scholarly journals The effect of β-endorphin on the functional parameters of the isolated heart and lymphatic vessels of the white rat

2019 ◽  
Vol 11 (2) ◽  
pp. 43-48 ◽  
Author(s):  
Olga V. Nechaykina ◽  
Denis S. Laptev ◽  
Sergei G. Petunov ◽  
Andrei S. Radilov
Keyword(s):  
Opioid Receptors ◽  
Rat Heart ◽  
Isolated Heart ◽  
Experimental Studies ◽  
Lymphatic Vessels ◽  
Isolated Rat Heart ◽  
K Channel ◽  
Channel Blockers ◽  
K Channels ◽  
Isolated Rat

Objective. The work is devoted to the comparison of the mechanisms of β-endorphin action in isolated rat heart and lymphatic vessels. Materials and methods. The experiments were performed using the Langendorff System perfusion device (Panlab, Spain) and the multichannel wire myograph 620M (DMT). During the study, selective opioid receptor blockers, K + channel blockers were used. Conclusion. In the course of experimental studies it was found that the most likely target for β-endorphin in an isolated rat heart are δ-opioid receptors, in isolated lymphatic vessels of a rat - μ- and δ-opioid receptors. The inhibitory effect of β-endorphin in the heart muscle is associated with stimulation of ATP-sensitive K + channels. In isolated lymphatic vessels, the effect of β-endorphin is realized through the activation of both potential-dependent and ATP-sensitive K+ channels.

Ischemic preconditioning attenuates acidosis and postischemic dysfunction in isolated rat heart

1992 ◽  
Vol 263 (3) ◽  
pp. H887-H894 ◽  
Author(s):  
G. K. Asimakis ◽  
K. Inners-McBride ◽  
G. Medellin ◽  
V. R. Conti
Keyword(s):  
Rat Heart ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Isolated Rat Heart ◽  
Rate Pressure Product ◽  
Anaerobic Glycolysis ◽  
Rat Hearts ◽  
Ischemic Period ◽  
Tissue Acidosis ◽  
Isolated Rat

The hypothesis that brief ischemia (preconditioning) protects the isolated heart from prolonged global ischemia was tested. Isovolumic rat hearts were preconditioned with either 5 min of ischemia followed by 5 min of perfusion (P1) or two 5-min episodes of ischemia separated by 5 min of perfusion (P2). Control hearts received no preconditioning. All hearts received 40 min of sustained ischemia and 30 min of reperfusion. Preconditioning (P1 or P2) significantly (P less than 0.0005) improved recovery of the rate-pressure product; percentage recoveries were 17.8 +/- 3.2 (n = 14), 59.9 +/- 5.5 (n = 6), and 46.4 +/- 4.7 (n = 8) for control, P1, and P2, respectively. Improved functional recovery of preconditioned hearts was associated with reduced end-diastolic pressure and improved myocardial perfusion. During the 40-min ischemic period, myocardial pH decreased from approximately 7.4 to 6.3 +/- 0.1 (n = 7) in the control hearts and to 6.7 +/- 0.1 (n = 7) in the preconditioned hearts (P less than 0.01). Also during the 40-min ischemic period, myocardial lactate (expressed as nmol/mg protein) increased to 146 +/- 11 (n = 7) and 101 +/- 12 (n = 8) in control and preconditioned hearts, respectively (P less than 0.02). The results demonstrate that a brief episode of ischemia can protect the isolated rat heart from a prolonged period of ischemia. This protection is associated with decreased tissue acidosis and anaerobic glycolysis during the sustained ischemic period.

scholarly journals Effect of Chronic Continuous Normobaric Hypoxia on Functional State of Cardiac Mitochondria and Tolerance of Isolated Rat Heart to Ischemia and Reperfusion: Role of µ and δ2 Opioid Receptors

2019 ◽  
pp. 909-920 ◽  
Author(s):  
E.S. Prokudina ◽  
N.V. Naryzhnaya ◽  
A.V. Mukhomedzyanov ◽  
A.S. Gorbunov ◽  
Y. Zhang ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Opioid Receptors ◽  
Mitochondrial Function ◽  
Rat Heart ◽  
Contractile Function ◽  
Isolated Rat Heart ◽  
Retention Capacity ◽  
Calcium Retention ◽  
Calcium Retention Capacity ◽  
Isolated Rat

Chronic continuous normobaric hypoxia (CNH) increases cardiac tolerance to ischemia/reperfusion injury in vivo and this effect is mediated via µ and δ2 opioid receptors (ORs) activation. CNH has also been shown to be cardioprotective in isolated rat heart. In this study, we hypothesize that this cardioprotective effect of CNH is mediated by activation of µ and δ2 ORs and preservation of mitochondrial function. Hearts from rats adapted to CNH (12 % oxygen) for 3 weeks were extracted, perfused in the Langendorff mode and subjected to 45 min of global ischemia and 30 min of reperfusion. Intervention groups were pretreated for 10 min with antagonists for different OR types: naloxone (300 nmol/l), the selective δ OR antagonist TIPP(ψ) (30 nmol/l), the selective δ1 OR antagonist BNTX (1 nmol/l), the selective δ2 OR antagonist naltriben (1 nmol/l), the selective peptide μ OR antagonist CTAP (100 nmol/l) and the selective κ OR antagonist nor-binaltorphimine (3 nmol/l). Creatine kinase activity in coronary effluent and cardiac contractile function were monitored to assess cardiac injury and functional impairment. Additionally, cardiac tissue was collected to measure ATP and to isolate mitochondria to measure respiration rate and calcium retention capacity. Adaptation to CNH decreased myocardial creatine kinase release during reperfusion and improved the postischemic recovery of contractile function. Additionally, CNH improved mitochondrial state 3 and uncoupled respiration rates, ADP/O, mitochondrial transmembrane potential and calcium retention capacity and myocardial ATP level during reperfusion compared to the normoxic group. These protective effects were completely abolished by naloxone, TIPP(ψ), naltriben, CTAP but not BNTX or nor-binaltorphimine. These results suggest that cardioprotection associated with adaptation to CNH is mediated by µ and δ2 opioid receptors activation and preservation of mitochondrial function.

Role of Na-activated K channel, Na-K-Cl cotransport, and Na-K pump in [K]e changes during ischemia in rat heart

1992 ◽  
Vol 263 (2) ◽  
pp. H333-H340 ◽  
Author(s):  
A. Mitani ◽  
M. J. Shattock
Keyword(s):  
Rat Heart ◽  
Control Level ◽  
Isolated Rat Heart ◽  
Global Ischemia ◽  
K Channel ◽  
Extracellular Potassium ◽  
Potassium Accumulation ◽  
Early Rise ◽  
R 56865 ◽  
Isolated Rat

The contribution of Na-activated K channel, the furosemide-sensitive (Na-K-Cl) cotransport, and Na-K pump to extracellular potassium accumulation during global ischemia was investigated using pharmacological blockade of these pathways. R 56865 (a blocker of the Na-activated K channel), furosemide, or ouabain was included in the perfusate before ischemia in the isolated rat heart preparation, and the extracellular K concentration ([K]e) was monitored during 30 min of global ischemia. In control hearts, [K]e showed an early rise (up to 9.0 +/- 0.2 mM from the baseline of 5.9 mM), a fall (to a minimum of 6.7 +/- 0.2 mM), and a late rise (to 14.1 +/- 0.4 mM by the end of ischemia). R 56865 (0.1 and 1 microM) suppressed the early [K]e rise to 50% of the control level. The late rise in [K]e was also significantly suppressed by the higher dose of R 56865. Furosemide (0.1 and 1 mM) reduced the early K accumulation by 35% but did not affect the rise of [K]e during the late ischemic phase. Blockade of Na-K pump by 10 microM ouabain did not increase [K]e during any phase of ischemia and, in fact, 100 microM ouabain profoundly suppressed the early rise in [K]e. We therefore suggest that the Na-activated K channel, the furosemide-sensitive cotransport, and changes in the activity of the Na-K pump may all contribute to extracellular K accumulation during ischemia. However, in addition to these pathways, it seems likely that other pathways for transsarcolemmal K efflux contribute to cellular K loss during ischemia in the isolated rat heart.

scholarly journals A Study on the Perfusion Preservation, Resuscitation, and Transplantation of a Rat Heart Isolated for 96 Hours

2009 ◽  
Vol 18 (5-6) ◽  
pp. 529-534 ◽  
Author(s):  
Naoyuki Hatayama ◽  
Yu Yoshida ◽  
Kunihiro Seki
Keyword(s):  
Rat Heart ◽  
Isolated Heart ◽  
Isolated Rat Heart ◽  
Gas Mixture ◽  
Heart Chamber ◽  
Constant Rate ◽  
Isolated Rat

Krebs-Henseleit (KH) solution was used to fill the heart chamber of an isolated rat heart before it was immersed in perfluorocarbon (PFC), which is an inert fluid. A gas mixture (PCO2 = 150 hPa and PO2 = 850 hPa) was then aerated at a constant rate into the PFC solution, and the isolated heart was thereafter preserved for 96 h with KH solution perfused continuously at a rate of 0.1 ml/h from the aorta of the isolated heart through a cannula. After preservation, the preserved heart was heterotopically transplanted into the neck of a recipient rat and then it was resuscitated. Using this method for preserving mammalian organs, we attained reproducibility after perfusion preservation for 96 h.

Effect of Hydrogen Sulfide on Reactions of Isolated Rat Heart under Volume Load and Ischemia-Reperfusion

2013 ◽  
Vol 4 (3) ◽  
pp. 201-212
Author(s):  
Tetyana V Shimanskaya ◽  
Yulia V. Goshovska ◽  
Olena M. Semenykhina ◽  
Vadim F. Sagach
Keyword(s):  
Hydrogen Sulfide ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Volume Load ◽  
Isolated Rat
Sign in / Sign up

Export Citation Format

Share Document