toh, C. C. TohSearch for more papers by this author J. H. Humphrey, J. H. HumphreySearch for more papers by this authorC. C. Toh, C. C. TohSearch for more papers by this author First published: 28 May 1954 https://doi.org/10.1113/jphysiol.1954.sp005108Citations: 89AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume124, Issue2May 28, 1954Pages 300-304 RelatedInformation