Effect of Hypoxia on Coronary Flow before and after Disruption of Both NOS and ATP-Sensitive K Channel Activities in the Isolated Guinea Pig Heart

2002 ◽  
Vol 96 (Sup 2) ◽  
pp. A643
Author(s):  
Kaoru Okazaki ◽  
Masayuki Endou
Keyword(s):  
Guinea Pig ◽  
Coronary Flow ◽  
K Channel ◽  
Guinea Pig Heart ◽  
Before And After

Hypoxia-induced activation of KATP channels limits energy depletion in the guinea pig heart

1995 ◽  
Vol 269 (2) ◽  
pp. H734-H742 ◽  
Author(s):  
U. K. Decking ◽  
T. Reffelmann ◽  
J. Schrader ◽  
H. Kammermeier
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Monophasic Action Potential ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
Guinea Pig Heart

The functional role of ATP-dependent potassium (KATP) in hypoxic cardiac failure was investigated in isolated guinea pig hearts with glibenclamide and rimalkalim as inhibitor and activator, respectively. Monophasic action potential duration at 90% of repolarization (MAP50), left ventricular function, and cardiac energy status (31P nuclear magnetic resonance spectroscopy) were measured during normotoxic (95% O2) and hypoxic (20% O2) perfusion. In normoxic hearts, 1 microM glibenclamide did not affect MAP50, left ventricular function, and coronary flow (n = 4). In contrast, rimalkalim rapidly shortened MAP50 and left ventricular pressure (LVP) in a dose-dependent fashion (e.g., by 60.2 +/- 3.5 and 80.8 +/- 8.2%, respectively, with 0.6 microM rimalkalim). This latter effect was reversed by 1 microM (glibenclamide (n = 4). With hypoxic perfusion, a reduction in LVP was observed, along with a shortening of the action potential (MAP90; 202 +/- 13 vs. 164 +/- 9 ms) and an increase in coronary flow. Glibenclamide (1 microM) reversed the MAP90 shortening and the increase in coronary flow. In addition, glibenclamide increased LVP transiently (n = 4). When coronary flow of hypoxic hearts was kept constant, however, glibenclamide elicited a sustained positive inotropic effect (n = 7). After glibenclamide, an increase in LVP from 54 +/- 4 to 64 +/- 3 mmHg was observed, along with a reduction in the free energy change of ATP hydrolysis from -54.5 +/- 1.9 to -52.9 +/- 0.2 nJ/mol and a further increase in the coronary venous adenosine from 269 +/- 48 to 1,680 +/- 670 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals ATP is involved in myocardial and vascular effects of exogenous bradykinin in ejecting guinea pig heart

1999 ◽  
Vol 277 (2) ◽  
pp. H818-H825 ◽  
Author(s):  
Peter B. Anning ◽  
Bernard D. Prendergast ◽  
Philip A. MacCarthy ◽  
Ajay M. Shah ◽  
Derek C. Buss ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Coronary Flow ◽  
Pyridoxal Phosphate ◽  
Left Ventricular ◽  
Luciferase Assay ◽  
Disulfonic Acid ◽  
Vascular Effects ◽  
Guinea Pig Heart ◽  
Nitric Oxide Release

It has recently been reported that bradykinin induces selective left ventricular (LV) relaxation in isolated guinea pig hearts via the release of nitric oxide. Exogenous bradykinin also induces vasodilation, which is only partly due to nitric oxide release. In the present study we investigated the role of adenyl purines on these bradykinin-induced effects. Isolated ejecting guinea pig hearts were studied. LV pressure was monitored by a 2-Fr micromanometer-tipped catheter. ATP concentrations were measured using a luciferin-luciferase assay. Bradykinin (1 and 100 nM) caused a progressive acceleration of LV relaxation together with a transient increase in coronary flow. These effects were inhibited by the nonselective P2 purinoceptor antagonist suramin (1 μM, n = 6) but were unaffected by the selective P2x purinoceptor antagonist pyridoxal phosphate 6-azophenyl-2′,4′-disulfonic acid (1 μM, n = 6). These myocardial and vascular effects of bradykinin were associated with increased ATP levels in coronary effluent. These data suggest that the selective enhancement of LV relaxation and rise in coronary flow induced by exogenous bradykinin involve endogenous ATP and the subsequent stimulation of P2 purinoceptors.

Effect of Acetaldehyde on the Isolated, Non-working Guinea-Pig Heart: Independence of the Coronary Flow Increase from Changes in Heart Rate and Oxygen Consumption

1974 ◽  
Vol 52 (3) ◽  
pp. 602-612 ◽  
Author(s):  
Minh-Hau Nguyen ◽  
L. Gailis
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Guinea Pig ◽  
Gas Phase ◽  
Coronary Flow ◽  
Constant Pressure ◽  
Guinea Pig Heart ◽  
Bicarbonate Buffer

Guinea-pig hearts were perfused at constant pressure with Krehs–Henseleit bicarbonate buffer equilibrated with 95% O2 – 5% CO2. Acetaldehyde at 1 and 5 mM increased coronary flow, oxygen consumption, and heart rate. At 0.2 mM, it increased coronary flow and oxygen consumption only. In the rapidly paced heart, 1 mM acetaldehyde increased coronary flow, but not heart rate or oxygen consumption. Acetaldehyde increased coronary flow and oxygen consumption of the potassium-arrested heart. Acetaldehyde increased all parameters of the hypoxic heart (25% O2 gas phase), but the anoxic heart was not affected (coronary flow was already maximal).Reserpine (in vivo) and catecholamine β blockers (dichloroisoproterenol and propranolol) (in vitro) blocked the heart rate increases and moderated the rise in oxygen consumption. Dichloroisoproterenol plus phentolamine blocked the increases of both heart rate and oxygen consumption. None of the compounds affected the increase of coronary flow produced by acetaldehyde. Epinephrine, norepinephrine, and tyramine increased the heart rate and oxygen consumption, but not the coronary flow. Theophylline increased all three parameters. Neither tranylcypromine nor atropine modified the acetaldehyde effect. We conclude that the increase in heart rate is mediated by catecholamine β receptors. The increase in coronary flow is independent of the increase in heart rate or oxygen consumption and is not mediated by catecholamines.

scholarly journals EFFECTS OF ARACHIDONIC ACID AND BRADYKININ ON THE CORONARY FLOW, RELEASE OF PGI2 AND CARDIAC FUNCTIONS IN THE PERFUSED GUINEA-PIG HEART

1982 ◽  
Vol 32 (2) ◽  
pp. 351-358
Author(s):  
Zen-ichi TERASHITA ◽  
Hiroshi FUKUI ◽  
Kohei NISHIKAWA ◽  
Minoru HIRATA ◽  
Shintaro KIKUCH
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Coronary Flow ◽  
Guinea Pig Heart ◽  
Cardiac Functions

Endothelial control of coronary flow in perfused guinea pig heart

1995 ◽  
Vol 90 (2) ◽  
pp. 119-124 ◽  
Author(s):  
R. J. Gryglewski ◽  
S. Chlopicki ◽  
P. Niezabitowski
Keyword(s):  
Guinea Pig ◽  
Coronary Flow ◽  
Guinea Pig Heart ◽  
Endothelial Control

scholarly journals Glibenclamide Specifically Blocks ATP-Sensitive K<+ Channel Current in Atrial Myocytes of Guinea Pig Heart

1990 ◽  
Vol 54 (4) ◽  
pp. 473-477 ◽  
Author(s):  
Eiji HAMADA ◽  
Reiko TAKIKAWA ◽  
Hiroyuki ITO ◽  
Mari IGUCHI ◽  
Akira TERANO ◽  
...  
Keyword(s):  
Guinea Pig ◽  
K Channel ◽  
Atrial Myocytes ◽  
Guinea Pig Heart ◽  
Channel Current

scholarly journals Obesity decreases the contribution of Kv channels to hypoxic coronary vasodilation

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Hannah E. Clark ◽  
Hana E. Baker ◽  
Adam G. Goodwill ◽  
Bianca S. Blaettner ◽  
Michael C. Kozlowski ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Functional Expression ◽  
K Channel ◽  
Coronary Vasodilation ◽  
Kv Channels ◽  
Arterial Blood ◽  
Before And After ◽  
Arterial Po2

Background and Hypothesis: Our group previously demonstrated that reductions in the functional expression of voltage-dependent K+ (Kv) channels contribute to impaired metabolic control of coronary blood flow in the setting of obesity. This study tested the hypothesis that obesity diminishes the contribution of Kv channels to coronary vasodilation in response to hypoxemia. Experimental Design or Project Methods: Control lean (n = 7) and obese (n = 5) swine were anesthetized and the heart exposed via left lateral thoracotomy. Coronary blood flow was measured in response to hypoxemia, before and after inhibition of Kv channels by 4-aminopyridine (4-AP; 0.3 mg/kg, iv), by a flow probe placed about the left anterior descending coronary artery. Hypoxemia was induced by progressive increases in the amount of nitrogen introduced into the ventilator. Arterial blood samples were obtained at each reduction in arterial oxygenation via a catheter placed in the femoral artery. Results: Blood pressure decreased from ~88 ± 5 mmHg to ~68 ± 6 mmHg (P = 0.01) as arterial PO2 was reduced below 50 mmHg in both lean and obese swine (P = 0.51). In lean swine, coronary flow progressively increased from ~0.6 to >3.0 ml/min/g as arterial PO2 was reduced. This response was decreased by ~40% in obese swine and by ~30% in lean swine treated with 4-AP. Administration of 4AP had no effect on coronary flow in obese swine. Conclusion and Potential Impact: These data support that Kv channels contribute to increases in coronary flow in response to hypoxemia in lean swine and that reductions in Kv channel function contribute to impaired hypoxic coronary vasodilation in obese swine. We propose that therapeutic targeting of obesity associated pathways (angiotensin-aldosterone system) known to influence K+ channel expression could improve coronary microvascular function and cardiovascular outcomes in subjects with obesity. Supported by R01 HL136386; T35 HL 110854.

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