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Biomedical subjects

S Nagy

Publications and source records attributed to S Nagy.

At least 55 records · Page 3Linked to original sources
PubMed1997

The role of mast cells in mucosal permeability changes during ischemia-reperfusion injury of the small intestine.

The objective of this study was to investigate the significance of mast cell-induced reactions in the mucosal functional and morphological alterations induced by 30 min segmental ischemia and 120 min reperfusion in anesthetized dogs. The rates of changes in permeability of the mucosa to sodium fluorescein (NaFL) in the plasma-to-lumen and lumen-to-plasma directions were studied, the local hemodynamics, intramucosal pH (pHi) alterations, mast cell number and degranulation, and degree of tissue injury were determined. The effects of pretreatments with cromolyn (a peritoneal-type mast cell stabilizer), quercetin (a mucosal-type mast cell stabilizer), and dexamethasone (an aspecific membrane stabilizer and mast cell depleter) were evaluated. We found that ischemia-reperfusion induced significant tissue injury, elevated the segmental vascular resistance, and decreased pHi. The plasma-to-lumen clearance of NaFL increased significantly during ischemia and reperfusion. Cromolyn and quercetin pretreatments significantly inhibited the permeability changes, but did not influence the pHi and morphological alterations induced by ischemia-reperfusion. Dexamethasone pretreatment did not influence the number of mast cells, but the degree of mast cell degranulation and fluorescein leakage decreased. We conclude that intestinal mast cells and mast cell-induced reactions contribute to the mucosal permeability alterations during reperfusion, but play only a minor role in ischemia-reperfusion-induced structural injury.

Animals↗
PubMed1997

Investigation of the thoracic electrical impedance during endotoxemia in dogs.

The purpose of our study was to examine the effect of sustained low-dose endotoxin infusion on changes in thoracic electrical impedances (Z0 at end-expiratory apnoea, Zmax at end-inspiration), Zmax-Z0, hematocrit (H) values, and extravascular lung water (EVLW) estimated with gravimetrical analysis (WW/DW) and the impedance method (dEVLWimp) in anesthetized dogs. To define the role of H in changes in the Z0 and Zmax, we applied splenectomy. To determine whether changes in respiration might be involved in changes in Z0 and Zmax, mechanically ventilated dogs were examined. During the infusion of endotoxin there was an increase in Z0, Zmax, H and the respiratory rate in the spontaneously breathing dogs. In splenectomized dogs both impedances slightly increased without any significant change in H. In the ventilated dogs Z0 and Zmax increased similarly, and H increased to a slightly lower level than in the spontaneously breathing dogs. In the ventilated-splenectomized dogs no changes were found in the impedances and in H. The EVLW values showed no serious edema in the endotoxemic groups. The results suggest that Z0 increased mainly in association with the increase in H. The Zmax-Z0 parameter proved to be a suitable parameter for demonstrating the changes in respiration.

Animals↗
PubMed1997

Effects of antiendothelin treatment on the early hemodynamic changes in hyperdynamic endotoxemia.

We have performed a series of experiments to study the effects of a newly developed antisense homology box-derived endothelin (ET) antagonist peptide (ETR-P1/fl) on the early hemodynamic changes in a hyperdynamic endotoxemic dog model. Mean arterial pressure (MAP), cardiac output (CO) and myocardial contractility (MC) were measured in closed-chest animals. Plasma levels of ET-1,2 were determined by radioimmunassay. A hyperdynamic circulatory response was elicited with a 2-hour infusion of 5.3 micrograms/kg of E. coli endotoxin (ETX). Control and ETX-treated animals received an infusion of ETR-P1/fl (0.1 mg/kg) i.v. ETX treatment decreased MAP and MC, increased initially CO, and a long lasting elevation in the plasma ET level was observed. In ETX-treated animals the administration of ETR-P1/fl significantly prolonged the increase in CO and inhibited the depression of MC. Our results suggest that treatment with the ET antagonist ETR-P1/fl may be advantageous in the early phase of endotoxemia.

Animals↗
PubMed1997

Mucosal permeability changes during intestinal reperfusion injury. The role of mast cells.

The objective of this study was to investigate the role of intestinal mast cells in mucosal functional and morphological alterations induced by 30 min segmental ischemia and 120 min reperfusion in anesthetized dogs. The time course of permeability changes of the mucosa to sodium fluorescein (NaFl) in blood-lumen and lumen-blood directions was studied in two separate series of experiments. Local hemodynamics, intramucosal pH (pHi) alterations, mast cell number and degranulation and the degree of tissue injury were determined. The effects of cromolyn (peritoneal-type mast cell stabilizer), quercetin (mucosal-type mast cell stabilizer), and dexamethasone (aspecific membrane stabilizer and mast cell depleter) pretreatments were evaluated. Ischemia-reperfusion induced significant tissue injury, elevated segmental vascular resistance, and decreased pHi. The blood to lumen clearance of NaFl increased significantly during ischemia and reperfusion. Cromolyn and quercetin pretreatment significantly inhibited permeability changes, but did not influence pHi and morphological alterations induced by ischemia-reperfusion. Dexamethasone pretreatment did not influence the number of mast cells, however, the degree of mast cell degranulation and the degree of mucosal damage decreased. These results demonstrate that mast cells or mast cell-induced reactions contribute to the mucosal permeability alterations and barrier lesions during reperfusion, but play a minor role in reperfusion-induced structural injury.

Animals↗
PubMed1997

Endothelin-1-induced circulatory response in the rat: the role of ETA and ETB receptors.

Production of the powerful vasoconstrictor endothelin-1 (ET1) is increased in a number of pathological conditions. This study was performed 1. to assess the effects of a twofold elevation of circulating ET1 on global hemodynamics and cardiac function, and 2. to determine the ET receptor subtypes that are responsible for this action. We have used the ETA receptor-selective antagonist BQ 610, the novel ETA receptor antagonist ETR-Pl/fl peptide and the specific ETB receptor antagonist IRL 1038 to investigate the role of these receptor subtypes in mediating circulatory changes induced by ET1 in anesthetized Wistar rats. ET1 infusion produced a significant rise in mean arterial pressure (MAP), elevated total peripheral resistance (TPR), and decreased cardiac output (CO). BQ 610 and ETR-Pl/fl pretreatment significantly attenuated the ET1-induced hemodynamic changes. Pretreatment with IRL 1038 had no effect on CO, but significantly reduced MAP and TPR elevation 20 min after ET1 infusion. These results suggest that ET1 may contribute to circulatory failure in conditions with increased ET1 production via a mechanism involving ETA receptors. ETB receptors, albeit to a lesser extent than ETA receptors, are also involved in mediating ET1-induced peripheral vasoconstriction in the rat.

Animals↗
PubMed1997

Effects of nitric oxide synthase inhibition on the hemodynamic changes in hyperdynamic endotoxemia.

In this study we compared the circulatory effects of the arginine analogue non-specific nitric oxide synthase (NOS) inhibitor N omega-nitro-L-arginine (NNA), and the specific inducible NOS (iNOS) inhibitor S-methylisothiourea (SMT) and S-(2-aminoethyl)-isothiourea (AEST) in a hyperdynamic endotoxemic dog model. Mean arterial pressure (MAP), cardiac output (CO), and myocardial contractility (MC) were measured. A hyperdynamic circulatory response was elicited with a 2-h infusion of a total dose of 5.3 micrograms/kg E. coli endotoxin (ETX). NOS inhibitory treatment (2 mg/kg) was administrated from the 45th min of endotoxemia. ETX induced a hyperdynamic circulatory response, and a significant myocardial depression. NNA induced a prolonged, SMT a transient increase in MC, both drugs elevated MAP, but decreased CO. AEST significantly prolonged the elevation in CO, but did not affect MAP. Selective inhibition of the iNOS may be a beneficial in sepsis.

Animals↗
PubMed1996

Activity of histamine metabolizing and catabolizing enzymes during reperfusion of isolated, globally ischemic rat hearts.

Myocardial ischemia-reperfusion injury increases both tissue levels and release of histamine. To study the possible effects of ischemia-reperfusion on histamine metabolism tissue activities of histidine decarboxylase (HDC), histamine N-methyl transferase (HNMT) and diamine oxidase (DAO) were investigated in isolated rat hearts subjected to either 20 min global ischemia and 40 min reperfusion (n = 10) or control perfusion (n = 8). Histamine in the coronary effluent increased from 21 +/- 4 nmol/min (mean +/- SEM) before ischemia to 55 +/- 5 and 50 +/- 7 nmol/min after 4 and 10 min reperfusion (p < 0.004 and p < 0.004). Tissue HDC activity did not change during observation in any group. HNMT activity was unchanged in controls, but increased from 0.37 +/- 0.04 to 0.84 +/- 0.18 and 0.96 +/- 0.22 pmol methylhistamine/mg protein hour after 4 and 10 min reperfusion (p < 0.008 and p < 0.01). DAO decreased similarly in controls and ischemic-reperfused hearts during observation. In conclusion, the previously observed increase of tissue histamine during reperfusion cannot be explained by increased histamine synthesis or decreased histamine catabolism.

Amine Oxidase (Copper-Containing)↗
PubMed1996

The impact of the technological care environment on the nursing role.

Proliferation of acute health care technology creates problems and benefits for nurses and patients. In this paper the impact of technology on the nursing work role is reviewed through the international literature. The thrust of the nursing literature has, not surprisingly, matured over time as the use of technology has become well established in the acute care environment, and three themes can be identified. The implications for acute care nurse specialists, including their educational needs, are set in context of the Australian health care system, with particular reference to the cardiac care environments.

Australia↗
PubMed1996

Effect of nitric oxide synthase inhibition on myocardial contractility in anesthetized normal and endotoxemic dogs.

Nitric oxide (NO) produced by the induced NO synthase (NOS) enzyme has been implicated in the mechanisms of the circulatory changes that occur in the later stages of sepsis. As NO produced by the constitutive form of the enzyme is known to play a role in the regulation of normal circulation, we have performed a series of experiments to study the early circulatory effects of inhibition of NOS in a hyperdynamic endotoxemic dog model. Pentobarbital-anesthetized animals were used. Cardiac output (CO) was measured by thermodilution. Myocardial contractility (MC) was estimated from the slope of the left ventricular end-systolic pressure-diameter relationship obtained from sonomicrometer- and catheter-tip manometer signals in closed chest animals. All animals received a 15 mL/kg/h infusion of Ringer's lactate. A hyperdynamic response was elicited by a 2 h infusion of a total dose of 5.3 micrograms/kg Escherichia coli O55:B5 endotoxin (ETX). CO increased initially by about 25%, and total peripheral resistance decreased by 35%. These changes subsided in 60-90 min, after which a sustained decrease in CO occurred. MC elevated transiently by 25% after the first 30 min of ETX infusion, then decreased gradually below the control level. Administration of 2 mg/kg of the NOS inhibitor N-nitro-L-arginine (NNA) between the 45th and 55th min of the ETX infusion increased MC to the level in the control group, but accelerated the decline of the initially increased CO and caused a sustained increase in total peripheral resistance to about 50% above the control level. In normal (nonendotoxin treated) dogs, NNA also caused a similar increase in MC which, however, lasted at least 3 h. Left ventricular diameter increased in the NNA-treated groups. This increase also occurred in the endotoxin-only group but with a delay of about 2.5 h. Our results demonstrate the participation of constitutive NOS-produced NO in the early hyperdynamic response of endotoxemia. Suppression of NO is associated with increased myocardial contractility. NNA treatment may be favorable for the restoration of depressed cardiac contractility during endotoxemia, but this treatment is probably detrimental for the compensatory systemic flow (CO) increase.

Anesthesia↗
PubMed1996

Comparative study of the circulatory effects of aminoguanidine and N-nitro-L-arginine in hyperdynamic endotoxemia.

We have studied the effects of NG-nitro-L-arginine (NNA) a nitric oxide synthase (NOS) inhibitor, and aminoguanidine (AG) a diamine oxidase inhibitor, on hemodynamic parameters and plasma histamine level using a dog model in which a hyperdynamic circulatory response was elicited with a 2-hour infusion of a low dose (13.75 micrograms/kg) of E. coli 055:B5 endotoxin (ETX). AG (50 mg/kg) or NNA (0.5 mg/kg) was administered intravenously as pretreatment. Hemodynamic variables were studied for 4 hours after the beginning of the ETX infusion. The ETX-elicited hyperdynamic response was abolished by NNA and partially inhibited by AG. AG prevented the increases in cardiac output and heart rate and delayed the early decrease in total peripheral resistance (TPR). The plasma histamine concentration elevation was higher in animals receiving AG than in those receiving only ETX. In the group treated with ETX plus NNA the cardiac output was lower and the TPR was higher than in the ETX plus AG group. In future studies, AG should be considered as one of the possible therapeutic tools in sepsis, as its adverse effect on the compensatory hyperdynamic response is less than that of NOS inhibitors of the L-arginine analog type, while it may favourably influence the deleterious excessive activity of the inducible NOS in the later stages.

Animals↗
PubMed1995

Cardiac release of histamine after ventricular fibrillation and defibrillation during insertion of implantable cardioverter defibrillators (ICD).

Histamine has inotropic, chronotropic, arrhythmogenic, and vasoactive effects, and is released from the heart in ischaemia-reperfusion injury. The effect of ventricular fibrillation (VF) and defibrillation (DEF) on histamine release was investigated in 9 anaesthetized patients undergoing transvenous implantation of ICD. Concomitant arterial and coronary sinus (CS) blood samples were drawn before induction of VF (duration 20 seconds), immediately after, and 2 and 5 min after DEF (18-24 Joules). Basal arterial histamine was 2.5 +/- 6 nmol/l, and did not increase after VF. The histamine level in CS was 1.1 +/- 0.2 nmol/l before VF (p < 0.008 compared to arterial), and increased to 2.5 +/- 0.6 nmol/l immediately after (p < 0.045 compared to basal), to 3 +/- 1.1 nmol/l 2 min after (p < 0.45), and to 2.4 +/- 0.8 nmol/l 5 min after VF. In the basal state there was an uptake of histamine across the coronary circulation. After VF/DEF the level of histamine increased in coronary venous blood, suggesting cardiac release of histamine.

Aged↗
PubMed1995

A comparison of the stressors experienced by parents of intubated and non-intubated children.

When children are ill enough to require admission to paediatric intensive care, parents may become distressed about their child's medical condition and this distress may be compounded by the unfamiliar nature of the highly technological environment. Parents of children who are sick enough to warrant intubation are particularly likely to be exposed to a frightening array of technological equipment. Seventy-one parents of intubated and non-intubated children completed the Parental Stressor Scale: Paediatric Intensive Care Unit (PSS:PICU). Overall the findings suggest that parents were most distressed (a) by the painful procedures to which their children were subjected, (b) by the sights and sounds of the intensive care unit and (c) by their children's reactions to intensive care. The behaviour of staff towards parents and the way that staff communicated with them caused the least distress. When the levels of stress reported by parents of intubated children were compared with those reported by parents of non-intubated children, different patterns of stress were found. Painful procedures were a source of greater stress to parents of intubated children whereas the behaviour of staff and the children's reactions to the intensive care experience caused greater stress to the parents of the non-intubated children. In general the findings suggest that the needs of parents of non-intubated children are being overlooked, with staff focusing more of their attention on the parents of intubated children.

Adolescent↗
PubMed1995

Adverse factors associated with forced sex among southern adolescent girls.

OBJECTIVE: To identify adverse behavioral and psychological factors associated with forced sex experiences of adolescent girls compared with their sexually active counterparts. METHOD: An anonymous self-report survey examining an array of psychosocial items, to which 3124 grade 8 and grade 10 female students responded. RESULTS: Sexually abused girls were more likely to have been pregnant, to have initiated sexual intercourse at a younger age, to indicate illegal drug use, to have feelings of depression, to express more frequent suicidal ideation, and to have been physically abused. CONCLUSIONS: Behaviors such as gateway drug use, truancy, binge drinking of alcohol, and participation in violent episodes that were previously identified as indicators of sexual abuse did not distinguish between sexually active adolescents and those who had been sexually abused. Physicians should consider carefully a structured series of questions relating to behaviors as one approach in determining the risk of sexual abuse. Positive responses to young sexual initiation, pregnancy, illegal drug use, negative mental health states, and evidence of physical abuse are potential markers of sexual abuse in adolescent female clients.

Adolescent↗
PubMed1994

Open heart surgery increases the levels of histamine in arterial and coronary sinus blood.

The possible release of histamine into the coronary circulation during reperfusion of the cold, cardioplegic heart was investigated during open heart surgery in 13 patients (cardioplegic arrest 54 (35-120 min) (median (range)), cardiopulmonary bypass (CPB) 96 (65-360) min. Samples were drawn concomitantly from coronary sinus and arterial blood before cardioplegia and during myocardial reperfusion for measurement of histamine (radioenzymatic method). Additional arterial samples were drawn pre-, per- and postoperatively. CPB induced a sustained increase in arterial histamine (from 4.02 +/- 2.71 nmol/l preoperatively (mean +/- SD) to maximum 16.31 +/- 7.12 nmol/l, p < 0.009). Immediately before cardioplegia histamine levels were higher in arterial than coronary sinus blood (9.24 +/- 4.85 versus 4.04 +/- 2.07 nmol/l, p < 0.002). During myocardial reperfusion coronary sinus histamine increased to levels similar to that of arterial blood. In conclusion, histamine is released during CPB. Before cardioplegic arrest, there is a net uptake of histamine by the heart, which is abolished during reperfusion, possibly due to increased cardiac release of histamine.

Aged↗
PubMed1994

The role of histamine in the increased cardiac output in hyperdynamic endotoxemia.

The role of histamine in the hyperdynamic circulatory response to endotoxin (ETX) was investigated in 32 anesthetized dogs by means of histamine H1- and H2-receptor blockade. A hyperdynamic circulation was elicited with a prolonged, slow infusion of a low dose of ETX, and hemodynamic parameters were examined in control and histamine receptor-blocked groups. The following groups were studied: Group ETX received a 2 h infusion of Escherichia coli 055:B5 endotoxin in a total dose of 13.75 micrograms/kg at a rate of 10 micrograms/kg for 45 min and then 5 micrograms/kg for 75 min. In addition to the same dose of ETX, Groups ETX+TPA and ETX+RAN received 0.5 mg/kg of the H1-blocker tripelennamine (TPA) or 2 mg/kg of the H2-blocker ranitidine (RAN), respectively. Infusion of ETX caused a moderate decrease in arterial pressure in Group ETX, whereas TPA but not RAN inhibited this pressure fall. The cardiac output (CO) increased by 41% above the baseline level in Group ETX. Both TPA and RAN prevented this rise in CO. The total peripheral resistance was considerably lowered by ETX, but this decrease was significantly attenuated in the TPA or RAN-treated groups. The heart rate rose significantly after ETX infusion and was unaffected by TPA or RAN. The stroke volume remained unchanged following ETX but was decreased both by TPA and by RAN. TPA or RAN, when given alone, did not affect any of the measured hemodynamic parameters. These experiments provide evidence of the participation of histamine in the hyperdynamic circulatory response in endotoxemia.

Animals↗