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M Koltai

Publications and source records attributed to M Koltai.

At least 19 recordsLinked to original sources
PubMed1997

Loss of pacing-induced preconditioning in rat hearts: role of nitric oxide and cholesterol-enriched diet.

We examined whether the inhibition of nitric oxide (NO) synthesis by NG-nitro-L-arginine (lNNA) abolished pacing-induced preconditioning, and if prolonged exposure to cholesterol-enriched diet led to the loss of preconditioning due to decreased cardiac NO formation. Therefore, Wistar rats fed 2% cholesterol-enriched diet or standard diet for 24 weeks were treated with a single dose of 1 mg/kg lNNA or its solvent at the end of the week 24, respectively. Isolated hearts from all groups were subjected to either preconditioning induced by three consecutive periods of pacing at 600 beats/min for 5 min, with 5-min interpacing periods, or time-matched non-preconditioning perfusion, followed by a 10-min coronary occlusion, respectively. In the control group, coronary occlusion after a non-preconditioning protocol decreased aortic flow (AF) from 45.4+/-2.4 to 15.6+/-1.5 ml/min, and resulted in a lactate dehydrogenase (LDH) release of 219+/-55 mU/min/g, however, preconditioning attenuated the consequences of coronary occlusion [AF: 27.3+/-1.7 ml/min (P<0.05); LDH: 44+/-14 mU/min/g (P<0.05)]. Preconditioning did not confer protection in the lNNA-treated (AF: 17.4+/-1.5 ml/min; LDH: 151+/-21 mU/min/g), and/or in the high-cholesterol-fed groups (AF: 15.7+/-1.2 ml/min; LDH: 168+/-22 mU/min/g). Preconditioning was preserved however, when hearts were treated with lNNA after the preconditioning protocol [AF: 29.6+/-2.2 ml/min (P<0.05); LDH: 48+/-17 mU/min/g (P<0.05)]. Both lNNA treatment and cholesterol-enriched diet markedly decreased cardiac NO content assayed by electron spin resonance spectroscopy. We conclude that NO may be involved in the triggering mechanism of pacing-induced preconditioning, the protective effect of which is blocked by sustained exposure to dietary cholesterol, possibly by influencing cardiac metabolism of NO.

Animals↗
PubMed1997

The effect of continuous versus intermittent treatment with transdermal nitroglycerin on pacing-induced preconditioning in conscious rabbits.

1. Tolerance to the hypotensive effect of nitroglycerin (NG) blocks preconditioning induced by rapid ventricular pacing (RVP) in rabbits. In the present work the effect of continuous versus intermittent treatment with transdermal nitroglycerin on the pacing-induced preconditioning phenomenon was studied in conscious rabbits. 2. RVP (500 beats min-1 over 5 min) increased left ventricular end-diastolic pressure (LVEDP) from baseline 4.1 +/- 0.9 to postpacing 13.8 +/- 2.9 mmHg (P < 0.001) with a right intraventricular ST-segment elevation of 1.25 +/- 0.13 mV, two indicators of myocardial ischaemia. These changes were significantly attenuated when the RVP period was preceded by a preconditioning pacing of the same rate and duration with an interpacing interval of 5 min. 3. Protection by preconditioning was abolished when the animals had been made tolerant to the vasodilator effect of 30 micrograms kg-1 NG by the application of transdermal NG (approx. 0.07 mg kg-1 h-1) over 7 days. Furthermore, transdermal NG per se attenuated both RVP-induced ST-segment elevation and LVEDP-increase over the 7 day period. 4. With intermittent transdermal NG treatment (12 h 'patch on' vs 'patch off'), neither development of vascular tolerance nor attenuation of the NG- or preconditioning-induced anti-ischaemic effects were observed. However, the severity of pacing-induced myocardial ischaemia was significantly increased during the 'patch off' periods. 5. In a second set of experiments, postpacing changes in cardiac cyclic GMP and cyclic AMP levels were determined by means of radioimmunoassay in chronically instrumented anaesthetized open-chest rabbits with the same NG-treatment protocols. Preconditioning reduced postpacing increase in cyclic AMP with an increase in cyclic GMP concentrations in hearts of the untreated animals and in those given patches intermittently during both 'patch on' and 'patch off' periods. However, the preconditioning effect on either cyclic nucleotide was blocked in the tolerant animals. 6. Transdermal NG increased resting levels of both cardiac cyclic nucleotides in the non-tolerant but not in the tolerant state. The postpacing increase in cyclic AMP content was inhibited by transdermal NG, independent of vascular tolerance development, whereas an cyclic GMP content was exclusively seen in the non-tolerant animals. 7. We conclude that the anti-ischaemic effect of NG is independent of the cyclic GMP mechanism in the tolerant state. While intermittent NG therapy prevents development of vascular tolerance and preserves preconditioning, the nitrate-free periods yield an increased susceptibility of the heart to ischaemic challenges.

Administration, Cutaneous↗
PubMed1996

[Amantadine in the prevention of nosocomial influenza].

Amantadine prophylaxis was performed in 91 patients during influenza A epidemics. It was used for patients with chronic heart, pulmonary and metabolic disease, for immundeficienty and elderly patients. Patients with gravidity, lactation, epilepsy, peptid ulcer or serious liver disorder were excluded from prophylaxis. The daily dose was 200 mg, which was reduced to 100 mg in people over 65. The chemoprophylaxis was combined with killed influenza vaccine in 6 patients. No influenza-like illness occurred among patients with prevention. Light side-effect was observed in 5 patients. Ten peoples who were excluded from prophylaxis caught serologic proven influenza. Amantadine prophylaxis is appropriate for prevention of nosocomial influenza among high-risk patients in institutions because of other diseases.

Aged↗
PubMed1995

[Successfully treated Salmonella enteritidis endocarditis].

The 60 year old man was admitted because of aphasia and hemiparesis. After cranial computed tomography 15 ml parietal hematoma was removed by stereotaxic biopsy. The patient had hyperpyrexia, combined mitral vitium and atrial fibrillation. There was no symptom of gastroenteritis. Salmonella enteritidis was cultured from blood three times. The vegetation was proved by transoesophageal echocardiography. Ampicillin + gentamycin, amoxicillin-clavulanate + amikacin therapy was ineffective, respectively. During ciprofloxacin therapy of usual dose ceased the toxicosis and hyperpyrexia, but remained fever to 38.5 degrees C. During 750 mg ciprofloxacin t. i. d. intravenous followed 750 mg t. i. d. per os plus 1.5 g cefuroxin t. i. d. intravenous for 46 days became the patient afebrile and the vegetation was disappeared. No side effect was observed with ciprofloxacin of unusual high daily dose.

Brain Diseases↗
PubMed1995

The loss of pacing-induced preconditioning in atherosclerotic rabbits: role of hypercholesterolaemia.

A brief rapid pacing has been shown to protect rabbit heart against global myocardial ischaemia induced by subsequent longer pacing. We studied whether pacing-induced preconditioning was reproducible in experimental hypercholesterolaemia. In conscious rabbits with an implanted right ventricular electrode and left ventricular polyethylene catheters, pacing of 500 bpm over 20 min induced an intracavitary ST-segment elevation of 3.2 +/- 0.41 mV, shortened ventricular effective refractory period and increased left ventricular end-diastolic pressure from prepacing 105 +/- 3.9 ms and 4.0 +/- 0.93 mmHg to post-pacing 62 +/- 6.4 ms and 27.9 +/- 7.2 mmHg, respectively. A 10-min preconditioning pacing followed by a 5-min interval markedly attenuated these test pacing-induced ischaemic changes. Rabbits were fed a cholesterol-enriched diet over 4, 8 and 12 weeks, responded to a 5- or 10-min pacing with ischaemic changes of the same degree as did controls to a 10- or 20-min pacing, respectively. A 4-week diet elevated total serum cholesterol from 1.7 +/- 0.4 to 24.1 +/- 2.9 mmol/l without apparent atherosclerotic lesions in the thoracic aorta assessed by Oil-Red O staining and planimetry, but it abolished protection induced by a 5-min preconditioning pacing. A 12-week diet increased serum cholesterol and lesion surface area to 26.9 +/- 3.2 mmol/l and 89.6 +/- 6.4%, respectively, and continued to block preconditioning. When these animals were refed normal chow over additional 6 weeks, serum cholesterol level dropped to 2.6 +/- 0.80 mmol/l with no change in atherosclerotic lesions, the preconditioning effect, however, recovered. We conclude that hypercholesterolaemia blocks preconditioning irrespective of the development of atherosclerosis.

Animals↗
PubMed1995

Ventricular overdrive pacing-induced preconditioning and no-flow ischemia-induced preconditioning in isolated working rat hearts.

To examine preconditioning induced by short periods of ventricular overdrive pacing (VOP) as compared with that induced by no-flow ischemia, we subjected isolated working rat heart to 10-min coronary artery occlusion (test ischemia) followed by 3-min reperfusion after three intermittent periods of VOP (10 Hz) or 5-min no-flow ischemia, respectively. In the nonpreconditioned group, coronary occlusion decreased aortic flow (AF) from 46.6 +/- 2.4 to 13.7 +/- 1.7 ml/min and increased left ventricular end-diastolic pressure (LVEDP) from 0.53 +/- 0.05 to 2.02 +/- 0.07 kPa. Preconditioning by VOP or no-flow ischemia significantly increased AF to 25.1 +/- 2.3 ml/min (p < 0.001) and to 27.3 +/- 1.4 ml/min (p < 0.001) and decreased LVEDP to 1.38 +/- 0.1 kPa (p < 0.001) and to 1.65 +/- 0.05 kPa (p < 0.05), respectively, after test ischemia. Glibenclamide 10(-7) M which blocked the anti-ischemic effect of the ATP-sensitive K(+)-channel (KATP) opener cromakalim, inhibited VOP-induced protection (AF 20.3 +/- 2.3 ml/min; LVEDP 1.82 +/- 0.15 kPa), but did not affect no-flow ischemia-induced preconditioning [AF 26.6 +/- 2.4 ml/min (p < 0.001), LVEDP 1.60 +/- 0.07 kPa (p < 0.01)]. VOP and no-flow ischemia precondition heart, however their cardioprotective mechanisms may be different in terms of KATP activation in rats.

Animals↗
PubMed1995

Nitroglycerin-induced direct protection of the ischaemic myocardium in isolated working hearts of rats with vascular tolerance to nitroglycerin.

We investigated whether nitroglycerin (NTG) was able to produce an anti-ischaemic effect in isolated working hearts of rats with vascular tolerance to NTG. Hearts isolated from tolerant and non-tolerant rats were subjected to 10 min coronary occlusion in the presence of 10(-7) M NTG and/or its solvent. NTG alleviated ischaemia-induced deterioration of cardiac function and decreased lactate dehydrogenase release whilst having no effect on coronary flow nor the area of the ischaemic zone both in hearts isolated from NTG-tolerant and non-tolerant rats. The magnitude of the effect was similar in the two groups. These results suggest that the anti-ischaemic effect of NTG involves direct myocardial mechanisms independent of its vascular action and that vascular tolerance to NTG does not affect this direct protective action.

Animals↗
PubMed1995

KATP channel modulation in working rat hearts with coronary occlusion: effects of cromakalim, cicletanine, and glibenclamide.

OBJECTIVES: We studied the effects of ATP-sensitive potassium channel (KATP) modulation on ischemic cardiac performance and reperfusion-induced ventricular fibrillation (VF), and assessed the contribution of KATP to the cardioprotective and anti-arrhythmic effect of the anti-hypertensive drug cicletanine. METHODS: Isolated working rat hearts, subjected to a 10-min coronary occlusion followed by reperfusion, were perfused in the presence of vehicle, 0.1-60 microM cromakalim, an opener of KATP; 3-60 microM cicletanine; and 0.1-10 microM glibenclamide, a blocker of KATP, respectively. RESULTS: All concentrations of cicletanine, similarly to 0.1-10 microM cromakalim, attenuated ischemia-induced deterioration of aortic flow, left ventricular developed pressure, and left ventricular end-diastolic pressure. In contrast to cromakalim, cicletanine did not increase coronary flow. Cicletanine (60 microM) and cromakalim (10 and 60 microM) significantly reduced the incidence of reperfusion-induced VF; however, 60 microM cromakalim triggered VF during ischemia. Lower concentrations of cromakalim and cicletanine did not produce an anti-arrhythmic effect. Cardiac functional parameters were concentration dependently worsened by glibenclamide, and the drug did not change the incidence of VF. Glibenclamide (0.1 microM) did not significantly affect cardiac performance, but it did abolish the anti-ischemic effect of cromakalim (1-10 microM) and cicletanine (60 microM). Glibenclamide suppressed the anti-arrhythmic effect of 10 and 60 microM cromakalim; however, it did not affect the anti-arrhythmic effect of cicletanine. CONCLUSIONS: (i) The anti-ischemic but not the anti-arrhythmic effect of cicletanine may involve opening of KATP. (ii) opening of KATP attenuates, inhibition of the channel exacerbates functional consequences of coronary occlusion, and (iii) KATP opening attenuates reperfusion-induced VF, but it triggers ischemia-induced VF. KATP blocking does not affect VF.

Animals↗
PubMed1994

Secretion of phospholipase A2 induced by interactions of human platelets with monocytes.

Phospholipase A2 (PLA2) activity was found and measured in the cell-free supernatants of human mononuclear cells (monocytes and lymphocytes) cultured with platelets for 48 h at 37 degrees C. The relative molecular mass of purified, calcium-dependent PLA2 was 14 kD. The amount of PLA2 in the supernatants correlated positively with the number of monocytes and platelets in the cultures. Electron microscopically, direct cell-to-cell interactions of monocytes and platelets were observed. Cultivation of suspensions of human mononuclear cells with platelets in serum-free medium was found to be an efficient way to produce and purify human secretable PLA2. In the release of secretable PLA2 in peripheral blood, the interactions between platelets and monocytes may play a considerable role.

Blood Platelets↗
PubMed1994

Cromakalim and cicletanine against pacing-induced myocardial ischemia in conscious rabbits.

Myocardial ischemia assessed by intracavital ST-segment elevation, shortening of ventricular effective refractory period (VERP), and increase in left ventricular end-diastolic pressure (LVEDP) was provoked by ventricular overdrive pacing (VOP) in conscious rabbits. Cromakalim (10 micrograms/kg), an ATP-sensitive K+ channel opener, and cicletanine (30 mg/kg), a cGMP-phosphodiesterase inhibitor, reduced VOP-induced ST-segment elevation and LVEDP-increase. Under resting conditions, cromakalim lowered blood pressure, increased heart rate (HR), and shortened VERP, whereas cicletanine decreased HR, prolonged VERP without changing blood pressure. Co-administration of cromakalim and cicletanine additively reduced VOP-induced ST-segment elevation, shortening of VERP, and LVEDP-increase. Cicletanine did not change cromakalim-induced hypotension but abolished reflexogenic tachycardia. This suggests that VERP shortening is not a prerequisite for the anti-ischemic effect of cromakalim, and the combination of these drugs may afford a potent and safe anti-ischemic effect without affecting hypotension induced cromakalim.

Animals↗
PubMed1994

Loss of preconditioning in rabbits with vascular tolerance to nitroglycerin.

A preceding right ventricular overdrive pacing (VOP) of 500 b.p.m. for 5 min, markedly reduced the severity of global myocardial ischaemia produced by a subsequent 5-min VOP in conscious rabbits. This VOP-induced preconditioning developed in parallel with an increase in cardiac cyclic guanosine 3':5'-monophosphate (cyclic GMP) content. VOP-induced preconditioning was abolished when the animals had been made tolerant to the vasodilator effect of nitroglycerin (NG). In the heart of the NG-tolerant rabbits, neither VOP nor preconditioning increased cyclic GMP content. This suggests that changes by NG tolerance of cyclic GMP metabolism may account for the loss of VOP-induced preconditioning.

Animals↗
PubMed1994

Ventricular overdrive pacing-induced anti-ischemic effect: a conscious rabbit model of preconditioning.

To study whether ventricular overdrive pacing (VOP) induces preconditioning, rabbits were equipped with right ventricular electrode catheters for pacing and intracavital recording and polyethylene cannulas in the left ventricle and right carotid artery to measure intraventricular pressure and blood pressure. One week after surgery in conscious animals, VOP at 500 beats/min over 2, 5, or 10 min resulted in an intracavital S-T segment elevation, shortening of ventricular effective refractory period, decrease in maximum rate of pressure development and blood pressure, and increase in left ventricular end-diastolic pressure proportional to the duration of stimulation. A 5-min preconditioning VOP applied 5 or 30 min before a 10-min VOP markedly attenuated ischemic changes, whereas a 2-min VOP had no effect. In anesthetized rabbits, a 5-min VOP slightly increased guanosine 3',5'-cyclic monophosphate (cGMP) and profoundly elevated adenosine 3',5'-cyclic monophosphate (cAMP) content in left ventricular samples. When this VOP was preceded (5 or 30 min) by a preconditioning VOP, the cAMP increase was significantly attenuated, whereas the cGMP increase was amplified. We conclude that a single 5-min VOP induces preconditioning in association with alterations in cardiac cyclic nucleotide contents.

Animals↗
PubMed1993

Zaprinast, cicletanine, and verapamil attenuate overdrive pacing-induced myocardial ischemia in conscious rabbits.

In conscious rabbits equipped with right ventricular electrode and left ventricular polyethylene catheters, zaprinast and cicletanine, inhibitors of phosphodiesterase (PDE) V and PDEs I and V, respectively, as well as verapamil, a Ca2+ channel blocker, decreased intracavital ST-segment elevation induced by ventricular overdrive pacing (VOP). Zaprinast and cicletanine attenuated VOP-induced QT reduction and increase in left ventricular end-diastolic pressure (LVEDP), whereas verapamil increased LVEDP. These results suggest that inhibition of cGMP-PDEs can protect heart against ischemia.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1993

Cicletanine attenuates overdrive pacing-induced global myocardial ischemia in rabbits: possible role of cardiac cyclic nucleotides.

BACKGROUND: This study examined whether cicletanine, an antihypertensive drug with cGMP phosphodiesterase inhibitory effect, could alleviate ventricular overdrive pacing-induced myocardial ischemia in chronically instrumented rabbits. METHODS: An electrode-catheter implanted into the right ventricle was used for pacing (500 bpm over 5 min) and for measuring intracavital ST-segment elevation and ventricular effective refractory period (VERP). PQ and QT intervals were measured in the chest-lead ECG, and dP/dtmax as well as left ventricular end-diastolic pressure (LVEDP) were recorded through a left intraventricular catheter. In separate groups, mean arterial blood pressure (MABP) was monitored from the right carotid artery. Experiments were performed on conscious rabbits after a week of convalescence. In anesthetized, open-chest rabbits, samples were taken from the left ventricle before and after drug treatment and/or overdrive pacing for determination of cGMP and cAMP contents by radioimmunoassay. RESULTS: Intravenous cicletanine, 30 mg/kg body weight, did not change resting MABP, dP/dtmax, and LVEDP, but it did reduce heart rate and prolonged PQ and QT intervals and VERP. Overdrive pacing produced intracavital ST-segment elevation, increased LVEDP, and decreased dP/dtmax and MABP. Cicletanine administered 15 minutes before pacing significantly attenuated ST-segment elevation, increased LVEDP, and decreased dP/dtmax and MABP. In anesthetized animals, cicletanine itself slightly increased cardiac cGMP and cAMP contents. Overdrive pacing moderately increased cGMP and profoundly elevated cAMP, and in overpaced rabbits, cicletanine further increased cGMO and markedly attenuated cAMP content increased by overdrive pacing. CONCLUSIONS: These results suggest that in correlation with alterations of cardiac cycle nucleotide contents, cicletanine protects the heart against pacing-induced myocardial ischemia.

Animals↗