Tyrode Solution for Bath Perfusion:

2015 ◽  
Vol 2015 (4) ◽  
pp. pdb.rec079574
Keyword(s):  
Tyrode Solution

scholarly journals THE CULTIVATION OF TISSUES FOR PROLONGED PERIODS IN SINGLE FLASKS

1936 ◽  
Vol 64 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Raymond C. Parker
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Connective Tissue ◽  
Breast Muscle ◽  
Cell Multiplication ◽  
Tyrode Solution ◽  
Low Level ◽  
Further Development

1. Fragments of breast muscle from a 12 day old chick embryo have been kept alive in single flasks for an entire year without being transferred. The nutrient materials were supplied by frequent applications of adult fowl serum diluted with Tyrode solution. 2. When fragments of fixed tissues are cultivated in serum, cell multiplication and cell death are both reduced to an extremely low level. 3. The presence of a plasma coagulum is not essential to the continued survival and further development of tissues cultivated inserum. 4. The fibrinogen, prothrombin, and fibrin of coagulated plasma are not essential to the development of connective tissue fibers in vitro.

scholarly journals Positive Inotropic Effects of ATP Released via the Maxi-Anion Channel in Langendorff-Perfused Mouse Hearts Subjected to Ischemia-Reperfusion

2021 ◽  
Vol 9 ◽  
Author(s):  
Hiroshi Matsuura ◽  
Akiko Kojima ◽  
Yutaka Fukushima ◽  
Yu Xie ◽  
Xinya Mi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Organic Anion ◽  
Left Ventricular ◽  
Transient Increase ◽  
Tyrode Solution ◽  
Inotropic Effects ◽  
Cl Channel ◽  
Short Period ◽  
Cl Channels ◽  
Normal Tyrode Solution

The organic anion transporter SLCO2A1 constitutes an essential core component of the ATP-conductive large-conductance anion (Maxi-Cl) channel. Our previous experiments using Langendorff-perfused mouse hearts showed that the Maxi-Cl channel contributes largely to the release of ATP into the coronary effluent observed during 10-min reperfusion following a short period (6 min) of oxygen-glucose deprivation. The present study examined the effect of endogenous ATP released via Maxi-Cl channels on the left ventricular contractile function of Langendorff-perfused mouse hearts, using a fluid-filled balloon connected to a pressure transducer. After the initial 30-min stabilization period, the heart was then perfused with oxygen-glucose-deprived Tyrode solution for 6 min, which was followed by a 10-min perfusion with oxygenated normal Tyrode solution in the absence and presence of an ATP-hydrolyzing enzyme, apyrase, and/or an adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). In the absence of apyrase and DPCPX, the left ventricular developed pressure (LVDP) decreased from a baseline value of 72.3 ± 7.1 to 57.5 ± 5.5 mmHg (n = 4) at the end of 6-min perfusion with oxygen-glucose-deprived Tyrode solution, which was followed by a transient increase to 108.5 ± 16.5 mmHg during subsequent perfusion with oxygenated normal Tyrode solution. However, in the presence of apyrase and DPCPX, the LVDP decreased to the same degree during 6-min perfusion with oxygen-glucose-deprived Tyrode solution, but failed to exhibit a transient increase during a subsequent perfusion with oxygenated normal Tyrode solution. These results strongly suggest that endogenous ATP released through Maxi-Cl channels contributes to the development of transient positive inotropy observed during reperfusion after short-period hypoxia/ischemia in the heart.

scholarly journals CYTOLOGICAL AND PHARMACOLOGICAL OBSERVATIONS ON THE RELEASE OF HISTAMINE BY MAST CELLS

1954 ◽  
Vol 100 (2) ◽  
pp. 217-224 ◽  
Author(s):  
Don W. Fawcett
Keyword(s):  
Mast Cells ◽  
Peritoneal Fluid ◽  
Appreciable Amount ◽  
Fluid Solution ◽  
Tyrode Solution ◽  
Morphological Effect ◽  
Liberation Of Histamine ◽  
To Come ◽  
Histamine Liberator ◽  
Extensive Release

Experimental solutions known to affect mast cells or to cause liberation of histamine from the tissue were introduced into the peritoneal cavity of rats. Samples of the peritoneal fluid were withdrawn at intervals afterward and assayed for histamine and the condition of the mast cells was subsequently ascertained by microscopic examination of stained spreads of the mesenteries. Intraperitoneal injection of distilled water caused osmotic disruption of the mast cells and the appearance of an appreciable amount of histamine in the peritoneal fluid. Injection of Tyrode solution alone was not particularly damaging to the mast cells and little or no histamine was released. Injection of Tyrode solution containing compound 48/80 resulted in extensive release of granules from mast cells and the appearance of large amounts of histamine in the fluid. Solution of 48/80 failed however to cause histamine release when injected into rats whose subserosal mast cells had previously been destroyed. A series of increasing doses of compound 48/80 had a graded morphological effect upon mast cells and resulted in a graded increase in the amount of histamine that appeared in the peritoneal fluid. It is unlikely therefore that this compound acts by simply lysing the plasma membrane. It is concluded that mast cells in the rat are extraordinarily rich in histamine which is liberated under conditions which cause mast cells to release their granules. The histamine set free by the potent histamine liberator, compound 48/80, appears to come principally from the tissue mast cells.

scholarly journals Intermittent Hypoxia Inhibits Na+-H+ Exchange-Mediated Acid Extrusion Via Intracellular Na+ Accumulation in Cardiomyocytes

2018 ◽  
Vol 46 (3) ◽  
pp. 1252-1262 ◽  
Author(s):  
Huai-Ren Chang ◽  
Chih-Feng Lien ◽  
Jing-Ren Jeng ◽  
Jen-Che Hsieh ◽  
Chen-Wei Chang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intracellular Calcium ◽  
Intracellular Ph ◽  
Recovery Rate ◽  
Intermittent Hypoxia ◽  
Ros Production ◽  
Tyrode Solution ◽  
Neonatal Cardiomyocytes ◽  
Cardioprotective Effects ◽  
Acid Extrusion

Background/Aims: Intermittent hypoxia (IH) has been shown to exert preconditioning-like cardioprotective effects. It also has been reported that IH preserves intracellular pH (pHi) during ischemia and protects cardiomyocytes against ischemic reperfusion injury. However, the exact mechanism is still unclear. Methods: In this study, we used proton indicator BCECF-AM to analyze the rate of pHi recovery from acidosis in the IH model of rat neonatal cardiomyocytes. Neonatal cardiomyocytes were first treated with repetitive hypoxia-normoxia cycles for 1-4 days. Cells were then acid loaded with NH4Cl, and the rate of pHi recovery from acidosis was measured. Results: We found that the pHi recovery rate from acidosis was much slower in the IH group than in the room air (RA) group. When we treated cardiomyocytes with Na+-H+ exchange (NHE) inhibitors (Amiloride and HOE642) or Na+-free Tyrode solution during the recovery, there was no difference between RA and IH groups. We also found intracellular Na+ concentration ([Na+]i) significantly increased after IH exposure for 4 days. However, the phenomenon could be abolished by pretreatment with ROS inhibitors (SOD and phenanathroline), intracellular calcium chelator or Na+-Ca2+ exchange (NCX) inhibitor. Furthermore, the pHi recovery rate from acidosis became faster in the IH group than in the RA group when inhibition of NCX activity. Conclusions: These results suggest that IH would induce the elevation of ROS production. ROS then activates Ca2+-efflux mode of NCX and results in intracellular Na+ accumulation. The rise of [Na+]i further inhibits the activity of NHE-mediated acid extrusion and retards the rate of pHi recovery from acidosis during IH.

scholarly journals Energy expenditure by Ba2+contracture in rat ventricular slices derives from cross-bridge cycling

1999 ◽  
Vol 277 (1) ◽  
pp. H74-H79 ◽  
Author(s):  
Hisaharu Kohzuki ◽  
Hiromi Misawa ◽  
Susumu Sakata ◽  
Yoshimi Ohga ◽  
Hiroyuki Suga ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Energy Expenditure ◽  
Cyclopiazonic Acid ◽  
Left Ventricular ◽  
Basal Metabolism ◽  
Dependent Manner ◽  
Tyrode Solution ◽  
Cross Bridge ◽  
Butanedione Monoxime ◽  
Dose Dependent

To clarify the energy-expenditure mechanism during Ba2+ contracture of mechanically unloaded rat left ventricular (LV) slices, we measured myocardial O2 consumption (V˙o 2) of quiescent slices in Ca2+-free Tyrode solution andV˙o 2 during Ba2+ contracture by substituting Ca2+ with Ba2+. We then investigated the effects of cyclopiazonic acid (CPA) and 2,3-butanedione monoxime (BDM) on the Ba2+ contractureV˙o 2. The Ca2+-freeV˙o 2 corresponds to that of basal metabolism (2.32 ± 0.53 ml O2 ⋅ min−1 ⋅ 100 g LV−1). Ba2+ increased theV˙o 2 in a dose-dependent manner (from 0.3 to 3.0 mmol/l) from 110 to 150% of basal metabolic V˙o 2. Blockade of the sarcoplasmic reticulum (SR) Ca2+ pump by CPA (10 μmol/l) did not at all decrease the Ba2+-activatedV˙o 2. BDM (5 mmol/l), which specifically inhibits cross-bridge cycling, reduced the Ba2+activatedV˙o 2 almost to basal metabolic V˙o 2. These energetic results revealed that the Ba2+-activatedV˙o 2 was used for the cross-bridge cycling but not for the Ca2+ handling by the SR Ca2+ pump.

Effects of hormones on 3', 5' -cyclic adenosine monophosphate in choroid plexus.

1977 ◽  
Vol 232 (4) ◽  
pp. E353
Author(s):  
D Rudman ◽  
B M Hollins ◽  
N C Lewis ◽  
J W Scott
Keyword(s):  
Effective Dose ◽  
Choroid Plexus ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Tyrode Solution ◽  
Minimal Effective Dose ◽  
Camp Content ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

Choroid plexus of rabbit and rat was incubated for 2-30 min at 37 degrees C under 95% O2-5% CO2 in Tyrode solution containing 10 mM glucose and 1 mM theophylline with these agents: epinephrine, norepinephrine, isoproterenol, dopamine, histamine, serotonin, arginine, and lysine vasopressins, oxytocin, angiotensin, adrenocorticotropin (ACTH), beta-melanocyte-stimulating hormone, and choroid plexus peptide IIF. After incubation, tissue and medium were analyzed for 3', 5' -cyclic adenosine monophosphate (cAMP) content. Each amine or peptide was tested initially at 1,000 microng/ml. Only ACTH and serotonin affected cAMP content of rabbit choroid plexus. At 1,000 microng/ml, these agents caused a 10 and 4 times (respectively) increase in cAMP content of tissue + medium at 2-10 min with decline in content at 10-30 min. More than 90% of the increment was located in tissue, less than 10% in medium. Minimal effective dose (MED) to cause a significant (P less than .05) accumulation of cAMP was 0.1 microng/ml (2.2 x 10(-8) M) for ACTH and 10 microng/ml (5.7 x10(-3) M) for serotonin. Only isoproterenol, epinephrine, and norepinephrine influenced cAMP content of rat choroid plexus. MED's for this effect by isoproterenol, epinephrine, and norepinephrine were .001, .01, and 10 microng/ml (4.7 x 10(-9), 5.5 x 10(-8), and 5.9 x 10(-5) M), respectively.

Na+-dependent activation of Na+-K+ pump in human myocardium during recovery from acidosis

1989 ◽  
Vol 256 (1) ◽  
pp. H256-H264 ◽  
Author(s):  
H. H. Rasmussen ◽  
E. J. Cragoe ◽  
R. E. ten Eick
Keyword(s):  
Cardiac Cells ◽  
Right Atrial ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Tyrode Solution ◽  
Human Right ◽  
Pump Activity ◽  
Acid Load ◽  
Right Atrial Appendage ◽  
Dimethyl Amiloride

In cardiac cells of some species, an intracellular Na+ load and enhanced electrogenic Na+ pumping can develop during recovery from acidosis. We examined whether this can also occur in human heart. Specimens of human right atrial appendage were incubated in cold (2 degrees C) NH4Cl-substituted (for NaCl) Tyrode solution and then transferred to warm (30 degrees C) Na+-Tyrode solution containing 20 mM K+ to induce an intracellular acid load. After transfer, resting membrane potential (Em) transiently hyperpolarized to a maximal level (Emax) of -58.6 +/- 1.3 mV (n = 8), a level significantly (P less than 0.001) more negative than the equilibrium potential for K+. Decreasing K+ conductance with 0.5 mM Ba2+ increased Emax to -74.0 +/- 2.7 mV (n = 6, P less than 0.001), indicating that the hyperpolarization was not due to efflux of NH+4 through K channels. Acetylstrophanthidin (0.5 microM) reduced Emax to -37.5 +/- 3.1 mV (n = 5, P less than 0.001), indicating that an increased level of Na+-K+ pump activity was involved in the hyperpolarization. The Na+-K+ pump-induced hyperpolarization was abolished (Emax = -22.6 +/- 1.6 mV, n = 8, P less than 0.001) by 10 microM 5-(N,N-dimethyl)amiloride and, when the extracellular Na+ concentration was reduced to 50 mM, by 50 mM Li+. These findings suggest that Na+-H+ exchange can produce a Na+ load which then can stimulate electrogenic Na+ pumping in human cardiac cells during recovery from acidosis.

Effect of solute-coupled volume absorption on oxygen consumption in cat ileum.

1979 ◽  
Vol 236 (2) ◽  
pp. E198
Author(s):  
J D Valleau ◽  
D N Granger ◽  
A E Taylor
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Absorption ◽  
Tyrode Solution ◽  
Recovery Method ◽  
Volume Absorption ◽  
All Solutions ◽  
Volume Recovery ◽  
Oxygen Requirements ◽  
Increased Blood Flow

The effects of solute-coupled volume absorption on blood flow, oxygen consumption, and vascular resistance were analyzed in autoperfused segments of cat ileum. Intestinal absorption was stimulated by placing either Tyrode solution, Tyrode + glucose, or Tyrode + taurocholate into the ileal lumen. Net volume absorption rates (Jv,m) were determined using a volume recovery method. Oxygen consumption (VO2) increased during the absorption of all solutions. The absorption of Tyrode solution plus glucose caused the greatest increase in VO2, whereas Tyrode plus taurocholate resulted in the smallest increase. For Tyrode solution and Tyrode plus glucose absorption, the increased VO2 was due predominantly to an increased blood flow, whereas the increased VO2 with taurocholate resulted from an increased oxygen extraction. A linear relationship between the change in VO2 during transport and Jv,m was aquired for Tyrode solution, and Tyrode + glucose. The results indicate that the oxygen requirements of the absorbing intestine are dependent on both the rate of transport and the solutes being transported.

Apamin, a highly specific Ca2+ blocking agent in heart muscle

1985 ◽  
Vol 248 (6) ◽  
pp. H961-H965 ◽  
Author(s):  
G. Bkaily ◽  
N. Sperelakis ◽  
J. F. Renaud ◽  
M. D. Payet
Keyword(s):  
Heart Muscle ◽  
Blocking Agent ◽  
Tyrode Solution ◽  
Tetraethylammonium Chloride ◽  
Naturally Occurring ◽  
Ventricular Cells ◽  
Dose Dependent Fashion ◽  
K Concentration ◽  
Dose Dependent ◽  
Slow Action Potentials

Apamin, a bee venom polypeptide, was recently reported to block specifically the Ca2+-dependent K+ channels that are not blocked by tetraethylammonium chloride in muscle cells. We report here that apamin blocked the naturally occurring slow action potentials (APs) in cultured cell reaggregates from chick hearts. The effects of apamin were not reversible on washout with Tyrode solution only (up to 24 h), but quinidine (10(-8) M) reversed the apamin blockade of the slow channels. Apamin also blocked the isoproterenol-induced slow APs in freshly isolated chick ventricular cells depolarized by 22 mM extracellular K+ concentration ([K+]o) in a dose-dependent fashion (10(-12) to 10(-10) M). Apamin at 5 X 10(-11) M blocked the isoproterenol-induced slow APs without affecting the membrane potential. Washout (with Tyrode solution containing 22 mM [K+]o and 10(-6) M isoproterenol) did not recover the slow APs. However, recovery of the slow APs was possible only when quinidine (10(-8) M) was added to the superfusion medium. The fast APs were rapidly restored by washout with Tyrode solution only. The present data show that apamin is a highly specific compound that tightly binds to the Ca2+ slow channels, thus blocking the slow APs in heart muscle. In addition, quinidine antagonizes the apamin binding on the slow APs.

EFFECTS OF CELL ADHESION PEPTIDE, Arg-Gly-Asp-Ser (RGDS), ON RESPONSES OF WASHED PLATELETS FROM HUMANS, RABBITS AND RATS

1987 ◽  
Author(s):  
E J Harfenist ◽  
M A Packham ◽  
J F Mustard
Keyword(s):  
Cell Adhesion ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Independent Component ◽  
Tyrode Solution ◽  
Significant Extent ◽  
Aggregation Mechanism ◽  
Rabbit Platelets ◽  
Induced Aggregation ◽  
Rat Platelets

Fibrinogen (Fbg) is a cofactor in the aggregation of human platelets, and washed platelets do not aggregate to a significant extent in response to ADP unless Fbg is added to the suspension; however, exogenous Fbg is not required for ADP-induced aggregation of washed platelets from rabbits or rats. Since, with human platelets, Arg-Gly-Asp-Ser (RGDS) inhibits aggregation and the binding of 125I-Fbg to ADP-stimulated platelets, its effects on the responses of rabbit and rat platelets were studied in an attempt to elucidate the differences in Fbg requirements of platelets from the three species. Aggregation and Fbg binding were studied using washed platelets suspended in Tyrode solution containing albumin, apyrase and 2 mM Ca2+. 50 μM RGDS caused over 80% inhibition of the aggregation of human platelets stimulated with 9 yM ADP in the presence of 0.2 yM Fbg, but only 3-9% inhibition of the ADP-induced aggregation of rabbit or rat platelets regardless of whether exogenous Fbg was added. 50 yM RGDS also inhibited the aggregation of human platelets stimulated with thrombin (0.9 U/mL), but produced no more than 3% inhibition with rabbit or rat platelets. The binding of 125I-Fbg to ADP-stimulated human platelets was inhibited by 80-90% by 30 yM RGDS, but even at 50 μM, RGDS inhibited Fbg binding to rabbit or rat platelets by only 15-27%. The differences were due to the species of platelets, since, with both human and rabbit platelets, human Fbg could be replaced by rabbit Fbg without significantly changing the results. RGDS, added to human platelets that had been aggregated with thrombin, did not cause deaggregation, but did partially inhibit aggregation when added within 1 min; this inhibitory effect was less than when RGDS was added before thrombin, and decreased progressively as the length of time before the addition of RGDS was increased. These observations indicate a difference in aggregation mechanism between human platelets and those from rabbits and rats, and are consistent with a Fbg-independent component to the aggregation of rabbit and rat platelets.

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