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S Nagy

Publications and source records attributed to S Nagy.

At least 109 records · Page 6Linked to original sources
PubMed1986

Cytoprotective effect of free radical scavengers against mucosal damage produced by different antirheumatic drugs.

Following 200 mg aspirin, 20 mg indomethacin or 100 mg diclofenac, gastric mucosal damage was evoked after five hours in rats. By administering vitamin A, vitamin E, MTDQ (6,6-methylenebis-2,2,4-trimethyl-1,2-dihydroquinoline), vitamin C, lipoic acid and penicillamine intragastrically at the time of the application of the damaging agent, the authors studied the beneficial effect of these free-radical scavengers upon the mucosal lesions. Vitamin C and penicillamine exerted no significant protective effect. Among the other drugs, the most effective were the lipid-soluble ones: vitamin A, vitamin E and MTDQ. The authors hypothesized that the gastric damage may be connected with the degradation of the polyunsaturated fatty acid components of the cellular membranes and thus the lipid-soluble free radical scavengers were able to offer protection.

Animals↗
PubMed1986

Histamine level changes in the plasma and tissues in hemorrhagic shock.

Histamine (H) levels have been reported during various types of shock, but there is a paucity of such data during hemorrhagic shock. The present study demonstrates a rapid, severalfold increase of radioenzymatically measured plasma H in conscious and anesthetized dogs subjected to experimental hemorrhagic shock. Shock was elicited by bleeding to a mean arterial blood pressure of 5.3 kPa, and maintained until 20% of the maximal bleeding volume (MBV) was taken back by the animal. The corresponding figures in the anesthetized group were 4 kPa and 30% uptake. The increased H level persisted in both groups during hypovolemia and remained above the control value following reinfusion. Survival was examined in the conscious group. At MBV, survivors had significantly higher H levels and H/norepinephrine and H/renin activity ratios in the plasma than nonsurvivors. The H level increased in the liver, lungs, spleen, left atrium and ventricle, and blood vessel walls (superior mesenteric artery, small jejunal arteries and veins, femoral artery and vein). The H/norepinephrine ratio increased in the left ventricle and blood vessel walls. The increase of H in the blood plasma and blood vessels during hemorrhagic shock may exemplify a counterregulation against excessive vasoconstriction and could be a positive factor in survival.

Animals↗
PubMed1986

Minor modifications of the fluorimetric determination of glycosylated haemoglobin.

The fluorimetric method of Gallop et al [3] for the detection of the glycosylated haemoglobin was tested. Some minor modifications of the method are described and results of measurements performed in healthy subject are presented. The fluorimetric technique is compared to a colorimetric method and a chromatographic assay.

Fluorometry↗
PubMed1985

The effect of anaesthesia on the haemodynamic and sympathoadrenal responses of the dog in experimental haemorrhagic shock.

Studies were carried out to demonstrate the effect of sodium pentobarbital and morphine-pentobarbital anaesthesia on the haemodynamic and sympathoadrenal responses of dogs in haemorrhagic shock. The results were compared to those of conscious dogs and of dogs receiving only morphine. The reactivity of the cardiovascular system to exogenous adrenaline was also studied in every group. Pentobarbital did not change the resting plasma level of catecholamines but reduced the increase of plasma catecholamines in shock. In the pentobarbital-anaesthetized dogs in which shock was less severe, the reactivity of blood vessels to adrenaline was higher than in conscious dogs. In the haemodynamic response to shock the increase of heart rate predominated in the conscious dogs while the rise of blood pressure was more pronounced in the pentobarbital-anaesthetized animals. Subcutaneously injected morphine decreased the heart rate and increased the plasma catecholamine and histamine levels. Morphine-pentobarbital anaesthesia decreased the resting arterial pressure and increased the plasma histamine level while the plasma catecholamines were near their initial levels. Morphine alone increased the plasma catecholamines, and the subsequent shock could not induce as high a sympathoadrenal response as in the conscious dogs. Pentobarbital administered following morphine decreased the plasma level of catecholamines nearly to the conscious level but could not inhibit the sympathoadrenal activation induced by shock. Anaesthesia is a significant additional factor in the evaluation of shock experiments carried out on anaesthetized animals.

Adrenal Glands↗
PubMed1985

Effect of the rate of blood loss on the plasma catecholamine response.

In the present experiments the influence on the sympatho-adrenal system of the rate of haemorrhage-induced blood pressure fall in dogs was studied by measuring the plasma catecholamine response. Bleeding to a mean arterial pressure of 5.3 kPa in either 10 or 40 minutes caused an identical increase in the plasma catecholamine level. Similarly, there was no difference in bleeding volumes between the two groups. Within these limits the magnitude of the early catecholamine response was independent of the rate of the haemorrhage-induced decrease of blood pressure. The magnitude of the sympatho-adrenal response depended on the amount of lost blood. Bleeding for 80 minutes to the same pressure resulted in a considerably larger loss of blood and higher plasma catecholamine levels. No relationship was, however, found between the extent of the catecholamine response and the amount of the bleeding volume, probably due to some interaction with other control mechanisms.

Adrenal Glands↗
PubMed1983

Mechanism of functional residual capacity increase in haemorrhagic shock.

Shock was elicited in anaesthetized dogs by maintaining a haemorrhagic hypotension of 4 kPa until 30 per cent spontaneous refusion, followed by total reinfusion. Functional residual capacity (FRC) and minute ventilation increased considerably similarly to our previous experiments. Lactate content in both the external intercostal and the biceps femoris muscles increased significantly in advanced shock. The expiratory external abdominal oblique muscle showed electromyographic signs of fatigue. At the height of the FRC changes tonic contraction of the external intercostal muscle could be demonstrated electron microscopically. This tonic contraction is the main factor in the large FRC rise in late shock forming the basis of a hitherto unknown vicious circle.

Abdominal Muscles↗
PubMed1983

Relationship to survival of catecholamine levels and dopamine-beta-hydroxylase activity in experimental haemorrhagic shock.

Changes of plasma catecholamine levels, dopamine-beta-hydroxylase (DBH) activity and survival were studied in pentobarbital anaesthetized dogs during haemorrhagic hypotension. Shock was elicited by bleeding the animals to a mean arterial pressure of 4 kPa. This pressure was maintained until 15% of the maximum bleeding volume had been taken up spontaneously, then the remaining shed blood was reinfused. Twelve out of 28 animals died within 24 hours. Catecholamine and DBH levels were measured by radioenzymatic methods. Haemorrhagic hypotension caused a significant rise in the plasma catecholamine and DBH levels but the magnitude and time course of the rise was different. The increase of the plasma catecholamine level was higher than that of DBH activity. The highest catecholamine level was observed at the time of the maximum bleeding volume. DBH activity reached its peak during spontaneous blood re-uptake, whereas at the same time the catecholamine level decreased. These results suggest that the decrease of sympathetic activity, as represented by the decreasing catecholamine level was not followed immediately by a similar trend in DBH activity, presumably due to the delayed transport of the enzyme. Both the catecholamine and the DBH levels were significantly higher in non-surviving animals in which an extremely high level represents the stage of irreversibility of the shock.

Animals↗
PubMed1983

Lack of protective effect of adrenaline tolerance haemorrhagic shock in conscious dogs.

Dogs were made tolerant to lethal doses of adrenaline by treatment with increasing doses of the hormone up to 1 mg/kg. The conscious animals were then subjected to haemorrhagic shock with a hypovolaemic period of 3 hours. Survival was 8/17 in the pretreated group and 15/18 in the control group. 12 of 29 dogs died already during adrenaline treatment. Plasma catecholamine levels were higher in the treated group already before bleeding and also during hypovolaemia. Catecholamine induced myocardial lesions were found in the treated group. No evidence of a blunting of the sympathetic response or a protective effect in haemorrhagic shock was seen in adrenaline tolerance.

Animals↗
PubMed1982

Parameter estimation of transpulmonary mechanics by a nonlinear inertive model.

Transpulmonary mechanics of anesthetized intubated dogs were studied during control breathing and hemorrhage-induced hyperventilation by least-mean-squares parameter estimation using several model versions. The classical elastance-resistance model was modified to include nonlinear elastic and viscous pressure terms with and without a linear inertive pressure component. Inclusion of the nonlinear terms decreased the root-mean-square error of fitting (q) of the classical model on the average to 67% in the control period and to 58% during hyperventilation. An additional decrease due to inertance was 4% (control) and 22% (hyperventilation) and was associated with acceptable estimates of inertance [0.056 +/- 0.02 (SD) and 0.063 +/- 0.008 cmH2O . l-1 . s2, respectively]. When inertance alone was added to the classical model, negligible improvement in q and unrealistic values of inertance were obtained. Conventional measures (Edyn and midvolume resistance) were close to the corresponding least-mean-squares estimates (E and R) of all model versions, except that in hyperventilation neglecting the inertance caused Edyn to markedly overestimate E of nonlinear inertive model.

Animals↗
PubMed1982

Increase of functional residual capacity in hemorrhagic shock.

Functional residual capacity (FRC) was measured by body plethysmography in anesthetized dogs subjected to hemorrhagic shock. This was elicited by bleeding the animals to a mean arterial blood pressure of 4 kPa. Reinfusion was done at 30% spontaneous uptake of the maximal bleeding volume. During the initial rapid bleed-out and early hypovolemia, the FRC increased proportionally to the bleeding volume by an average factor of 0.19. Subsequently FRC increased further to about 50% above the control level, and it remained elevated even after reinfusion. Minute ventilation reached a peak value of about 2.5 times of that of the control state, and then declined to almost control values in late hypovolemia when FRC was still very high. The mechanism of the significant increase in FRC is not clear, but it is suggested that the balance of its effects is unfavorable to the maintenance of adequate ventilation in late shock.

Animals↗
PubMed1981

Pulmonary and systemic circulatory responses elicited by hyperosmotic solutions injected into the bronchial artery.

In open chest anaesthetized dogs the haemodynamic effects of solutions of equal hyperosmolarity (viz. NaHCO3 8%, NaCl k.6%, and glucose 34.3%, solutions) given into the bronchial artery were studied. Administration of any of these solutions directly into the bronchial artery resulted in increased cardiac output, stroke volume, bronchial blood flow, and bronchial fraction of the cardiac output, and decreased heart rate and bronchial as well as pulmonary vascular resistances. When given into the pulmonary circulation, the same solutions evoked similar reactions of smaller magnitude. To exclude the effect of major surgical trauma and the open-chest condition, another experimental model closer to the physiological situation was also developed. In this preparation NaHCO3 failed to produce the above haemodynamic response even when given into the bronchial artery. After a one-hour bleeding period resulting in a drop of arterial blood pressure to 40 mmHg, while using the same preparation, the administration f NaHCO3 solution into the bronchial artery caused a significant rise in blood pressure in both the systemic and pulmonary arteries. In these experiments a correlation was found between arterial oxygen tension and the extent of change in blood pressure. The exact mechanism of action of the observed haemodynamic changes is still not clear. However, it is likely that receptors localized in the area of the bronchial circulation and sensitive to hypoxia might have played a role in the development of the haemodynamic effects described.

Animals↗
PubMed1981

The effect of haemorrhagic shock on blood pressure and heart rate responses to adrenaline in the conscious dog.

The effects of haemorrhagic shock on blood pressure and heart rate responses to exogenous adrenaline (2 microgram/kg i.v.) were studied in conscious dogs with chronically implanted vascular cannulae. The animals were bled to a mean arterial pressure of 40 mmHg, the duration of hypovolaemia being two hours. Adrenaline was injected before bleeding, at the beginning and at the end of controlled hypotension, before and 15 minutes after reinfusion. Plasma adrenaline and noradrenaline levels were determined by a radioenzymatic method. In shock, blood pressure responses and their duration decreased. Heart rate responses were changed from a bradycardia type before bleeding to a tachycardia during shock. After reinfusion biphasic responses were dominating. A significant negative correlation was found between plasma noradrenaline levels and blood pressure responses to adrenaline.

Animals↗
PubMed1980

Effects of previous repeated bleedings on the response of plasma epinephrine and norepinephrine levels of conscious dogs in hemorrhagic shock.

A study was conducted on the effects of repeated hemorrhages and reinfusions on the sympathoadrenal response to subsequent hemorrhagic shock. Conscious dogs with carotid and jugular venous cannulae were subjected to hypovolemia of progressively increasing duration for three days. Plasma catecholamines were measured radioenzymatically. Prehemorrhaged animals subjected to hemorrhage shock on Day 4 demonstrated less increase of catecholamines and earlier return toward normal levels. Nonsurviving animals showed higher catecholamine levels than survivors. After three days of conditioning bleedings, prehemorrhaged animals had lower resting heart rates, but larger increases during shock than control animals. Bleeding volumes and hematocrits were also lower in the prehemorrhaged group. The study demonstrates that, by repeated exposure to hypovolemia, the sympathoadrenal response can be decreased in hemorrhagic shock.

Adrenal Cortex↗