Lack of Evidence for a Role of Mast Cell Degranulation in Acute Hypoxia /Reoxygenation-induced Injury in the Isolated Rat Heart

1996 ◽  
Vol 28 (2) ◽  
pp. 363-373 ◽  
Author(s):  
C VANHAASTER ◽  
W ENGELS ◽  
A DUIJVESTIJN ◽  
P LEMMENS ◽  
G HORNSTRA ◽  
...  
Keyword(s):  
Mast Cell ◽  
Rat Heart ◽  
Acute Hypoxia ◽  
Isolated Rat Heart ◽  
Mast Cell Degranulation ◽  
Isolated Rat ◽  
Hypoxia Reoxygenation

Antigen-evoked mast cell degranulation in the isolated rat heart: No effect on subsequent ischemia-reperfusion induced damage

1997 ◽  
Vol 46 (2) ◽  
pp. 40-45 ◽  
Author(s):  
W. Engels ◽  
C. M. C. J. Van Haaster ◽  
W. Vleeming ◽  
G. J. Van der Vusse
Keyword(s):  
Mast Cell ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Mast Cell Degranulation ◽  
Isolated Rat

scholarly journals ROLE OF SDF-1α/CXCR4 AXIS TO THE CARDIOPROTECTIVE EFFECT OF ISCHEMIC POST-CONDITIONING IN ISOLATED RAT HEART

2013 ◽  
Vol 61 (10) ◽  
pp. E217
Author(s):  
Jeong-Su Kim ◽  
Ju-Hyun Park ◽  
Kook-Jin Chun ◽  
Young-Ho Jang ◽  
June-Hong Kim ◽  
...  
Keyword(s):  
Rat Heart ◽  
Isolated Rat Heart ◽  
Cardioprotective Effect ◽  
Cxcr4 Axis ◽  
Isolated Rat

Evaluating the possible role of mitochondrial ATP-sensitive potassium channels in the cardioprotective effects of morin in the isolated rat heart

Life Sciences ◽  
2021 ◽  
Vol 264 ◽  
pp. 118659
Author(s):  
Maryam Rameshrad ◽  
Seyedeh Farzaneh Omidkhoda ◽  
Bibi Marjan Razavi ◽  
Hossein Hosseinzadeh
Keyword(s):  
Potassium Channels ◽  
Rat Heart ◽  
Isolated Rat Heart ◽  
Cardioprotective Effects ◽  
Isolated Rat

Mechanisms of antifibrillatory effect of acidic reperfusion: role of perfusate bicarbonate concentration

1993 ◽  
Vol 264 (3) ◽  
pp. H783-H790 ◽  
Author(s):  
C. Ibuki ◽  
D. J. Hearse ◽  
M. Avkiran
Keyword(s):  
Heart Rate ◽  
Ventricular Fibrillation ◽  
Rat Heart ◽  
Coronary Flow ◽  
Isolated Rat Heart ◽  
Acidic Ph ◽  
Bicarbonate Concentration ◽  
Left And Right ◽  
Isolated Rat

Transient (2 min) acidic (pH 6.6) reperfusion with low [HCO3-] solution suppresses reperfusion-induced ventricular fibrillation (VF) in the isolated rat heart. Using this preparation, we tested whether the effect was mediated by the high [H+] or the low [HCO3-] of perfusate. Left and right coronary beds were independently perfused with HCO3(-)-containing (25.0 mmol/l) solution at pH 7.4. Regional ischemia was then induced by stopping flow to the left coronary bed for 10 min. Hearts were subsequently assigned to four groups (n = 12 hearts/group), and the left coronary bed was reperfused with either HCO3(-)-containing (25.0 or 4.0 mmol/l) or HCO3(-)-free (5.0 mmol/l HEPES) solution, at pH 7.4 throughout (control reperfusion) or at pH 6.6 for the first 2 min and at pH 7.4 from 2 to 5 min (acidic reperfusion). Regardless of the buffer, controls exhibited a high (92 and 100%) incidence of VF; this was reduced to 42% in both of the acidic reperfusion groups (P < 0.05). There were no intergroup differences in heart rate, coronary flow, or size of ischemic zone. Thus high [H+], rather than low [HCO3-], appears to mediate the antifibrillatory effect of transient acidic reperfusion.

scholarly journals Acute reoxygenation injury in the isolated rat heart: role of resident cardiac mast cells.

1988 ◽  
Vol 63 (6) ◽  
pp. 1044-1052 ◽  
Author(s):  
A M Keller ◽  
R M Clancy ◽  
M L Barr ◽  
C C Marboe ◽  
P J Cannon
Keyword(s):  
Mast Cells ◽  
Rat Heart ◽  
Isolated Rat Heart ◽  
Reoxygenation Injury ◽  
Isolated Rat

scholarly journals Modulation ofN-methyl-d-aspartate receptors in isolated rat heart

2017 ◽  
Vol 95 (11) ◽  
pp. 1327-1334 ◽  
Author(s):  
Ivan Srejovic ◽  
Vladimir Zivkovic ◽  
Tamara Nikolic ◽  
Nevena Jeremic ◽  
Isidora Stojic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Heart ◽  
Isolated Rat Heart ◽  
Albino Rats ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Combined Application ◽  
Wistar Albino Rats ◽  
Isolated Rat

Considering the limited data on the role of NMDA-Rs in the cardiovascular system, the aim of the present study was to examine the effects of NMDA and DL-Hcy TLHC, alone and in combination with glycine, memantine, and ifenprodil, in the isolated rat heart. The hearts of Wistar albino rats were retrogradely perfused according to the Langendorff technique at a constant perfusion pressure. The experimental protocol for all experimental groups included the stabilization period, application of estimated substance for 5 min, followed by a washout period of 10 min. Using a sensor placed in the left ventricle, we registered the following parameters of myocardial function: dp/dtmax, dp/dtmin, SLVP, DVLP, HR; CF was measured using flowmetry). We estimated the following oxidative stress biomarkers in the coronary venous effluent using spectrophotometry: TBARS, NO2−, O2−, and H2O2. NMDA alone did not induce any change in any of the observed parameters, while DL-Hcy TLHC alone, as well as a combined application of NMDA and DL-Hcy TLHC with glycine, induced a reduction of most cardiodynamic parameters. Memantine and ifenprodil induced a reduction of cardiodynamic parameters and CF, as well as some oxidative stress biomarkers.

ATP-sensitive potassium channels regulate stimulated ANF secretion in isolated rat heart

1996 ◽  
Vol 271 (6) ◽  
pp. H2339-H2345 ◽  
Author(s):  
T. Xu ◽  
J. H. Jiao ◽  
R. A. Pence ◽  
A. J. Baertschi
Keyword(s):  
Potassium Channels ◽  
Potassium Channel ◽  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Left Atrial ◽  
Channel Blocker ◽  
Acute Hypoxia ◽  
Isolated Rat Heart ◽  
Perfused Hearts ◽  
Isolated Rat

Perfused hearts (n = 127) were exposed to acute hypoxia (10% O2 for 12 or 20 min) or left atrial stretch (increase in atrial pressure) in the presence or absence of 100 mumol/l ATP-sensitive potassium channel blocker (tolbutamide) or openers (pinacidil and diazoxide). Hypoxia alone elicited a prolonged atrial natriuretic factor (ANF) release, peaking at 74% over baseline (P < 0.01); with tolbutamide, ANF secretion peaked at 132% over baseline (P < 0.01). Pinacidil and diazoxide abolished the ANF response to hypoxia (P < 0.01). Atrial stretch alone (1 mmHg) transiently (2 min) increased ANF by 56% (P < 0.05); with tolbutamide, ANF increased transiently by 124% and showed a prolonged increase of 52% (P < 0.05). With tolbutamide, graded stretch (0.5-2.3 mmHg) induced a bell-shaped transient (2-min) increase of ANF release [-3% at 0.5 mmHg, 124% (P < 0.05) at 1.0 mmHg, 80% (P < 0.05) at 1.48 mmHg, and 14% at 2.22 mmHg] and a saturating prolonged ANF response. Tolbutamide increased the ANF response nonsignificantly at lower doses (30 mumol/l) and had no effect at 1 mumol/l. Pinacidil abolished the stretch-induced ANF release. These results suggest that ATP-sensitive potassium channels are extremely potent modulators of stimulated ANF secretion.

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