Coagulation Changes of Septic Shock in the Sub-Human Primate and Their Relationship to Hemodynamic Changes

Abstract

COAGULOPATHIES suggestive of disseminated intravascular coagulation are frequently observed in clinical septic shock. 3' 6, 8,14 Although there is no clear explanation of its cause, the disseminated intravascular coagulation (DIC) has usually been attributed to hypercoagulability of blood secondary to blood stasis and acidosis occurring in shock. Experimental studies have shown that alterations of hemostasis can be produced by injection of bacterial endotoxin into dogs 16 and rabbits.2 However, several authors have pointed out that primates respond differently to endotoxin shock than other mammalian orders.4'13. 8,27 Also, Guenter et al. have noted differences in the response of primates to live bacteria in contrast to bacterial endotoxin,9 although Thomas et al. did not find this to be the case.26 To make our results as applicable as possible to the clinical situation, we have studied the shock produced by administration of live bacteria in a primate species.

Identified plasma proteins related to vascular structure are associated with coarctation of the aorta in children

“…It was found that most of the DEPs enriched in the four categories of KEGG pathway which were the immunity-related proteins, the coagulation-related proteins, the myocardium-related proteins and the vascular structure-related proteins. Considering the succeeding cardiovascular processes after atrial stenosis, the other categories of KEGG pathway except vascular structure-related proteins may be activated or inhibited after vascular structure alteration; for example, the change in the level of myocardium-related proteins was correlated with elevated LV load [20,21], and vascular structure alteration can influence immunity [22,23] and coagulation [24,25]. Finally, we focused on the vascular structure-related proteins to track the pathogenesis of CoA.…”

Release of Plasminogen Activator from Viable Leukocytes of Man, Baboon, Dog and Rabbit

“…It is of interest to mention that Lack (13) used endotoxin to free plasminogen activator from the lysosomal fractions of rabbit polymorphs. The ability of endotoxin to enhance plasminogen activator release may have pathogenic significance in states of endotoxemia associated with increased blood fibrinolysis ( 14). This possibility should be kept in mind when endotoxin effects are studied in animals of the species used in this report.…”

Coagulation and fibrinolysis during the infusion of Corynebacterium parvum in man

“…White cells may release proteases or plasminogen activators (Gans, 1964) and this would result in an increase in fibrinolytic activity. Furthermore, the overall response to infusion of C. parvum is similar to the response seen after endotoxin infusion, which can bring about intravascular clotting, fibrinolytic activation and endothelial damage (McKay, 1966;Horwitz et al, 1972) although C. parvum is not a Gram-negative organism which releases lipopolysaccharide endotoxins.…”