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2542. Acute elevation of endogenous prolactin does not influence glucose homeostasis in healthy men
- Creator:
- Vigaš, M., Klimeš, I., Jurčovičová, J., and Ježová, D.
- Type:
- article, model:article, and TEXT
- Subject:
- plasma prolactin, glucose, C-peptide, insulin, and insulin receptors
- Language:
- English
- Description:
- The diabetogenic effect of prolactin observed in patients with pathological hyperprolactinaemia was verified in healthy subjects. Plasma prolactin elevation was induced by administration of a dopamine antagonist drug domperidone (Motilium 10 mg orally, 9 subjects) and 2 h later the oral glucose tolerance test was performed. The influence of dopamine receptor stimulation on glucose homeostasis was tested by dopamine infusion (0.3 mg in saline or 20 % glucose, 1 g/min for 60 min, 11 subjects). After the blockade of dopamine receptors, a significant and prolonged increase of prolactin concentration was found. However, the levels of glucose, insulin, and C- peptide either before or after the glucose load were not different from control ones. The decreased number of insulin receptors (1.97±0.41 vs 0.51 ±0.14 pmol per 2.109 red blood cells) was compensated by increased affinity (0.51 ±0.17 vs 1.00±0.22 K* 108 mol.-1 per 1]) of insulin receptors. The stimulation of dopamine receptors showed a negligible effect on glucose regulation. It may be suggested that an endogenous increase of prolactin concentration in the physiological range does not participate in the regulation of glucose homeostasis in healthy subjects.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
2543. Acute experimental tabun-induced intoxication and its therapy in rats
- Creator:
- Krejčová, Gabriela
- Type:
- model:article and TEXT
- Language:
- English
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
2544. Acute generalized exanthematous pustulosis induced by olanzapine
- Creator:
- Christen, Susanne
- Type:
- model:article and TEXT
- Language:
- English
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
2545. Acute glycemic changes in brain and subcutaneous tissue measured by continuous glucose monitoring system in hereditary hypertriglyceridemic rat
- Creator:
- Michal Žourek, Pavlína Kyselová, Zdeněk Rušavý, and Daniela Čechurová
- Format:
- print, bez média, and svazek
- Type:
- model:article and TEXT
- Subject:
- fyziologie člověka, human physiology, Glucose, Brain, Continuous glucose measurement system, Rat, 14, and 612
- Language:
- English
- Description:
- Parallel glucose measurements in blood and other different tissues give us knowledge about dynamics of glycemia changes, which depend on vascularization, distribution space and local utilization by tissues. Such information is important for the understanding of glucose homeostasis and regulation. The aim of our study was to determine the time-lag between blood, brain, and adipose tissue during rapid glucose changes in a male hHTG rat (n=15). The CGMS sensor Guardian RT (Minimed/Medtronic, USA) was inserted into the brain and into the abdominal subcutaneous tissue. Fixed insulin and variable rate of glucose infusion was used to maintain euglycemia during sensor calibration period. At 0 min, 0.5 g/kg of bolus of glucose was administered, and at 50 min, 5 IU/kg of bolus of insulin was administered. Further glucose and insulin infusion was stopped at this time. The experiment was finished at 130 min and animals were euthanized. The time-shift between glycemia changes in blood, brain, and subcutaneous tissue was calculated by identification of the ideal correlation function. Moreover, the time to achieve 90 % of the maximum glucose excursion after intervention (T90) was measured to compare our data with the literature. The time-lag blood vs. brain and blood vs. subcutaneous tissue was 10 (10; 15) min and 15 (15; 25) min, respectively. The difference was statistically significant (P=0.01). T90 after glucose bolus in brain and subcutaneous tissue was 10 min (8.75; 15) and 15 min (13.75; 21.25), respectively. T90 after insulin bolus in brain and subcutaneous tissue was 10 min (10; 15) and 20 min (20; 27.5), respectively. To the contrary, with literature, our results showed earlier glucose level changes in brain in comparison with subcutaneous tissue after glucose and insulin boluses. Our results suggest that glucose dynamics is different within monitored tissues under rapid changing glucose level and we can expect similar behavior in humans. Improved knowledge about glucose distribution and dynamics is important for avoiding hypoglycemia., M. Žourek, P. Kyselová, D. Čechurová, Z. Rušavý., and Seznam literatury
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
2546. Acute hypoxic pulmonary vasoconstriction: a model of oxygen sensing
- Creator:
- Michelakis, E. D., Archer, S. L., and Weir, E. K.
- Type:
- article, model:article, and TEXT
- Language:
- English
- Description:
- One explanation of the mechanism of hypoxic pulmonary vasoconstriction (HPV) suggests that hypoxia shifts the redox status of the pulmonary artery smooth muscle cell towards a more reduced state, through changes in the redox couples and the activated oxygen species generation. The outward K+ current is then reduced and the membrane depolarized, leading to Ca++ influx through the voltage dependent Ca++ channels and vasoconstriction. The response of both pulmonary and systemic vessels to hypoxia may depend on the expression of different K+ channels in the two sites. While the oxygen sensor in pulmonary artery smooth muscle cells may be the delayed rectifier K+ channel, in the systemic arteries, hyperpolarization of the smooth muscle cell membrane, leading to vasodilatation, probably represents the effect of hypoxia in opening ATP-sensitive and Ca++-dependent K+ channels. The similarities between oxygen sensing mechanisms in several oxygen sensing cells (pulmonary artery smooth muscle cell, carotid body type 1 cell, neuroepithelial body) are striking. It is very likely that the mechanisms by which hypoxia is sensed at the molecular level are highly conserved and tightly regulated.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
2547. Acute hypoxic vasoconstriction in isolated rat small and large pulmonary arteries
- Creator:
- Zhang, F., Woodmansey, P. A., and Morice, A. H.
- Type:
- article, model:article, and TEXT
- Subject:
- hypoxic pulmonary vasoconstriction, pulmonary artery, and pulmonary resistance vessels
- Language:
- English
- Description:
- Hypoxic vasoconstriction (HPV) has been shown to consist of a biphasic contraction change. The first phase of the hypoxic response peaks at approximately five minutes. The second phase is at about 30 minutes. The force of contraction of both phases of HPV were found to be significantly greater in pulmonary resistance vessels (PRV) than in pulmonary artery (PA) (P<0.01). The endothelium modulates the hypoxic response, especially of the second phase of HPV (68 % reduction in PRV) (P<0.05). In Ca2+-free solution, the first peak and the second peak of HPV were reduced to 11 and 32 % contraction in PRV and to 26 and 21 % contraction in PA. A calcium channel antagonist (amlodipine) caused significant dose-dependent inhibition of the first phase of HPV (P=0.001), with a significantly greater effect on PRV compared to PA (P<0.01). Levcromakalim caused a dose- dependent inhibition of HPV in PRV (58 % at 10 /utA). In contrast, HPV in PA was not significantly inhibited by levcromakalim. In conclusion, this study has confirmed that hypoxia induces a biphasic contractile response in isolated pulmonary arteries requiring extracellular calcium. Both amlodipine and levcromakalim inhibit hypoxic pulmonary vasoconstriction and these agents may be of value in the treatment of pulmonary hypertension.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
2548. Acute liver failure induced by thioacetamide : Selection of Optimal Dosage in Wistar and Lewis Rats: selection of optimal dosage in wistar and lewis rats
- Creator:
- Eva Koblihová, Mrázová, I., Zdenka Vernerová, and Ryska, M.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, játra, liver, acute liver failure, thioacetamide, wistar rats, lewis rats, 14, and 612
- Language:
- English
- Description:
- Acute liver failure (ALF) is a clinical condition with very high mortality rate. Its pathophysiological background is still poorly understood, which necessitates a search for optimal experimental ALF models with features resembling those of the human disorder. Taking into consideration reproducibility of induction of ALF, adequate animal size, cost of animals, the required time gap between insult and death of animals (“therapeutic window”), potential risk to investigator and other aspects, administration of thioacetamide (TAA) in rats is currently most recommended. However, the fundamental details of this ALF model have not yet been evaluated. This prompted us to investigate, first, the course of ALF as induced by intraperitoneal TAA at doses increasing from 175 to 700 mg/kg BW per day. The animals’ survival rate, plasma alanine and aspartate aminotransferase activities, and bilirubin and ammonia levels were determined over the follow-up period. Second, we examined whether Wistar and Lewis rats exhibit any differences in the course of ALF induced by different TAA doses. We found that the optimal dose for ALF induction in rats is 350 mg.kg-1 i.p., given as a single injection. Wistar rats proved more susceptible to the development of TAA-induced ALF compared with Lewis rats. Collectively, our present findings provide a sound methodological background for experimental studies aimed at evaluation of pathophysiology and development of new approaches in the therapy of ALF., E. Koblihová, I. Mrázová, Z. Vernerová, M. Ryska., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
2549. Acute lung injury - from pathophysiology to treatment
- Creator:
- Mokra, Daniela
- Format:
- počítač and online zdroj
- Type:
- model:article and TEXT
- Subject:
- acute lung injury, acute respiratory distress syndrome, pathophysiology, therapy, and ARDS subtypes
- Language:
- English
- Description:
- Acute lung injury is characterized by acute respiratory insufficiency with tachypnea, cyanosis refractory to oxygen, decreased lung compliance, and diffuse alveolar infiltrates on chest X-ray. The 1994 American-European Consensus Conference defined “acute respiratory distress syndrome, ARDS” by acute onset after a known trigger, severe hypoxemia defined by PaO2/FiO2≤200 mm Hg, bilateral infiltrates on chest X-ray, and absence of cardiogenic edema. Milder form of the syndrome with PaO2/FiO2 between 200-300 mm Hg was named „acute lung injury, ALI“. Berlin Classification in 2012 defined three categories of ARDS according to hypoxemia (mild, moderate, and severe), and the term “acute lung injury” was assigned for general description or for animal models. ALI/ARDS can originate from direct lung triggers such as pneumonia or aspiration, or from extrapulmonary reasons such as sepsis or trauma. Despite growing understanding the ARDS pathophysiology, efficacy of standard treatments, such as lung protective ventilation, prone positioning, and neuromuscular blockers, is often limited. However, there is an increasing evidence that direct and indirect forms of ARDS may differ not only in the manifestations of alterations, but also in the response to treatment. Thus, individualized treatment according to ARDS subtypes may enhance the efficacy of given treatment and improve the survival of patients.
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
2550. Acute occlusion of abdominal aorta
- Creator:
- Ševčíková, Hana
- Type:
- model:article and TEXT
- Language:
- English
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public