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211. International symposium Nitric Oxide from Molecular Level to Clinical Application: Bratislava, June 27-29, 1999

Creator:
Oľga Pecháňová and Iveta Bernátová
Format:
print, bez média, and svazek
Type:
article, úvodníky, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, odborné časopisy, konference, physiology, professional journals, conferences, 14, and 612
Language:
English
Description:
Oľga Pecháňová, Iveta Bernátová.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

212. Intracelullar mediators in regulation of leptin secretion from adipocytes

Creator:
Szkudelski, Tomasz
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Biochemie. Molekulární biologie. Biofyzika, fyziologie, leptin, mastné kyseliny, adenosin, vápník, physiology, fatty acids, adenosine, calcium, adipocity, mTOR, adenosin trifostát (ATP), cyklický adenosinmonofosfát (cAMP), malonyl-CoA, adipocytes, mTOR (mammalian target of rapamycin), adenosine triphosphate (ATP), cyclic adenosine monophosphate (cAMP), 2, and 577
Language:
English
Description:
Leptin is a hormone primarily secreted by adipocytes and participating in the regulation of food intake and energy expenditure. Its blood levels usually correlate with adiposity. The secretion of this hormone is affected, among others, by food consumption, insulin, fasting and cold exposure. Regulation of leptin secretion depends on many intracellular events. It is known that the activation of mTOR (the mamma lian target of rapamycin) as well as increase in ATP and malonyl-CoA content in adipocytes enhance secretion of leptin. The rise in intracellular cAMP and fatty acids is thought to evoke the opposite effect. Moreover, the undisturbed action of endogenous adenosine in adipocytes and the proper intracellular Ca2+ concentration in these cells were also found to have an important function in leptin release. The role of mTOR, ATP, cAMP, fatty acids, malonyl-CoA, adenosine and Ca2+ in the regulation of leptin secretion from adipocytes is discussed., T. Szkudelski., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

213. Intracerebroventricular injection of oxidant and antioxidant molecules affects long-term potentiation in urethane anaesthetized rats

Creator:
Viggiano, A., Viggiano, E., Monda, M., Ascione, S., Amaro, S., and de Luca, B.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Experimentální medicína, fyziologie, experimentální medicína, anestezie, physiology, experimental medicine, anesthesia, oxidant molecules, antioxidant molecules, intracerebroventricular injection, long-term potentiation, urethane anesthesia, 14, and 616-092
Language:
English
Description:
Production of superoxide anions in the incubation medium of hippocampal slices can induce long-term potentiation (LTP). Other reactive oxygen species (ROS) such as hydrogen peroxide are able to modulate LTP and are likely to be involved in aging mechanisms. The present study explored whether intracerebro-ventricular (ICV) injection of oxidant or antioxidant molecules could affect LTP in vivo. With this aim in mind, field excitatory post-synaptic potentials (fEPSPs) elicited by stimulation of the perforant pathway were recorded in the dentate gyrus of the hippocampal formation in urethane-anesthetized rats. N-acetyl-L-cysteine, hydrogen peroxide (H2O2) or hypoxanthine/xanthine-oxidase solution (a superoxide producing system) were administrated by ICV injection. The control was represented by a group injected with saline ICV. Ten minutes after the injection, LTP was induced in the granule cells of the dentate gyrus by high frequency stimulation of the perforant pathway. Neither the H2O2 injection or the N-acetyl-L-cysteine injection caused any variation in the fEPSP at the 10-min post-injection time point, whereas the superoxide generating system caused a significant increase in the fEPSP. Moreover, at 60 min after tetanic stimulation, all treatments attenuated LTP compared with the control group. These results show that ICV administration of oxidant or antioxidant molecules can modulate LTP in vivo in the dentate gyrus. Particularly, a superoxide producing system can induce potentiation of the synaptic response. Interestingly, ICV injection of oxidants or antioxidants prevented a full expression of LTP compared to the saline injection., A. Viggiano, E. Viggiano, M. Monda, A. Viggiano, S. Ascione, S. Amaro, B. de Luca., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

217. Involvement of actin microfilament in regulation of pacemaking activity increased by hypotonic stress in cultured ICCs of murine intestine

Creator:
Wang, Z. Y., Huang, X., Liu, D. H., Lu, H. L., Kim, Y. C., and Xu, W. X.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, stres (fyziologie), physiology, stress (physiology), ICCs, hypotonic stress, actin microfilament, pacemaking activity, calcium oscillation, 14, and 612
Language:
English
Description:
Distension is a regular mechanical stimulus in gastrointestinal (GI) tract. This study was designed to investigate the effect of hypotonic stress on pacemaking activity and determine whether actin microfilament is involved in its mechanism in cultured murine intestinal interstitial cells of Cajal (ICCs) by using whole-cell patch-clamp and calcium imaging techniques. Hypotonic stress induced sustained inward holding current from the baseline to -650±110 pA and significantly decreased amplitudes of pacemaker current. Hypotonic stress increased the intensity of basal fluorescence ratio (F/F0) from baseline to 1.09±0.03 and significantly increased Ca2+ oscillation amplitude. Cytochalasin-B (20 μM), a disruptor of actin microfilaments, significantly suppressed the amplitudes of pacemaker currents and calcium oscillations, respectively. Cytochalasin-B also blocked hypotonic stress-induced sustained inward holding current and hypotonic stress-induced increase of calcium oscillations. Phalloidin (20 μM), a stabilizer of actin microfilaments, significantly enhanced the amplitudes of pacemaker currents and calcium oscillations, respectively. Despite the presence of phalloidin, hypotonic stress was still able to induce an inward holding current and increased the basal fluorescence intensity. These results suggest that hypotonic stress induces sustained inward holding current via actin microfilaments and the process is mediated by alteration of intracellular basal calcium concentration and calcium oscillation in cultured intestinal ICCs., Z. Y. Wang, X. Huang, D. H. Liu, H. L. Lu, Y. C. Kim, W. X. Xu., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

218. Involvement of the periaqueductal gray in the descending antinociceptive effect induced by the central nucleus of amygdala

Creator:
Bourbia, N. and Pertovaara, A.
Format:
print, bez média, and svazek
Type:
model:article and TEXT
Subject:
fyziologie, physiology, amygdala, descending pain control, mechanical nociception, N-methyl-D-aspartate receptor, periaqueductal gray, 14, and 612
Language:
English
Description:
Here we studied whether descending control of mechanical nociception by glutamate in the central nucleus of the amygdala (CeA) of healthy control animals is induced by amygdaloid NMDA receptors and relayed through the midbrain periaqueductal gray (PAG). Mechanical nociception in the hind paws was assessed in rats with chronic guide cannulae for glutamate administration in the right CeA and for inducing local anesthesia in the PAG. In a separate electrophysiological study, ON-like PAG neurons giving an excitatory response to noxious pinch of the tail were recorded in anesthetized rats following glutamate administration into the CeA. A high dose of glutamate (100 μg) in the CeA induced mechanical antinociception in the contra- but not ipsilateral hind limb. Antinociception was prevented by an NMDA receptor antagonist in the CeA or local anesthesia of the PAG. Discharge rate of ON-like PAG neurons was increased by a high dose of glutamate (100 μg) in the CeA and this increase was prevented by an NMDA receptor antagonist in the CeA. The results indicate that amygdaloid NMDA receptors in the CeA may induce contralaterally mechanical antinociception through a circuitry relaying in the PAG. Activation of ON-like PAG neurons is associated with the descending antinociceptive effect. Mechanisms and causality of this association still remain to be studied., N. Bourbia, A. Pertovaara., and Obsahuje bibliografii
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

219. Is NO the king? Pathophysiological benefit with uncertain clinical impact

Creator:
Fedor Šimko
Format:
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Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, fyziologie, nitric oxide, physiology, NO donor, cardiovascular mortality, clinical trial, 14, and 612
Language:
English
Description:
NO is the “hero” molecule of the last few decades. It is a ubiquitous and omnipotent radical with both hemodynamic and antiproliferative effects within the cardiovascular system. NO is an important counterregulatory factor for vasoconstrictors and growth promoting substances. Endothelial dysfunction with decreased NO production is related to many cardiovascular disorders, such as coronary artery disease, heart failure and hypertension. Despite the important role of NO within the circulation, there is only limited evidence in the form of large clinical trials that NO delivery can reduce cardiovascular morbidity and mortality. Thus, NO donors are not in the first line therapy in ischemic heart disease, heart failure or arterial hypertension and NO delivery is recommended only in particular clinical situations, when a well established treatment is contraindicated or has an insufficient effect. It is concluded that the insufficient NO production is the principal disorder in endothelial dysfunction, which is related to cardiovascular pathology with deteriorated prognosis, but the impact of therapeutically increased NO bioactivity on the morbidity and mortality is inferior to well established treatment with ACE-inhibitors, AT1 receptor blockers, beta-blockers, statins and certain antihypertensive drugs. There is little doubt that NO is king in the circulation, but kings seldom decide the battles., Fedor Šimko., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

220. Is postconditioning effective in prevention against long-lasting myocardial ischemia in the rabbit?

Creator:
Létienne, Robert, Calmettes, Y., and Le Grand, B.
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, ischemie, human physiology, ischemia, postconditioning, preconditioning, ischemia-reperfusion, 14, and 612
Language:
English
Description:
The goal of the study was to determine whether postconditioning protects against different ischemia durations in the rabbit. Rabbits were assigned to a 20-, 25-, 45- or 60-min coronary occlusion followed by 24-h of reperfusion. Rabbits received no further intervention (control) or were postconditioned with four cycles of 30-s occlusion and 30-s reperfusion after myocardial infarction. Plasma levels of troponin I were quantified throughout reperfusion. In control conditions, infarct sizes (% area at risk using triphenyltetrazolium chloride) after 20, 25, 45 and 60 min of coronary occlusions were 23±3, 51±4, 70±3 and 81±3 %, respectively. With 20 and 25 min occlusion, postconditioning reduced infarct size by 43±10 and 73±21 %, respectively. On the other hand, with 45 or 60 min occlusion, postconditioning had no significant effects on infarct size (61±3 and 80±2 % of area at risk). Preconditioning protocol was performed with 25- and 60-min coronary occlusion. As expected, preconditioning significantly reduced infarct size. In conclusion, in the rabbit, the cardioprotection afforded by postconditioning is limited to less than 45 min coronary occlusion., R. Létienne, Y. Calmettes, B. Le Grand., and Obsahuje seznam literatury
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public