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223. 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

224. 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

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

Creator:
Fedor Šimko
Format:
print, bez média, and svazek
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

226. 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

227. Ischemic preconditioning fails to confer additional protection against ischemia-reperfusion injury in the hypothyroid rat heart

Creator:
Mourouzis, I., Dimopoulos, A., Saranteas, T., Tsinarakis, N., Livadarou, E., Spanou, D., Kokkinos, A. D., Xinaris, C., Pantos, C., and Cokkinos, D. V.
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, ischemická choroba srdeční, hormony štítné žlázy, hypotyreóza, physiology, ischemic heart disease, thyroid hormones, hypothyreosis, ischemic preconditioning, JNKs, p38 MAPK, 14, and 612
Language:
English
Description:
There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfus ion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts ( P<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts ( P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts., I. Mourouzis ... [et al.]., and Obsahuje seznam literatury
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

228. Ivan Djaja (Jean Giaja) and the Belgrade School of Physiology

Creator:
Pavle R. Andjus, Stanko S. Stojilković, and Gordana Cvijić
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, bioenergetika, fyziologie, dějiny, bioenergetics, physiology, history, history of physiology, Sorbonne, University of Belgrade, thermoregulation, neuroendocrine regulation, 14, and 612
Language:
English
Description:
The founder of physiology studies in the Balkans and the pioneer of research on hypothermia, Ivan Djaja (Jean Giaja) was born 1884 in L’Havre. Giaja gained his PhD at the Sorbonne in 1909. In 1910 he established the first Chair of Physiology in the Balkans and organized the first Serbian In stitute for Physiology at the School of Philosophy of the University of Belgrade. He led this Institute for more than 40 subsequent years. His most notable papers were in the field of thermoregulation and bioenergetics. Djaja became member of the Serbian and Croatian academies of science and doctor honoris causa of Sorbonne. In 1952 for the seminal work on the behavior of deep cooled warm blooded animals he became associate member of the National Medical Academy in Paris. In 1955 the French Academy of Sciences elected him as associate member in place of deceased Sir Alexander Fleming. Djaja died in 1957 during a congress held in his honor. He left more than 200 scientific and other papers and the golden DaVincian credo “Nulla dies sine experimento”. His legacy was continued by several generations of researchers, the most prominent among them being Stefan Gelineo, Radoslav Andjus and Vojislav Petrović ., P. R. Andjus, S. S: Stojilkovic, G. Cvijic., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

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