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Biomedical subjects

T Mózes

Publications and source records attributed to T Mózes.

At least 19 recordsLinked to original sources
PubMed1993

Protective effect of diclofenac sodium against endotoxic shock in anaesthetized pigs.

The effect of diclofenac sodium was investigated on haemodynamics, haematologic and blood glucose values as well as the release of eicosanoids, tumor necrosis factor (TNF) and platelet activating factor (PAF) in anaesthetized pigs receiving 5 micrograms.kg-1 Escherichia coli lipopolysaccharide (LPS) over 60 min into the superior mesenteric artery. The animals were observed for an additional period of 2 h after the termination of LPS infusion. 15 of the 31 animals infused with LPS and not treated with diclofenac sodium died within 30 min after the commencement of LPS infusion (non-survivors), while the other 16 survived the experimental period of 3-h, though in a shock state (survivors). No alterations were observed in plasma concentrations of PAF or eicosanoids (TXB2, 6-keto PGF1 alpha and LTB4), but a marked increase was detected in TNF release in the non-survivors. A significant, though transient, increase in concentrations of PAF, TNF and eicosanoids studied characterized the survivors. Another group of 7 LPS-infused pigs was treated with diclofenac sodium (2 mg, kg-1, i.v. bolus 60 min before the start of LPS infusion, followed by a continuous infusion of 1 mg kg-1 h-1) 1 mg/kg-1/h-1. This treatment prevented death and shock despite the high concentrations of TNF and PAF. Concentrations of both cyclooxygenase and 5-lipoxygenase enzymes products were reduced. These data indicated that the beneficial effect of diclofenac sodium in LPS induced shock may be related to the reduced production of eicosanoids.

Animals↗
PubMed1991

Significance of platelet-activating factor in mesenteric ischemia-reperfusion.

Reperfusion of the ischemic mesenterium is frequently followed by acute circulatory collapse. This review focuses on the possible role of platelet-activating factor (PAF) in ischemia-induced damage. It provides evidence that (i) PAF concentrations are elevated in the mesenteric circulation following temporary ischemia; (ii) administration of exogenous PAF into the superior mesenteric vein mimics many events observed during reperfusion; and (iii) pretreatment of the experimental animals with specific PAF receptor antagonists prevent the circulatory collapse. These findings suggest that PAF may play an important role in the development of circulatory collapse caused by mesenteric ischemia-reperfusion.

Animals↗
PubMed1991

Serum levels of tumor necrosis factor determine the fatal or non-fatal course of endotoxic shock.

The role of tumor necrosis factor alpha (TNF alpha) in endotoxin-induced shock was investigated in pigs receiving 5 micrograms kg-1 of Escherichia coli endotoxin (LPS) during 60 min of continuous infusion into the superior mesenteric artery. LPS concentration in aortic plasma, as determined by a chromogenic Limulus amoebocyte lysate (LAL) test, reached a peak of approximately 1000 ng l-1 during LPS infusion, and declined rapidly after discontinuation of the infusion. Serum TNF levels were determined by a bioassay using the L929 murine transformed fibroblast line. Eight of the 17 animals infused with LPS died within 30 min after beginning LPS administration, while the other 9 pigs survived beyond the experimental observation period of 3 h, although they were in a state of shock. No difference in LPS concentration was found between the survivors and the non-survivors. However, the serum TNF levels in non-survivors were significantly higher than in survivors when measured at 30 min after beginning LPS administration. In survivors, the peak increase in serum TNF levels was measured at 60 min after the beginning of LPS injection and returned rapidly to the baseline values. Although the role of TNF inducing rapid death seems to be dominant, the hemodynamic, hematology and blood chemistry disturbances seen during shock continued in survivors long after the return of TNF to baseline levels. These findings indicate that besides TNF other mediators are also involved in the LPS infusion-induced shock.

Anaphylaxis↗
PubMed1991

Sequential release of eicosanoids during endotoxin-induced shock in anesthetized pigs.

The release of eicosanoids during endotoxin shock was investigated in anesthetized pigs receiving 5 micrograms/kg Escherichia coli lipopolysaccharide (LPS) over 60 min into the superior mesenteric artery. TXB2, 6-keto PGF1 alpha and LTB4 concentrations in blood obtained from the superior mesenteric vein (SMV), right ventricle (RV) and aorta, during LPS infusion and an additional period of 2 h, were assessed along with hemodynamic variables, blood gases and pH and laboratory parameters. Half of the animals died within 30 min after termination of LPS infusion (non-survivors, n = 8), while the other half survived the experimental period of 3 h, though in a shock state (survivors, n = 9). The non-surviving pigs demonstrated progressively reduced cardiac output, hypotension and hypoperfusion in all organs. The surviving pigs demonstrated also a reduced cardiac output, which however was compensated by an elevated systemic vascular resistance resulting in a maintenance of arterial blood pressure. After exhausting this compensation the flow to non-vital organs increased and consequently arterial blood pressure was reduced resulting in hypoperfusion. In survivors a marked, though, transient increase was measured in concentrations of TXB2 and 6-keto PGF1 alpha level. A significant increase was measured in plasma concentration of LTB4 in SMV without any elevation in RV and aorta. LTB4 production started when prostanoid release had decreased. In contrast to survivors, no changes could be observed in eicosanoid release for non-survivors. A correlation was observed between systemic vascular resistance and TXB2 to 6-keto PGF1 alpha ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Sequential release of tumour necrosis factor, platelet activating factor and eicosanoids during endotoxin shock in anaesthetized pigs: protective effects of indomethacin.

1. The effects of indomethacin were investigated on haemodynamics, haematological and blood glucose values, and the release of tumour necrosis factor (TNF), platelet activating factor (PAF) and eicosanoids in anaesthetized pigs receiving 5 micrograms kg-1 E. coli lipopolysaccharide (LPS) over 60 min into the superior mesenteric artery. The animals were observed for an additional period of 2 h after the termination of LPS infusion. 2. Eight of the 17 animals infused with LPS and not treated with indomethacin died within 30 min after the beginning of LPS infusion (non-survivors), while the other 9 survived the experimental period of 3 h though in a state of shock (survivors). 3. No alterations were observed in plasma concentrations of PAF and eicosanoids (thromboxane B2 (TXB2), 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) and leukotriene B4 (LTB4] in non-survivors. However, a marked increase was detected in TNF release. A significant, though transient, increase in concentrations of PAF, TNF and eicosanoids occurred in the survivors. The peak in the concentrations of PAF and TXB2 preceded the maximum in TNF values in survivors. 4. Another group of 7 LPS-infused pigs was treated with indomethacin (2 mg kg-1, i.v. bolus 60 min before the start of LPS infusion, followed by a continuous infusion of 3 mg kg-1 h-1). This treatment prevented death and shock despite the high concentrations of circulating TNF and PAF. Concentrations of cyclo-oxygenase enzyme products were reduced, whereas LTB4 release was not affected. The effect of indomethacin on haemodynamic changes occurred earlier than on cyclo-oxygenase products.5. In another group of 6 pigs indomethacin (2mg kg- 1, i.v.) was given 20-25 min after the start of LPS infusion at which time mean arterial blood pressure (MABP) had decreased below 40mmHg indicating imminent death. This indomethacin treatment immediately reversed the hypotension, restored the organ perfusion, delayed the haemoconcentration and thrombocytopenia and prevented death. However, TNF and PAF concentrations remained elevated. Concentrations of cyclo-oxygenase products studied were reduced by the end of the observation period, whereas LTB4 production was unaffected.6. The decrease in MABP induced by exogenous PAF was temporarily prevented by indomethacin.7. These data indicate that the beneficial effect of indomethacin in LPS-induced septic shock is related to cyclo-oxygenase inhibition as well as to a direct vasoconstrictor property of the drug.

Anesthesia↗
PubMed1991

Interactions between platelet-activating factor and prostanoids during mesenteric ischemia-reperfusion-induced shock in the anesthetized dog.

The effects of platelet-activating factor (PAF) on prostanoid release during mesenteric ischemia-reperfusion-induced shock were investigated in anesthesized dogs 1) by measuring plasma levels of prostaglandin (PG)F2 alpha, 6-keto-PGF1 alpha and thromboxane (TX)B2 in the superior mesenteric vein during reperfusion following 2 hr occlusion of the superior mesenteric artery; 2) by monitoring the effects of BN 52021, a specific PAF receptor antagonist and indomethacin on hemodynamic parameters and prostanoid levels; and 3) by studying circulatory responses to PAF and PGF2 alpha injected into the superior mesenteric vein in the presence of BN 52021 or indomethacin. Restoration of the blood flow following 2 hr ischemia resulted in an immediate dramatic decrease in mean arterial blood pressure, with a concomitant increase in mean portal venous pressure, hematocrit values, and plasma prostanoid levels. Pretreatment of the animals either with BN 52021 (4 mg.kg-1) or indomethacin (2 mg.kg-1 plus 3 mg.kg-1hr-1) prevented the circulatory collapse and the increase in prostanoid levels during reperfusion. Administration of exogenous PAF (0.1 micrograms.kg-1) or PGF2 alpha (10 micrograms.kg-1) into the superior mesenteric vein evoked hypotension similar to that observed during reperfusion. Pretreatment of the animals with BN 52021 completely prevented the effects of PAF but failed to modify the responses to PGF2 alpha. Indomethacin at a dose that inhibited prostanoid formation was highly effective to attenuate the hypotensive response to exogenous PAF. These data suggest that prostanoid formation may be secondary to PAF release in circulatory collapse evoked by intestinal ischemia-reperfusion and give further support to the notion of the importance of PAF prostanoid interaction during ischemia-reperfusion-induced shock.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Platelet activating factor is one of the mediators involved in endotoxic shock in pigs.

The role of platelet activating factor (PAF) in endotoxic shock was investigated in anaesthetized pigs receiving 5 micrograms/kg E. coli endotoxin (LPS) into the superior mesenteric artery over a 60 min period. Concentrations of PAF and tumor necrosis factor (TNF) were measured in blood obtained from the superior mesenteric vein and aorta before, during and 60 min after the LPS infusion. The effect of 4 mg/kg of BN 52021, a PAF receptor antagonist, given as a bolus injection 5 min prior to LPS infusion and/or PAF administration into the superior mesenteric vein was studied on systemic and regional hemodynamic variables. Eight of the 17 animals infused with LPS died within 30 min after start of LPS, while the other 9 survived the experimental period of 3 h, though in a shock state. In survivors, PAF concentration in both superior mesenteric vein and aorta increased twenty-fold at 30 min of endotoxaemia, but rapidly returned back towards normal values. No changes in PAF release, but a marked rise in TNF production were measured in non-survivors. Exogenous administration of PAF (0.01 micrograms/kg) produced similar hemodynamic effects as observed in survivors. BN 52021 markedly reduced the effects of PAF on arterial blood pressure for over 1 h. Treatment with BN 52021 (4 mg/kg), injected 5 min prior to LPS infusion, failed to exert any effect on the surviving rate. However, in survivors all circulatory and laboratory parameters studied were improved after treatment with BN 52021. PAF release observed during LPS infusion in survivors may play a role in the development of shock; however, its role in the rapid death seems to be negligible. Present results clearly demonstrate that endotoxin shock is not crucially dependent on one class of mediators.

Animals↗
PubMed1989

Increased levels of platelet-activating factor in blood following intestinal ischemia in the dog.

The possible role of platelet-activating factor (PAF) in superior mesenteric artery occlusion induced circulatory collapse was studied in anesthetized dogs. PAF was measured by platelet aggregation assay. Identity of PAF-like product in blood was ascertained by thin layer chromatography, high pressure liquid chromatography and alkaline treatment. Low amount of PAF was detected in the mesenteric blood under normal conditions, during reperfusion PAF levels were significantly higher. Pretreatment of the animals with BN 52021, a specific PAF receptor antagonist abolished the fall in mean arterial pressure and the rise in hematocrit due to ischemia/reperfusion. These findings suggest that PAF may play an important role in mesenteric ischemia-induced circulatory collapse.

Animals↗
PubMed1989

Role of PGF2 alpha in the superior mesenteric artery-induced shock.

The role of PGF2 alpha in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring PGF2 alpha levels in superior mesenteric vein, right ventricle, aorta, and femoral vein during superior mesenteric artery occlusion-induced shock by comparing the circulatory effects of exogenous PGF2 alpha injected into either the superior mesenteric or the femoral vein and by inhibiting of prostanoid synthesis with indomethacin. Release of the superior mesenteric artery occlusion caused a dramatic decrease in mean arterial blood pressure; an increase in mean portal venous pressure, and more than fivefold increases in plasma PGF2 alpha levels in superior mesenteric vein, right ventricle, and aorta. In spite of the decreased mean arterial blood pressure, postocclusion blood flow in the mesenteric artery did not fall below preocclusion values. Indomethacin in itself, significantly reduced plasma PGF2 alpha levels as well as intestinal blood flow and increased mean arterial blood pressure in animals without superior mesenteric artery occlusion. Furthermore, indomethacin attenuated the magnitude of postocclusion hypotension and completely prevented PGF2 alpha production during superior mesenteric artery occlusion shock. Exogenous PGF2 alpha 10 micrograms/kg injected into the superior mesenteric or femoral vein produced hypotension or hypertension, respectively. When PGF2 alpha was injected into the superior mesenteric vein, the plasma level of PGF2 alpha in the aorta was similar to that observed during superior mesenteric artery occlusion shock, whereas PGF2 alpha injected into the femoral vein gave a significantly higher concentration. Pulmonary metabolism of PGF2 alpha was significantly reduced in shock. The present results suggest that PGF2 alpha released by intestinal tissues might play an important role in shock caused by intestinal ischemia.

Animals↗
PubMed1989

Intestinal and arterial plasma thromboxane and prostacyclin levels in shock: effects of indomethacin.

The role of thromboxane and prostacyclin in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring their stable metabolites, thromboxane B2 (TXB2) and 6-keto-PGF1 alpha, respectively, in superior mesenteric vein (SMV), right ventricle (RV), and aorta during superior mesenteric artery occlusion-induced (SMAO) shock and by inhibiting prostanoid synthesis with indomethacin (IM). Release of the SMAO caused a dramatic decrease in mean arterial blood pressure and a significant increase in 6-keto-PGF1 alpha levels in SMV, RV, and aorta within 5 min. Thereafter, 6-keto-PGF1 alpha concentration decreased so that at 60-min postrelease it was not significantly different from the control values. TXB2 levels rose continuously during shock. IM significantly attenuated the magnitude of postocclusion hypotension and reduced both TXB2 and 6-keto-PGF1 alpha production.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Role of prostanoids in respiratory failure during circulatory shock of intestinal origin in dogs.

The role of prostanoids in respiratory failure during circulatory shock of intestinal origin was investigated in anesthetized, non-ventilated dogs by measuring PGF2 alpha thromboxane B2 (TXB2) and 6-keto prostaglandin F1 alpha (PGF1 alpha) in arterial and mixed venous (right ventricle) blood samples during superior mesenteric artery occlusion-induced (SMAO) shock. Release of the SMAO caused a dramatic decrease in mean arterial blood pressure (MABP), arterial and mixed venous pO2, hyperventilation and a more than 2 fold increase in levels of prostanoid studied within 5 min. At the same time, arterial and mixed venous pCO2 and pH remained unchanged. Thereafter, 6-keto PGF1 alpha concentration decreased so that at 60 min post release it was not significantly different from that of control values. PGF2 alpha and TXB2 levels rose continuously during shock. Respiratory failure which occurred after declamping was characterized by low pO2 and oxygen saturation and hyperventilation throughout the experiment. Pulmonary metabolism of PGF2 alpha was significantly reduced in shock. Indomethacin significantly attenuated the magnitude of postocclusion hypotension and respiratory failure, furthermore reduced prostanoid production. The present results suggest that PGF2 alpha and thromboxane A2 released by intestinal tissues might play an important role in the development of respiratory failure in shock caused by intestinal ischemia.

Animals↗
PubMed1989

Platelet-activating factor: an endogenous mediator of mesenteric ischemia-reperfusion-induced shock.

The role of platelet-activating factor (PAF) in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring PAF levels in the superior mesenteric vein during reperfusion after 2-h occlusion of the superior mesenteric artery; by monitoring the effects of BN 52021, a specific PAF receptor antagonist; and by studying the circulatory effects of exogenous PAF injected into the superior mesenteric vein. PAF was measured by a platelet-aggregation assay. Identity of PAF-like bioactivity was ascertained by thin-layer chromatography, high-pressure liquid chromatography, and alkaline treatment. Removal of the superior mesenteric artery occlusion caused an immediate dramatic decrease in mean arterial blood pressure with concomitant increase in mean portal venous pressure and hematocrit values. PAF concentration in the superior mesenteric vein increased from 0.2 +/- 0.1 to 2.8 +/- 0.4 ng/ml (n = 4, P less than 0.05) within the first 5 min of reperfusion. Administration of exogenous PAF (0.1 microgram/kg) injected into the superior mesenteric vein produced similar hemodynamical effects. Pretreatment of the animals with BN 52021 (4 mg/kg), a specific PAF receptor antagonist, prevented the circulatory collapse. The present results suggest that PAF release during intestinal ischemia may play an important role in the development of circulatory collapse caused by mesenteric artery occlusion.

Animals↗
PubMed1989

Changes in plasma kallikrein and PGF2 alfa concentrations during circulatory shock. Studies with superior mesenteric artery occlusion in anesthetized dogs.

Among the mediators for development of endotoxic shock, plasma kallikrein and prostanoids have been suggested to play an important role. The role of kallikrein and PGF2 alfa in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring inactive and active kallikreins and PGF2 alpha in superior mesenteric vein, right ventricle and aorta during shock induced by occlusion of the superior mesenteric artery. After removal of the clamp in dogs subjected to occlusion for 1 hour, the mean arterial blood pressure fell rapidly within 5 min and gradually increased over the next 60 min, with return to the control values. The plasma concentrations of PGF2 alfa in superior mesenteric vein, right ventricle and aorta increased three- to fivefold within 5 min of reperfusion. Thereafter the PGF2 alfa levels fell, so that at 60 min after declamping they did not significantly differ from the control values. No significant changes were observed in the levels of inactive and active kallikreins. The results suggest that PGF2 alfa released by intestinal tissues may contribute to the development of shock caused by intestinal ischemia.

Animals↗
PubMed1979

Effect on renal function and renin secretion of noradrenaline infused into the renal artery.

Effect of noradrenaline on renal function and renin secretion was studied during infusion into the renal artery of anaesthetized dogs. Experiments were performed with or without alpha or beta receptor blockade. Noradrenaline infusion resulted in a significant elevation of renin secretion associated with marked vasoconstriction. Urine flow rate, the filtered and excreted amounts of sodium were diminished due to the decreased GFR. Alpha receptor blockade suppressed renin secretion in the presence of changes in renal haemodynamics. The simultaneous infusion of noradrenaline enhanced renin release without affecting renal haemodynamics or reducing Na-excretion. Following simultaneous inhibition of alpha and beta receptors renin secretion dropped markedly; there were no further changes in either renin secretion or renal haemodynamics upon the simultaneous administration of noradrenaline. Based on the present findings it is suggested that renin secretion is controlled by both alpha and beta receptors. Beta receptor simulation exerts a direct action, whereas alpha stimulation appears to be mediated in part by indirect mechanisms such as renal haemodynamics.

Animals↗
PubMed1979

The role of beta receptors in the regulation of renin release.

The effect of the primarily beta 2 type adrenergic receptor stimulating terbutaline (10(-7)--10(-5) M) and of the beta 1 and beta 2 type adrenergic receptor stimulating isoproterenol (10(-7)--10(-5) M) was studied on renin release from incubated slices of renal cortex. Renin release and cAMP content of the slices were significantly higher in the presence of both terbutaline and isoproterenol. A logarithmic dose--response relationship was shown to be present between the beta mimetics and the renin concentration in the medium, and the cAMP content of tissue slices. In equal doses isoproterenol was about 1.5 times more potent than terbutaline. No change was seen in the renin content of the tissue slices. The results supports the view that beside the beta 1 type adrenergic receptors of the renal cortex--even if to a lesser extent--the beta 2 type adrenergic receptors, too, are involved in the regulation of renin release.

Animals↗
PubMed1979

Species differences in the effect of isoproterenol and pindolol on renin release in vitro.

The effects of selective beta adrenergic receptor stimulation with isoproterenol (3 X 10(-8) M) and of beta adrenergic blockade with pindolol (3 X 10(-5) M) on the renin release in vitro were investigated in incubated canine and rat kidney slices. Bioassay was used to measure the renin content of the tissue samples and incubation media; renin content in the canine incubation medium was measured also by radioimmunoassay. Isoproterenol in a concentration of 3 X 10(-8) M brought about a significant increase in the renin content of the incubation media as well as the tissue slices obtained from canine kidney, however, there was no change in these parameters under similar conditions if rat kidneys were incubated. Pindolol, on the other hand, in a concentration of 3 X 10(-5) M caused a significant decrease in the renin release from as well as in the renin content of the rat kidney slices, while canine kidney slices failed to respond to the same dose of the drug. The differences between the two species is suggested to be due to the differences in basal renin levels.

Animals↗
PubMed1979

Changes of plasma renin and renal renin concentration in HgCl2 induced acute renal failure in rats.

Acute renal failure (ARF) was produced by the single intraperitoneal injection of 3 mg/kg mercuric chloride (HgCl2) in male Wistar rats. Immediately after, and in the 1st, 3rd, 6th, 24th and 48th hour after HgCl2 administration the following variables were monitored: plasma renin concentration (PRC), renal renin concentration (RRC) blood-urea nitrogen (BUN), plasma sodium (PNa), plasma creatinine (PCr) concentrations and haematocrit (Ht). Haematocrit and PNa increased during the first hour and returned to the control value in the 3rd hour. Thereafter, their level remained unchanged. Plasma renin concentration increased threefold during the first six hours after the HgCl2 injection, however, by the 48th hour it returned to the control value. In the first 24 hours of ARF, RRC remained unchanged. However, by the 48th hour its level increased four times the control value. After mercury injection BUN and PCr increased progressively. We were not able to establish any significant correlation between the changes of PRC and BUN. A gradual increase of RRC was observed in the course of ARF.

Acute Kidney Injury↗