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Mean blood pressure and heart rate have been registered in the experiments on male Wistar rats. Kallikrein-kinin system (KKS) components have been evaluated in blood plasma: plasma kallikreinogen, kallikrein-inhibiting capacity, spontaneous esterase activity. The parameters were determined before and after hemorrhage in the volume accounting for 10, 20 and 30% of the circulating blood volume. The rats were administered enkephalin analogues--DAGO, DADL and naloxone. The administration of mu-agonist DAGO improved hemodynamics. DAGO effect was eliminated by naloxone. The administration of enkephalins did not affect KKS parameters, while naloxone potentiated KKS changes induced by hemorrhage. It has been shown that KKS is not involved into the mechanism of hemodynamic changes in response to enkephalin administration during hemorrhagic shock.

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The esterolytic activity of proteinases was measured in the gingival crevicular fluid from healthy and inflamed periodonts using BAEE as substrate. The BAEE-activity was significantly increased in crevices with inflamed periodonts.

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The present study shows results aimed at determining whether levels of a trypsin-like protease in gingival crevicular fluid are associated with disease activity as assessed by the level of gingival inflammation and probing attachment loss. Maximum enzyme level was significantly elevated by groups with gingival inflammation and periodontal destruction. In a long-time study we find a decrease of enzyme activity with clinical therapy by scaling and root planning.

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Content of adenine nucleotides, lactic and pyruvic acids, glucose and fructose-6-phosphate was studied in kidney of rats with hemorrhage constituting 3% of body mass after intravenous administration at a dose of 100 mg/kg of agonists of mu-opiate receptors DAGO and delta-opiate receptors DADL and dalargin. Stimulation of both these types of receptors amplifies the kidney ischemia developed after hemorrhage, which was expressed as increased decomposition of ATP, decrease in energetic charge of the adenine nucleotide system (DAGO) and increase in content of AMP (DADL, dalargin).

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The pretreatment of rats with the substance LPH and LXU caused decrease of lethality in endotoxin shock and suppression of the following changes 6 hours post endotoxin: Increase of plasma ICDH activity, decrease in platelet count, decrease of the hepatic energy state and increase of the ATP content in the lung. The catabolic glucose metabolism during endotoxin shock was not influenced by LPH and LXU administration.

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The effect of differences in sympathoadrenomedullary and pituitary-adrenocortical responses of individual animals to 35% hemorrhage on severity of shock induction has been studied in unanesthetized unrestrained rats by measuring plasma concentrations of adrenaline (A), noradrenaline (NA), corticosterone (CS) and adrenocorticotropin (ACTH). The responses of A, CS and ACTH were related to the decrease of blood volume and mean arterial pressure (MAP), whereas plasma NA remained unchanged. Higher susceptibility to blood loss was characterized by more pronounced hemorrhage-induced increase in blood lactate concentration and plasma enzyme activities as well as lethal outcome of hemorrhagic shock. In animals with irreversible hemorrhagic shock, enhanced catecholamine secretion and reduced ACTH release was observed. Furthermore, a revealed direct correlation between A and blood lactate concentration and plasma enzyme activities (aspartate aminotransferase, isocitric dehydrogenase, creatine kinase, lipase and glutathione-S-transferase) may indicate its possible participation in the mechanism of shock induction. In contrast, an inverse relationship of plasma CS to the indicators of shock severity was demonstrated. In conclusion, non-optimal neuroendocrine regulation of cardiovascular adjustments to hemorrhage in shock-prone animals might cause an exaggerated compensatory activation of adrenomedullary catecholamine secretion, which in turn has been shown to exert deleterious vascular and metabolic effects. The mechanisms responsible for reduced ACTH secretion in shock-prone animals remain to be established.

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Alveolar macrophages of normal and endotoxin--treated rats were stimulated in suspension by calcium ionophore A 23187. After solid phase extraction and isocratic separation by HPLC the lipoxygenase products (Leukotriene B4, 5-hydroxyeicosatetraenoic acid and 12-hydroxyeicosatetraenioc acid) were quantified. Unlike alveolar macrophages of control animals, alveolar macrophages of endotoxin treated rats showed an increased synthesis of lipoxygenase products (Leukotriene B4: 1.6fold; 5-hydroxyeicosatetraenoic acid: 2.1fold; 12-hydroxyeicosatetraenoic acid: 1.3fold). Our results suggest that in vivo endotoxin disturbs the mechanisms of arachidonic acid liberation in alveolar macrophages.

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Effects of Hageman factor fragment (factor XIIf) administration on shock induction were studied in anesthetized male Wistar rats with hemorrhagic shock. Administration of factor XIIf in non-hemorrhaged rats resulted in an immediate decrease of mean arterial pressure (MAP) for 5 min and in significant increases of blood glucose, lactate and hematocrit (Hct) as well as in a strong tendency for plasma kallikreinogen (KKN) to decrease. At the beginning of bleeding (15 min after factor XIIf administration) MAP has been normalized again. During subsequent hemorrhage pretreated rats showed a sharper decrease in MAP which remained significantly lower up to 25% of estimated blood volume (EBV) and recovered more slowly to normal level after hemorrhage. Blood glucose, lactate and Hct were significantly higher in pretreated animals after hemorrhage of 30% EBV. KKN depicted significant lower values during hemorrhage and in the posthemorrhagic period. Mortality within the observation time increased from 20% (control group) to 60% (pretreated animals). The results demonstrate that prehemorrhagic kallikrein-kinin system (KKS) activation induced an increased severity of shock state with higher mortality.

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The effect of a new shock-protective agent LPH on parameters of the kallikrein-kinin-system was studied in a standardized endotoxin shock model. Activation of KKS in endotoxin shock was not significantly influenced by LPH. On the other hand, LPH by itself caused activation of KKS. Decrease of kininogen level by endotoxin, however, was prevented by the pretreatment with LPH.

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Administration of factor XIIf prepared from human plasma activated the kallikrein-kinin system in vivo. In rats there was a decrease in kallikreinogen as well as a short decrease of the mean arterial blood pressure. The results described are of importance for the research of pathogenesis of shock.

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Protective effect of the investigated alpha-tocopherol solution regarding survival and changes of several biochemical parameters in rat endotoxin shock could already be demonstrated after application of the solvent (special oil HCO-60) alone. An additional effect of Vitamin E was observed only in DP IV activity and leukocyte counts.

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Metabolites of the energy and carbohydrate metabolism and mitochondrial function in the liver were compared in rats with reversible as well as with irreversible shock. 6 h after induction of shock there was a close correlation between the severity of shock and the energy state of the liver. Only rats with irreversible shock showed a marked deterioration in parameters of the adenylate system, whereas in animals with reversible shock the energy state remained at control levels. Liver glycogen and glucose stores declined similarly in all shocked rats. The capacity of isolated liver mitochondria to produce ATP did not essentially differ in reversible and irreversible shock. Further investigations should consider the intracellular environment in evaluating the mitochondrial function in vivo during endotoxin shock.

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The effects of enkephalin derivates with different opioid receptor subtype specificity and naloxone on cardiovascular responses and kallikrein-kinin system (KKS) were studied in anesthetized rats exposed to 30% hemorrhage. Administration of a mu-receptor agonist (DAGO) in early hemorrhage improved mean arterial blood pressure (MAP) responses to hemorrhage. This effect could be abolished by naloxone pretreatment. Moreover, a delayed MAP recovery after hemorrhage could be observed. Treatment with a delta-agonist (DADL) resulted in transient depression of MAP and heart rate (HR). Hemorrhage by itself caused only a slight activation of KKS as indicated by decreased plasma kallikreinogen concentration and reduced kallikrein inhibitor capacity after 20% blood loss. Enkephalin administration did not exert significant effects on KKS. Naloxone pretreatment, in contrast, induced prehemorrhagic activation of KKS, which was potentiated by subsequent hemorrhage. Naloxone-induced activation of KKS could be confirmed by an in vitro study. Taken together these results suggest that the KKS is not involved in MAP and HR responses to enkephalin administration during hemorrhage, whereas it might be implicated in naloxone-induced delayed posthemorrhagic MAP recovery.

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A competitive bradykinin enzymeimmunoassay (BK-EIA) for the determination of urinary kinins was developed. The BK-EIA was based on a stable BK-peroxidase conjugate and a BK-antirabbit-antiserum. Compared with a healthy control group, a significantly lower mean kinin excretion was found in patients with essential hypertension.

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In a well defined endotoxin (ET) shock model we compared the influence of a selective LOX-inhibitor FLM 5011 and the COX-inhibitor Acetylsalicylic acid (ASA) on survival as well as on their effects on TXB2 and 6-oxo-PGF1 and on selected parameters characterizing the shock syndrome. Pretreatment with both substances reduced the lethality rate. Neither TXB2 nor the PGF1 concentration revealed a consistent trend after therapeutic intervention. None of the investigated mediators could be identified as the primary "shock mediator".

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