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M Boros

Publications and source records attributed to M Boros.

At least 55 records · Page 3Linked to original sources
PubMed1995

Response of mucosal mast cells to intestinal ischemia-reperfusion injury in the rat.

The goals of this study were to investigate the in vivo effects of intestinal ischemia-reperfusion on mucosal mast cells, and to evaluate the morphological changes induced by standardized arterial occlusion in anesthetized rats. Complete segmental ileal ischemia was maintained for 15, 30, or 60 min, and was followed by a 30 min reperfusion period. Intestinal biopsies taken at the end of ischemia and in the 30th min of reperfusion were evaluated by image analysis, and the rate of release of type II rat mast cell protease, a marker of mast cell exocytosis, was determined from the venous effluent of the segment. Electron microscopy revealed cytoplasmic vacuolization of the mast cells of the villi after the 15 min ischemia. Ischemia induced a continuous diminution of the mucosal thickness and a significant fall in the number of mast cells in the villi; with immunoperoxidase staining with a monoclonal antibody that recognizes the AD1 mast cell surface antigen, the decrease was 57, 49, and 66% in the 15, 30, and 60 min ischemia groups, respectively. In these groups, the mucosal type II mast cell protease concentration increased to 2.4-, 2.5-, and 3.6-fold, respectively, and a significant increase in plasma protease levels was observed on reperfusion. These results lead us to conclude that mucosal mast cells are very sensitive to intestinal ischemia, with the majority of mast cells in the ileal villi already involved in the response to ischemia after a short period of arterial occlusion.

Animals↗
PubMed1994

Role of histamine in the intestinal flow response following mesenteric ischemia.

Sudden reperfusion of the gut following prolonged ischemia can itself have more deleterious consequences than the ischemia alone. Studies of vasodilator factors influencing the increased flow on reperfusion are therefore of importance. In the present study, a possible role of histamine in the postischemic flow response was examined after a period of total segmental ischemia. The artery supplying the terminal ileum was occluded in anesthetized dogs. Ischemia of 30 min duration was followed by a 30 min reperfusion period (control postischemic flow response), and the arterial blood flow to the segment was measured. After the control postischemic flow response, one of the following drugs was administered intravenously: histamine H1-or H2-blockers (tripelennamine, .5 mg/kg, cimetidine, 10 mg/kg, ranitidine, 2 mg/kg), cromolyn (a mast cell stabilizer, 25 mg/kg), and aminoguanidine (a diamine oxidase blocker, 50 mg/kg). The 30 min ischemia-30 min reperfusion cycle was then repeated (test postischemic flow response). A 30 min mesenteric ischemia-reperfusion period is reproducible once without a significant change in its hemodynamic parameters. The duration and volume of the postischemic flow response were significantly decreased by cimetidine, ranitidine, or cromolyn, and were increased by aminoguanidine. Tripelennamine did not affect the postischemic vasodilator response. At the onset of reperfusion, a release of endogenous histamine occurs from the gut, originating mainly from mast cells. It is proposed that histamine participates in the postischemic flow response through the H2-receptors.

Animals↗
PubMed1994

Intramucosal pH changes following complete segmental small intestinal ischemia, as compared with the effects of superior mesenteric artery occlusion.

Microcirculatory nonperfusion of the intestinal mucosa may result in a subsequent prolongation of tissue ischemia, even after restoration of the mesenteric blood flow. It was hypothesized that there is a relationship between mucosal no-reflow and the amount of previously ischemic tissues during intestinal ischemia reperfusion. Accordingly, an examination was made of the changes in intestinal and gastric intramucosal pH (pHi) in dogs after a 120-min complete occlusion of the superior mesenteric artery (SMA) and those observed following ischemia of an ileal segment only. pHi, as an indicator of the adequacy of mucosal microcirculatory perfusion, was calculated by the tonometer technique. Baseline values of intestinal pHi (mean 7.25 +/- 0.12) and gastric pHi (mean 7.23 +/- 0.27) were determined in sham-operated animals. The 120-min intestinal ischemia caused a progressive fall in intestinal pHi to a mean value of approximately 6.8. Reperfusion resulted in a slow return to nearly normal pHi levels in the ileal segment, but essentially no intestinal pHi elevation was observed during the 90-min period following occlusion of the SMA. The gastric pHi remained at the control level during segmental intestinal ischemia reperfusion, but declined below the normal range following release of the occlusion of the SMA. It is proposed that continuing microcirculatory nonperfusion could explain the failure to demonstrate a postreperfusion elevation of pHi following complete occlusion of the SMA.

Animals↗
PubMed1993

Reperfusion mucosal damage after complete intestinal ischemia in the dog: the effects of antioxidant and phospholipase A2 inhibitor therapy.

In a recent study, reperfusion mucosal injury was demonstrated in a rat model of total ischemia if venous congestion was avoided. The aims were to examine the possibility of reperfusion damage in a canine model involving 2 hours of complete segmental ischemia and to investigate the effects of antioxidant therapy or pretreatment with nonspecific phospholipase A2 inhibitors on postocclusive mucosal changes. Tissue samples were evaluated histologically in a blind manner, according to a 0 to V grade scale. The degree of mucosal damage was statistically significantly increased during the 30-minute reperfusion period. Similarly, 2 hours of total ischemia followed by 30 minutes of reperfusion produced significantly more tissue lesions than did 2 1/2 hours of ischemia without reperfusion. Oral allopurinol pretreatment supplemented by an intravenous dose, or oral allopurinol in combination with a superoxide radical scavenger, resulted in a significant amelioration of postischemic histologic changes. Pretreatment with a nonspecific phospholipase A2 inhibitor (methylprednisolone, dexamethasone, or quinacrine) was ineffective in diminishing the reperfusion injury in either case. The results suggest that reperfusion injury may develop even after complete intestinal ischemia, and this damage can be attenuated by inhibiting the capacity of xanthine oxidase to generate reactive oxygen intermediates.

Allopurinol↗
PubMed1992

Studies on the relationship between xanthine oxidase and histamine release during intestinal ischemia-reperfusion.

Recent studies have demonstrated a connection between xanthine oxidase-generated reactive oxygen intermediates and histamine release during ischemia-reperfusion. In the present work, the effect of modulation of the endogenous histamine level on the xanthine oxidase activity was examined during the reperfusion of a canine ileal segment following a 2 hr of complete ischemia. The xanthine oxidase activity and the plasma histamine level peaked simultaneously at the beginning of reperfusion, reaching mean values of 14.9 nmol/ml/min and 12.1 nmol/l, respectively. Pretreatment with aminoguanidine, a blocker of diamine oxidase (histaminase), resulted in significantly higher levels of histamine during reperfusion, but this elevation was not accompanied by a further increase in xanthine oxidase activity. Pretreatment with the mast cell stabilizer cromolyn significantly diminished the rise in plasma histamine level, with an unchanging activity of xanthine oxidase. No significant alteration could be observed in the postocclusive activity of xanthine oxidase following the intra-arterial administration of 0.5, 1, or 5 nmol of histamine during the last 10 min of the ischemic period. These data suggest that the amount of histamine liberated during reperfusion does not result in a further increase in the xanthine oxidase activity. The release of histamine is not a cause, but rather an effect of the elevated activity of intestinal xanthine oxidase.

Animals↗
PubMed1991

Effect of antioxidant therapy on cyclooxygenase-derived eicosanoid release during intestinal ischemia-reperfusion.

Conflicting data have been reported on the relationship between reactive oxygen intermediates and the formation of oxygenase-derived eicosanoids. Plasma levels of prostacyclin (PGI2, measured as the stable metabolite 6-keto-PGF1 alpha) and thromboxane A2 (TxA2, measured as TxB2) in the effluent blood of a canine ileal segment were determined following 1 or 2 h of ischemia. The synthesis of both eicosanoids was significantly stimulated during reperfusion, but extension of the ischemic interval from 60 to 120 min was not followed by a further increase. The role of oxidants potentially involved in the process was investigated by using materials that inactivate the xanthine-oxidase-generated intermediates. Previous studies on the same in vivo animal model had demonstrated the effectiveness of antioxidant therapy in reducing the postischemic histamine release. There was no significant alteration in the amount of eicosanoids synthesized following oral allopurinol, catalase, dimethylsulfoxide, mannitol or desferrioxamine treatment. Intravenously administered allopurinol, however, significantly elevated the postischemic 6-keto-PGF1 alpha/TxB2 ratio. The results suggest that these antioxidants at doses inhibitory to histamine liberation are not effective in influencing the postischemic eicosanoid release. Intravenously administered allopurinol could exert a potentially beneficial effect through a mechanism other than the blockade of xanthine oxidase.

Allopurinol↗
PubMed1991

Histamine release during intestinal ischemia-reperfusion: role of iron ions and hydrogen peroxide.

Reactive oxygen intermediates (ROI) play a major role in the mucosal damage developing during the reperfusion period following intestinal ischemia. We have shown previously that histamine (H) release is related to the ROI generated by xanthine oxidase during intestinal ischemia-reperfusion. The present study sought to determine the possible chain of events leading to H liberation. The artery supplying a segment of the ileum was occluded for 2 hr in 51 anesthetized dogs, and plasma levels of H were determined radioenzymatically in the venous effluent. Catalase was applied to scavenge hydrogen peroxide; dimethylsulfoxide and mannitol were used as hydroxyl radical scavengers; the role of catalytically active iron was assessed by using desferrioxamine. Pretreatment with either catalase or desferrioxamine, but not with dimethyl sulfoxide or mannitol, was effective in reducing the postocclusive H release. The results provide further in vivo evidence that ROI are causative agents in H liberation during reperfusion of the ischemic gut. Hydrogen peroxide can interact with catalytically active iron and generate highly reactive oxidants, which in turn are responsible for H release. The exact nature of these oxidants is still uncertain.

Animals↗
PubMed1990

A canine model of hyperdynamic sepsis induced by intestinal ischemia.

A hyperdynamic sepsis model was developed in dogs. It is based on a 3-hour clamping of the arteries supplying the middle portion of the jejunum. The ensuing sepsis has a course of several days, during which the animals were studied in the conscious state. 2/3 of the animals developed a sustained 32-108 per cent increase in cardiac output, and survived 7 days or more. In the other 1/3 of the animals, the cardiac output was lower than the control value and all these animals died within 5 days. There were no differences between the two groups in other parameters examined. Sepsis caused a steady, slight decrease in mean arterial pressure, an increase in heart rate, and leukocytosis. The plasma levels of epinephrine and norepinephrine showed a sustained, significant elevation. The level of thromboxane B2 was high only on the first day of sepsis, and that of plasma renin activity on the first 2 days. Necrosis and edema of jejunal villi were demonstrated histologically in the early period. Hemocultures were positive in only 5 of 11 animals examined, suggesting the predominant role of absorbed toxins. This model simulates human sepsis well and is suitable for the study of pathophysiologic mechanisms in hyperdynamic sepsis.

Alkaline Phosphatase↗
PubMed1989

Oxygen free radical-induced histamine release during intestinal ischemia and reperfusion.

Acute mesenteric ischemia is highly lethal and therefore a serious problem for surgery and intensive care medicine; accordingly its pathophysiology warrants further study. Oxygen free radicals (OFR) play a role in the intestinal mucosal damage that develops during reperfusion after ischemia. Histamine (H) is generally released in various types of tissue ischemia. The link between H release and OFR has only been studied in in vitro systems. We tested the hypothesis that OFR may be involved in H release following reperfusion of the ischemic gut. The artery supplying a segment of the ileum was occluded for 1 or 2 h in anesthetized dogs. On reperfusion, a release of H into the venous effluent of the segment was demonstrated. Pretreatment of the animals with allopurinol (an inhibitor of xanthine oxidase), or with MTDQ-DA [6,6'-methylene-bis(2,2-dimethyl-4-methanesulfonic acid sodium-1,2-dihydroquinoline)], a superoxide anion scavenger, or with a combination of allopurinol and MTDQ-DA resulted in an inhibition of H release. We conclude that OFR may play a role in the local H release following intestinal ischemia.

Allopurinol↗
PubMed1989

Intensive treatment and prognosis of patients with sepsis of gynaecological origin.

The treatment of 16 patients with severe sepsis of gynaecological origin admitted to the Institute of Anaesthesiology and Intensive Therapy of Albert Szent-Györgyi Medical University, Szeged between 1980 and 1985 is reported. According to the scoring system described by Elebute and Stoner, based on the clinical and laboratory findings typical of the septic state, efforts have been made to assess the severity of sepsis and to give prognostic sings for the chances of survival. The species and incidence of pathogenic agents isolated from different discharges of the patients are also reported. As a result of the complex intensive care only 3 died of the 16 female patients with severe sepsis.

Adolescent↗
PubMed1989

Humoral changes in shock induced by cardiac tamponade.

Cardiac tamponade was induced in dogs by the infusion of saline into the pericardial cavity. The mean arterial pressure dropped to approximately one-third and the cardiac output to one-fourth of the control level. This was accompanied by the release of vasoactive humoral mediators. Among the vasoconstrictor mediators measured in the plasma, the greatest rise during early tamponade occurred in vasopressin concentrations. Considerable elevations of epinephrine and nonrepinephrine concentrations and plasma renin activity were also demonstrated, these mediators reaching their maximum levels in late tamponade. This study for the first time demonstrates significant rises in plasma thromboxane B2 and histamine levels in cardiac tamponade. The histamine level elevation was greater in the portal venous blood than in the arterial blood. It is suggested that histamine may play a counterregulatory role in cardiac tamponade by attenuating excessive vasoconstriction caused by the activation of various vasoconstrictor systems.

Animals↗
PubMed1986

Plasma cortisol, prolactin and thyroxine levels related to midazolam anaesthesia.

Changes of plasma cortisol, prolactin and thyroxine levels as a result of surgical stress were examined in 11 patients undergoing abdominal hysterectomy. General anaesthesia was induced with the new benzodiazepine derivative midazolam (0.25 +/- 0.04 mg/kg) and maintained by nitrous oxide in oxygen. Plasma cortisol and thyroxine levels slightly decreased at the induction of anaesthesia and the beginning of surgery, while the prolactin level increased. By the end of surgery the cortisol and prolactin concentrations increased significantly, although the thyroxine level had barely changed. The highest hormone values were observed a few hours after the operation, but on the next morning hormone levels approached the normal range. On the basis of these results anaesthesia induction with midazolam can be said to have favourably affected the unwanted degree of hormonal changes related to surgery.

Adult↗
PubMed1985

The effects of benzodiazepines as anaesthesia inducing agents on plasma cortisol level in elective hysterectomy.

The effects of anaesthesia inducing benzodiazepines (diazepam, flunitrazepam, midazolam) on serum cortisol level, blood pressure and pulse rate were examined in patients undergoing elective hysterectomy. Diurnal variation of serum cortisol was established two days before operation. Either form of benzodiazepine provided good suppression of the cortisol response to stress during anaesthesia and surgery. The endocrine response to surgical stress was more pronounced at end of the operation in all three groups. Considering the relative changes of cortisol compared to the pre-operative values the smallest differences were seen in the group receiving midazolam. At 6 p.m. on the day of operation the cortisol level decreased in the flunitrazepam and midazolam groups. Especially in the patients who received midazolam at 6 a.m. on the following day the values did not differ from those observed in the control group. On the basis of these examinations it would appear that to prevent adverse stress-induced effects there is a slight advantage in using midazolam for induction of anaesthesia.

Adjuvants, Anesthesia↗
PubMed1985

Comparative study of intravenous anaesthetic techniques administered during short-term gynecological operations.

The effects of nine intravenous anaesthetic techniques on serum cortisol level and circulatory parameters were studied in healthy patients undergoing termination of pregnancy. Considering the increased pre-operation values and those of the pregnant control group as well as diurnal variations, it was found that the serum cortisol value changed during and after the procedure depending on the type of anaesthesia used. This might mean that the optimal type of anaesthesia for interruption could be designed by measuring the serum cortisol level, assuming that this parameter was one of the indicators of stress. The rating the different types of anaesthetics, the circulatory parameters were also considered. According to these criteria the best results were observed using methohexital in combination with fentanyl or diazepam.

Abortion, Legal↗
PubMed1984

Myoneural effects of pethidine and droperidol.

In vitro experiments on the rat phrenic nerve-hemidiaphragm preparation, stimulated directly or indirectly with supramaximal impulses at 0.1 Hz revealed that pethidine in concentrations greater than 5 micrograms ml-1 caused a rapid increase of the twitch. This was maximal (60% increase during direct and 70% increase during indirect stimulation) with pethidine 75 micrograms ml-1. With concentrations of pethidine greater than 40 micrograms ml-1, the initial increase was followed by a slowly developing inhibition of the twitch (50% depression with 46.0 and 50.4 micrograms ml-1 during direct and indirect stimulation, respectively). Droperidol caused no increase in twitch, but it depressed the twitch by 50% at concentrations of 9.8 and 6.9 micrograms ml-1 during direct and indirect stimulation, respectively. The increase in twitch produced by pethidine was augmented by 4-aminopyridine and inhibited by verapamil during both direct and indirect stimulation. Tubocurarine antagonized the augmentation of the twitch by pethidine only during indirect stimulation. The pethidine- and droperidol-induced inhibition of the twitch could be reversed by washout, but it was not antagonized by neostigmine or 4-aminopyridine. The inhibitory effect of pethidine and droperidol were additive. Sub-effective inhibitory concentrations of pethidine and droperidol, and those of tubocurarine, pancuronium and suxamethonium, independently of the sequence of their administration, mutually increased the myoneural effects of one another. The resulting twitch depression could be reversed by washout. The inhibition caused by the combination of pethidine with tubocurarine or pancuronium was partially antagonized by neostigmine or 4-aminopyridine.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗