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Biomedical subjects

K Tárnoky

Publications and source records attributed to K Tárnoky.

At least 19 recordsLinked to original sources
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↗
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↗
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

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↗
PubMed1987

Plasma catecholamine levels in the postoperative period in complication-free and "paralytic" ileus patients.

Plasma catecholamine concentrations were compared in a group of postoperative "paralytic" ileus patients and in another group of patients, who had undergone medium-size abdominal operations followed by uneventful recovery. The plasma epinephrine level was significantly in the former group, whereas no such difference was observed in the norepinephrine concentration. The data appear to confirm that the epinephrine released from the adrenal medulla appreciably contributes to the development of "paralytic" ileus. The therapeutically effective major tranquillizer and alpha-receptor blocking drug, trifluperidol, was found to reduce both epinephrine and norepinephrine levels in "paralytic" ileus patients. The decrease of the plasma epinephrine level was the higher, the greater its initial concentration. These findings seem to support the decisive role of increased catecholamine release in the development of postoperative motor inhibition ("postoperative" ileus) and also explain the success of sympatholytic treatment in such cases, i.e. the return of normal peristalsis.

Abdomen↗
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

Changes of small bowel motility and noradrenaline content of the intestinal wall in response to alpha- and beta-adrenergic blockade in dog.

In experiments on dogs, the spontaneous movements of the small bowel were in all cases enhanced by the alpha 2-blocker phentolamine, while they were not influenced, or were slightly decreased, by the beta 1-blocker practolol. Neither drug caused a change in the noradrenaline content of the intestinal wall. In the same animals, the joint administration of phentolamine and practolol led to a considerable increased small bowel motility, and to a significant decrease in the noradrenaline level of the intestinal wall. The results are in agreement with experimental data indicating that presynaptic alpha-receptors play a primary role in the sympathetic regulation of small bowel motility.

Animals↗
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

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↗
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↗