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E Monos

Publications and source records attributed to E Monos.

At least 37 records · Page 2Linked to original sources
PubMed1998

Direct relaxing effect of estradiol-17beta and progesterone on rat saphenous artery.

Although estrogen has been reported to relax large coronary arteries immediately, its direct acute effect on small vessel tone has not been fully defined. In this study, we investigated the effect of estradiol-17beta and progesterone on isolated rat saphenous artery segments-with an internal radius of 250 microm-by measuring the outer diameter of the vessels using in vitro angiometry. Estradiol and progesterone at concentrations of 1-100 and 8.6-86 microM induced a rapid, dose-dependent relaxation of the arterial segments precontracted with norepinephrine. Maximal changes of diameters were 85.8 +/- 10 and 90.9 +/- 8%. Clomiphene citrate, a cytoplasmic receptor antagonist, did not diminish this action of estradiol, with the exception of the highest concentrations of the hormone. Thus a nongenomic pathway for this effect can be suspected. Dexamethasone did not induce similar vasodilation. It is concluded that estradiol and progesterone have similar rapid vasorelaxing effects on small muscular arteries as found previously on coronary arteries.

Animals↗
PubMed1998

[150 years from the birth of Endre Hogyes, promotor of Hungarian medicine].

Endre Hogyes, one of the most prominent and internationally known leaders in the field of medical research, a specialist on the treatment of rabies, was born one hundred and fifty years ago in Hungary. E. Hogyes started his medical career and research in 1870. In 1889 he became vice-president of the Royal Hungarian society of Natural Sciences and was elected as member of the Hungarian Academy of Sciences (MTA) and member of the National Council of Public Health. The scientific career of E Hogyes was throughout closely linked to the physiological sciences. He contributed significantly in different fields of the physiological sciences. His most important scientific publications in this field deal with renal physiology, respiratory mechanics, cerebellar function and associated eye movements. Endre Hogyes was the first to organize Hungarian physiologists into a community. The "Special Physiological Conferences" were initiated within the Hungarian Royal Society of Natural Sciences in 1891. As a proof of appreciation, Hungarian physiologists and other medical professionals have proclaimed the year 1997 as a memorial year of Dr. Endre Hogyes.

History, 19th Century↗
PubMed1997

[Striking increase in mortality from venous diseases in Hungary].

The statistical data of the World Health Organisation were studied from 1970 to 1990 to evaluate changes in mortality caused by venous diseases in 9 European countries and in the USA. The data were analysed in process and mortality rates in Hungary and in other countries were compared. In 1970 data based on general population of Hungary indicated medium incidence of mortality due to vein pathology (10.8/100,000) compared to the economically more developed countries. Unfortunately by 1990 mortality due to venous diseases almost had doubled (19.8/100,000). During this 20 years period mortality rates caused by venous diseases gradually decreased in the USA and in most European countries, e.g. by 80% in Austria and by 70% in Finland. Even the relatively high mortality caused by venous diseases in Switzerland (10/100,000) comprises only 50% of that demonstrated in Hungary. While the significance of modern thromboprophylaxis was recognised in the Western European countries and the USA in the early seventies, a delay of the introduction of prophylaxis with low-dose heparin was observed in Hungary. Socio-economic and nutritional causes could have been contributed to the high mortality rates caused by venous diseases as well. Further epidemiologic investigations focusing on venous morbidity factors and wide scale application of organised preventive programme are suggested.

Adolescent↗
PubMed1997

Somatostatin induces vasodilatation in the cat mesenteric artery via endothelium-derived nitric oxide and prostaglandins.

Direct vascular effects of somatostatin (ST) were investigated in cat superior mesenteric artery (SMA) segments in vitro. Changes of outer diameter were measured at constant axial length and perfusion pressure. SMA segments in the resting state were not affected by ST, regardless of endothelial integrity. Noradrenaline-preconstricted SMA segments were dilated concentration-dependently by ST (EC50 10(-13) mol/l). At maximal dilatation (by 10(-11) mol/l ST) the preconstriction was diminished to 45 +/- 9% (P<0.001). Perfusion with Triton X-100, or NG-nitro-L-arginine nearly abolished the ST-induced dilatation, while indomethacin treatment partially suppressed it. We conclude that ST dilates preconstricted cat SMA segments mainly via the endothelial release of nitric oxide, and additionally via prostaglandins.

Animals↗
PubMed1997

Effect of a new nitric oxide donor on the biomechanical performance of the isolated ischaemic rat heart.

The effect of a new nitric oxide (NO) donor, a meso-ionic 3-aryl substituted oxatriazole-5-imine derivative, GEA 3162 was studied on constant flow-perfused ischaemic Langendorff rat heart. The perfusion was kept constant at a rate of 16 mL min-1. Ischaemia was induced by a low flow rate of 0.8 mL min-1 for 30 min, and was followed by a 40-minute reperfusion. In the first set of experiments the effects of GEA 3162-infusion were examined on perfusion pressure, left ventricular pressure, heart rate and left ventricular dP/dt. GEA 3162 infusion did not affect the pre-ischaemic maximum of left ventricular pressure. During reperfusion, maximal left ventricular pressure, maximal and minimal dP/dt values in the GEA 3162-treated group significantly exceeded those of the untreated controls (by 19.3, 36.0 and 18.0%, respectively). During reperfusion, perfusion pressure increased continuously in the control group indicating an increasing coronary resistance, but it was kept at a continuous low level with GEA 3162 treatment. In a second set of experiments bradykinin was infused in order to test the endothelial function before ischaemia and during late reperfusion. Bradykinin elicited significant vasodilation in the control group during reperfusion, meanwhile it did not cause further change in coronary resistance in the GEA 3162-infused group. We suggest, that GEA 3162 may have a protective effect on isolated rat heart in ischaemia and reperfusion, that results in an improved cardiac performance compared with untreated hearts.

Animals↗
PubMed1997

Venous myogenic tone and its regulation through K+ channels depends on chronic intravascular pressure.

In this study, we compared the level of myogenic tone and its negative-feedback control through specific K+ channels in two types of human veins (saphenous [SV] and cephalic [CV] veins), which experience different ranges of pressure in vivo. We also investigated whether an experimental model of increased venous pressure in rats exposed to head-up tilt for 2 weeks produced changes similar to those observed in the human veins. Cylindrical vein segments were cannulated, their diameters were measured, and the intraluminal pressure was set at different levels (2 to 30 mm Hg) in vitro. Acetylcholine test showed that during the regular harvesting process 76% of the human SVs exposed for coronary bypass grafts had no functional endothelium. We found significant myogenic tone in the human SV, where the in vivo pressure is high, but it was not present in the human CV, where the in vivo pressure is low. The nonspecific K+ channel antagonist, tetraethylammonium (TEA), decreased the diameter of the human SV but not the CV. Iberiotoxin and 4-aminopyridine, blockers of the Ca(2+)-sensitive (KCa) and voltage-gated K+ (KV) channels, also decreased the diameter of the human SV by 10.2 +/- 4.8% and 19.5 +/- 4.7%, respectively. In the rat SV, significant myogenic tone was found, but TEA had no effect, even after 2 weeks of in vivo pressure increase in the hindlimb by head-up tilt. We conclude that (1) an increased venous myogenic tone correlates with higher chronic intraluminal pressure loads, (2) KCa and KV channels counterregulate the myogenic tone in human, but not in rat, saphenous vein, (3) the counterregulatory effect is more effective at high than at low intraluminal in vitro pressure levels, and (4) its development is probably a long-term process.

Acetylcholine↗
PubMed1997

Mechanisms of vascular adaptation to long-term orthostatic gravitational loading.

Frequent symptoms and serious complaints related to orthostatic intolerance are among the important reasons for investigating the long-term control mechanisms of blood vessels especially those of veins. Previously we studied perfused and superfused saphenous vein segments from rats maintained in head-up tilt position for two weeks. It was found that passive lumen capacity and acute pressure induced myogenic response of these vessels increased substantially without measurable change in wall thickness. Sympathetic component of the smooth muscle cell membrane potential determined in vivo was also significantly enhanced in this vein, but no such change was seen in the saphenous artery and in the brachial vessels. In a separate study, rarefaction of microvessels was found in the hind limb oxydative muscles after two-week tilting, while muscular water content was unaltered. These results suggest that long-term gravitational loading may induce adaptive rearrangement of the blood vessel functions. The aim of the present study was to quantitate and compare the density of nerve fiber terminals as well as their synaptic vesicle population in the wall of saphenous vein and artery from tilted rats to those obtained from rats which were maintained in horizontal, control position. It was hypothetized that adaptation of blood vessels to long-term gravitational loading might include also a morphological restructuring of the vascular adrenergic innervation.

Adaptation, Physiological↗
PubMed1996

Prostacyclin and thromboxane production of rat and cat arterial tissue is altered independently by several vasoactive substances.

The modulation of the production of prostacyclin and thromboxane from cat and cat aortic tissue slices by different vasoactive agents has been studied in order to reveal whether the release of these main two vasoactive prostanoids goes in parallel or may be controlled independently. Norepinephrine, isoproterenol, phentolamine, propranolol, angiotensin II, vasopressin, bradykinin, thrombin, verapamil, gallopamil, dopamine or methionin enkephalin were added to the incubation medium and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and TxB2 (the stable metabolite of thromboxane) were determined in the supernatant by radioimmunoassay. The ratio of the release of prostacyclin and thromboxane was computed. Norepinephrine increased both prostacyclin and thromboxane release. Isoproterenol increased the ratio of prostacyclin and thromboxane released in cat aortic tissue slices. Phentolamine and propranolol had no effects. Angiotensin II induced a slight but statistically insignificant increase in the ratio of the two prostanoids released. Vasopressin increased thromboxane release only. Bradykinin stimulated the prostacyclin while thrombin stimulated the thromboxane release. Verapamil decreased both prostacyclin and thromboxane production. Gallopamil decreased prostacyclin release and increased thromboxane release from vessel wall slices in a certain concentration range causing a characteristic dose dependent minimum in the ratio of prostacyclin and thromboxane release. Dopamine separately increased prostacyclin release while enkephalin had no significant effect. The data obtained show that in vascular tissue some unidentified yet cytophysiological mechanisms might exist which specifically control the activities of the prostacyclin synthase and thromboxane synthase enzymes.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Myogenic responses of isolated rat skeletal muscle venules: modulation by norepinephrine and endothelium.

The pressure-induced myogenic response of large venules of skeletal muscle and its possible interactions with adrenergic receptor activation and endothelial factors have not yet been elucidated. Therefore, first-order venules of rat gracilis muscle were isolated, cannulated, and placed in an organ chamber. Changes in internal diameter of the vessels as a function of perfusion pressure (PP) were obtained. In response to increases in PP (0.5-17.5 mmHg), the diameter of venules increased from 197.1 +/- 23.96 to 369 +/- 14.1 microns. In passive conditions (in Ca(2+)-free solution), the pressure-diameter curve of venules shifted significantly upward. In the presence of norepinephrine (NE; 10(-6) M) in the bath solution, the pressure-diameter curve of active venules shifted significantly downward, and in the pressure-normalized diameter curve, a negative slope developed (-6.1 +/- 4.6). In both the absence and presence of NE, removal of endothelium significantly reduced venular diameters in the pressure ranges of 3-5 and 2-5 mmHg, respectively, but did not change significantly the characteristics of the pressure-diameter curves. These findings indicate that the smooth muscle of venules actively responds to changes in intraluminal pressure. This response is greatly facilitated by NE and modulated by the endothelium. The myogenic response of skeletal muscle venules, especially in the presence of NE, could have a role in the regulation of the resistance and capacitance of venules and, consequently, blood flow and tissue exchange in skeletal muscle.

Animals↗
PubMed1996

Nitric oxide-dependent opposite effects of somatostatin on arterial and venous caliber in situ.

The vascular effects of somatostatin (ST) and its mechanism of action are not well understood. In the present study, we investigated the direct effects of ST on the vascular tone of rat saphenous artery and vein using videomicroangiometry in situ. ST was administered either in superfusion or in infusion. We found opposite effects in arteries and veins: ST (10(-12)-10(-7) M) dilated the artery (outer diameter increased from 533 +/- 28 to 600 +/- 29 microns, administered in superfusion) and contracted the vein (from 709 +/- 26 to 640 +/- 26 microns and from 775 +/- 30 to 708 +/- 60 microns in superfusion and infusion, respectively). These effects of ST were completely abolished after deendothelization (air bolus maintained for 6 min in vessel lumen) and after local infusion of NG-nitro-L-arginine (L-NNA; 10(-4) M), a nitric oxide (NO) synthesis inhibitor. An NO-dependent basal vasodilator tone in the rat saphenous vein responsible for 10.9 +/- 0.3% of the total vessel diameter was found. After ST administration the venous diameter reduction was similar to that measured after deendothelization or L-NNA. We conclude that ST in situ induces NO release from endothelial cells of rat saphenous artery causing vasodilation, whereas, in contrast, it inhibits the basal NO-dependent vasodilator tone of the saphenous vein inducing vasoconstriction.

Animals↗
PubMed1996

In vivo dose-response characteristics of endothelin-1: studies on rat saphenous vein.

Microangiometric studies were made in vivo on rat saphenous vein to obtain dose-response contraction curves with endothelin-1. During superfusion of the drug, threshold concentrations were found to be in the range of 4 x 10(-11) -4 x 10(-10) moles/lit, maximal concentrations were about 4 x 10(-8) moles/lit. These values are close to published in vitro threshold values. During intravascular administration of the drug contraction could be observed in response to a dose as small as 4.37 femtomoles/s. The data presented show that characteristic dose response curves resembling those found in vitro can be recorded in vivo with endothelin on appropriate vascular preparata. The rat in situ saphenous vein microangiometric technic can be used for delicate pharmacologic examination of venoactive substances in vivo.

Animals↗
PubMed1996

Regional differences in nitric oxide-dependent vascular responses to somatostatin.

The mechanisms of the vascular effects of somatostatin (ST) are not well known. This study compares the direct effect of ST in different vascular regions and species. Isolated perfused segments of the cat superior mesenteric artery in vitro did not exhibit a vascular response in the resting state, however, ST-induced vasodilatation was observed with norepinephrine preconstriction. In contrast, ST only slightly dilated superior mesenteric vein segments. In the artery, NG-nitro-L-arginine inhibited both ST and endothelium-dependent nitric oxide (NO) mediated response. No regular dose-response curves were found when ST was applied on the large mesenteric artery in the cat, but rings of small mesenteric artery from both cats and dogs exhibited dose-dependent relaxations. These effects were also NO-dependent. Local application of ST on the rat saphenous artery in situ elicited NO-mediated dose-dependent vasodilatation. However, ST constricted rat saphenous veins in the case of either adventitial or intraluminal application. It is concluded that ST exerts different actions on the arterial and the venous vessel wall. The major response in arteries is endothelium-mediated vasodilatation seen in various species and vascular beds. Large and small arteries respond differently to ST but these differences require further elucidation.

Acetylcholine↗
PubMed1995

Optimization of hemodynamic energy expenditure in the arterial system.

Experimental evaluations and comparisons of the passive and active biomechanical properties of isolated blood vessels from different species (dog, pig, calf, human), as well as the nature of different arterial pressure oscillations, reveal that: 1) Characteristic impedance of middle-size and large arteries changes with intraluminal mean pressure usually resulting in a U-shaped function with a minimum value around the normal physiological 100 mmHg pressure; 2) Similarly, pressure dependent adrenergic diameter responses (active strain) of different large arteries also exhibit parabolic shape with an extreme (maximum) value at 50-100 mmHg intraluminal pressure, suggesting that biomechanical characteristics of the vessel wall may define an optimum for hemodynamic operations; 3) Changes in the arterial smooth muscle tone shift the characteristic impedance curve along the pressure axis and alter the slopes of the parabola; 4) There are significant interactions between the fast 1st-order (pulsatile) and the slow 3rd-order arterial pressure wave components. These and some other characteristics of the circulatory system suggest the existence of an "extremal" forced oscillation blood pressure control mechanism in the body, optimizing the afterload of heart and the blood perfusion of systemic microvessels by minimizing the pulsatile energy expenditure at the physiological mean pressure operation level. A versatile mathematical model of this hypothetical mechanism was developed by us on an IBM PC using Pascal and 8086 Assembly languages. Simulation experiments show that such a physiological adaptive system could control arterial pressure effectively. The computer model is available on a PC disc.

Animals↗
PubMed1995

Local control of veins: biomechanical, metabolic, and humoral aspects.

The incidence of vein diseases (varicosity, thrombophlebitis, phlebosclerosis, orthostatic intolerance) is extremely high. In several countries it may exceed that of the arterial pathology by an order of magnitude. In the last decades, this recognition and the rapid accumulation of experimental data have resulted in a progressive reevaluation of the physiological significance of the venous system, which had been rather neglected earlier by scientists. The major aim of this review is to provide a critical survey of recent selected literature related to different physiological functions of the venous system as well as to biomechanical, metabolic, and humoral (ionic, hormonal) aspects of the local venous control. Local neural control mechanisms, including effects of catecholamines and other transmitters, are regarded to be beyond the scope of this work. At present, the synthesis of information available in the literature meets certain difficulties, because occasionally poorly defined methodological techniques and physiological parameters have been applied. On the other hand, a significant part of works dealing with venous physiology is excellent and inspirational. We have good reason to believe that the fast accumulation of reliable scientific data on this very important field will soon reach a new critical level, then an even more effective integration of knowledge will be possible.

Animals↗
PubMed1995

The effect of long-term tilting on capillary supply in rat hindlimb muscles.

Rats were kept for three weeks tilted head-up at 45 degrees and their capillary supply (capillary density CD, number of capillaries/mm2, and capillary/fibre ratio C/F), fibre density FD, and muscle weights were compared with a group of animals with similarly restricted movement but at horizontal position, and with control freely moving animals. Movement restriction caused loss of muscle (but not body) weight in fast muscles in all rats, and gain of weight in slow postural soleus in the tilted group. Neither of these changes were due to changes in the content of water. Loss of weight was accompanied by increased fibre density indicative of muscle atrophy due to movement restriction. Capillary supply was not affected by movement restriction, but was significantly decreased, particularly in the oxidative part of tibialis anterior and in the soleus of tilted animals (C/F: 1.78 +/- 0.11 vs 2.11 +/- 0.05 and 2.06 +/- 0.08 vs 2.29 +/- 0.10). It is assumed that this reduction might be explained by changes in hemodynamic characteristics of the venous vascular bed due to a chronic increase in hydrostatic pressure load.

Animals↗
PubMed1993

Hyperpolarization of in situ rat saphenous vein in response to axial stretch.

The goal of this study was to measure the effect of axial stretch on vascular smooth muscle (VSM) transmembrane potential (Em) and external diameter (De) of intact and deendothelialized rat saphenous veins (SV). Incremental increases in length of SV were produced in situ by biaxial stretch of its perivascular connective tissue. Em was measured in situ with glass microelectrodes and De with a high-resolution eyepiece or on-line video microangiometer. Vessels were locally denervated by 20 min superfusion with 6-hydroxydopamine. Endothelium was removed by maintaining an air bolus in the lumen for 6 min. Axial stretch of endothelium-intact SV from a baseline length (Lo, at which there was no vessel buckling or folding) to 120% Lo induced a small depolarization from -56 +/- 1.2 to -53 +/- 0.8 mV. This was followed by a substantial hyperpolarization to -65 +/- 1.4 mV at 140% Lo. However, a depolarization was observed in deendothelialized SV from -47 +/- 1.3 mV at Lo to -43 +/- 1.8 mV at 140% Lo. Neither Em response was influenced by local denervation. Relative to Lo, 40% stretch also attenuated norepinephrine-induced vasoconstriction. These results suggest that axial stretch of SV can lead to release of endothelium-derived factor(s) that hyperpolarizes venous VSM and possibly attenuates stretch-induced and adrenergic vasoconstriction. Such a response may act as a protective mechanism to attenuate vasoconstriction induced by axial stretch.

Animals↗
PubMed1993

[Not Available].

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Academies and Institutes↗