Ultrastructure of rabbit myocardium in experimental histamine shock

The ultrastructure of rabbit myocardium was studied after experimental histamine release by Polymyxin-B-sulphate. As soon as 15 minutes after the histamine release mitochondria and sarcoplasmic reticulum showed alterations with appearance of lysosomes and partial destruction of contractile structures. The sarcolemm formed blistered protrusions with simultaneously expelled cytoplasmic elements. Whereas intramural vessels were inconspicuous, the pericapillar spaces showed a considerable enlargement. On the basis of these findings, we suppose that the changes were induced on the one hand by the increase of the permeability of capillaries produced by histamine and, on the other one, by local and general ischemia as a consequence of shock.     

Is lymphocyte histamine involved in the pathogenesis of rheumatoid arthritis?

Inflammation Research -     

An assessment of plasma histamine concentrations during documented endotoxic shock

Recent reviews of the literature involving histamine release during sepsis and endotoxemia have reported that the majority of the studies are inconclusive due to inadequate assays or experimental protocols. In a controlled experimental setting we have employed a specific and sensitive radioenzymatic assay to determine plasma histamine concentrations temporally during documented endotoxin-induced shock in the conscious rat. Cardiovascular and metabolic measurements for the control group (n=7) were normal during the study period. Endotoxin (n=8, LD/90-24 hrs.) induced an early transient hypotensive episode and increase in systemic vascular resistance and a sustained decrease in cardiac index and central venous pressure and increase in heart and respiratory rates. Hypoglycemia and hyperlacticemia were present at the end of the four-hour study period. The small intestine was severely hemorrhaged in all animals given endotoxin. Histamine concentrations for the control group were unchanged throughout the study period. Contrary to previous reports, this model of endotoxemia revealed unchanging histamine concentrations during the first 30 minutes which were temporally coincident with the characteristic early hypotensive episode evoked by endotoxin. The histamine concentrations at 60 and 240 minutes following endotoxin were increased two and three-fold, respectively, compared to the control group. Three of the 8 rats given endotoxin died before four hours; histamine concentrations in plasma taken when death appeared certain were 42, 91, and 174, compared to the control value of approximately 8 ng/ml. There was no clear association of the increases in plasma histamine with any of the parameters measured in this study; however, established histamine effects may have been masked by the pre-existing effects of other mediators known to be active during endotoxemia. In separate groups of animals endotoxin (n=5) elicited early increases in plasma concentrations of norepinephrine (5-fold) and epinephrine (8-fold) that remained elevated for the 4-hour study period while the control group (n=4) remained stable. This study establishes that a) plasma histamine concentrations are increased during endotoxemia, b) plasma histamine is not elevated during the initial hypotension episode following endotoxin, c) plasma histamine increases during the progression of endotoxic shock, and d) plasma histamine concentrations are extremely high prior to death.NIH guidelines for the use of experimental animals were strictly adhered to throughout this study.     

The ultrastructural bases of multiple organ failure in the pathogenesis of endotoxic shock]

The paper presents ultrastructural characteristics of polyvisceral lesions underlying organ insufficiency in endotoxin shock, demonstrates the role of initial intracellular changes in target organs in the mechanism of generalized disorders caused by endotoxin action.     

Inflammation mediators in pathogenesis of infection-toxic shock of meningococcal etiology

Up-to-date advances made in understanding of the events underlying meningococcal infection-toxic shock (ITS) are reviewed. Endotoxin properties, its interaction with transport protein and specific membrane receptors entailing activation of macrophages and secretion of cytokines TNF and IL-1 are described. Both of them are considered as major mediators of ITS. Recent information about activation of complement and coagulation cascades, changes of kinetic and functional properties of polymorphonuclear leukocytes are summarized. As to secondary mediators, the emphasis is placed on bioregulatory system L-arginine-NO. A scheme of pathogenesis of meningococcal ITS is provided. The latter is corresponding both clinically and morphologically to other endotoxin shocks and its peculiarities in excessive activation of coagulation system.