We are analyzing https://link.springer.com/article/10.1007/s00395-007-0657-0.

Title:
Independency of myocardial stunning of endothelial stunning? | Basic Research in Cardiology
Description:
Background and objective Vascular endothelial cells play an important role in the control of vascular tone. The reasons for coronary endothelial dysfunction are complex and may involve ischemia/reperfusion injury. We investigated whether endothelial, smooth muscle, and myocardial dysfunction are independent phenomena. Methods Rabbit hearts were rapidly excised without intermittent ischemia, connected to a modified Langendorff apparatus, and perfused with a modified Krebs-Henseleit solution containing bovine erythrocytes. Normoxic control hearts (n = 16) were perfused for 125 min. Postischemic hearts (n = 15) were perfused for 45 min, submitted to global ischemia (20 min) and reperfused (60 min). Both the normoxic and the postischemic hearts were divided into three groups that received either 0.9% NaCl (placebo), or 3-morpholinosydnonimine (SIN-1; 100 μM),or substance P (SP; 5 nM). Results After SIN-1, CBF in the normoxic hearts was increased by maximum 63% and after SP by 62%. 60 min after the onset of reperfusion, the postischemic hearts of both groups had recovered to 95% LVPmax. In the postischemic hearts, SIN-1 increased CBF still by 58%, while the endothelium-dependent vasomotion was impaired: SP improved CBF by only 9%. Summary and conclusions The particular protocol permitted differentiation between myocardial and vascular stunning. The results show that, while myocardial function has already recovered, endothelial cells are more severely impaired than smooth muscle cells, and that this injury persists beyond myocardial stunning. Thus, endothelial-dependent dysfunction can still impair vasodilatation while ventricular dysfunction has already resolved.
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Topics {✒️}

ischaemia-induced myocardial dysfunction month download article/chapter l-arginine blood cardioplegia modified krebs-henseleit solution alpha-adrenergic coronary vasomotion article basic research isolated rabbit heart nitric oxide-generating agents nitric oxide/hydrogen peroxide reversible cardiac failure impaired myocardial perfusion isolated rabbit hearts full article pdf darley-usmar vm improved perfusion reserve privacy choices/manage cookies involve ischemia/reperfusion injury increasing ischemia-reperfusion injury isolated working hearts isolated rat hearts postischemic rat heart adenosine receptor subtypes schipke jd increasing end-systolic cross-sectional study normothermic cardiac operation canine coronary artery coronary endothelial dysfunction smooth muscle cells sympathetic coronary innervation endothelial-dependent dysfunction endothelial cell dysfunction rabbit heart decreased space constant coronary artery occlusion ischemiareperfusion induces stunning regional myocardial functional coronary vascular reactivity european economic area original contribution published scope submit manuscript modified langendorff apparatus protocol permitted differentiation end-diastolic volumes refractory angina treated initiate lipid peroxidation glyceraldehyde- 3-phosphate dehydrogenase cell resistance/susceptibility action potential characteristics early gene expression

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Independency of myocardial stunning of endothelial stunning?
Independency of myocardial stunning of endothelial stunning?

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         description:Vascular endothelial cells play an important role in the control of vascular tone. The reasons for coronary endothelial dysfunction are complex and may involve ischemia/reperfusion injury. We investigated whether endothelial, smooth muscle, and myocardial dysfunction are independent phenomena. Rabbit hearts were rapidly excised without intermittent ischemia, connected to a modified Langendorff apparatus, and perfused with a modified Krebs-Henseleit solution containing bovine erythrocytes. Normoxic control hearts (n = 16) were perfused for 125 min. Postischemic hearts (n = 15) were perfused for 45 min, submitted to global ischemia (20 min) and reperfused (60 min). Both the normoxic and the postischemic hearts were divided into three groups that received either 0.9% NaCl (placebo), or 3-morpholinosydnonimine (SIN-1; 100 μM),or substance P (SP; 5 nM). After SIN-1, CBF in the normoxic hearts was increased by maximum 63% and after SP by 62%. 60 min after the onset of reperfusion, the postischemic hearts of both groups had recovered to 95% LVPmax. In the postischemic hearts, SIN-1 increased CBF still by 58%, while the endothelium-dependent vasomotion was impaired: SP improved CBF by only 9%. The particular protocol permitted differentiation between myocardial and vascular stunning. The results show that, while myocardial function has already recovered, endothelial cells are more severely impaired than smooth muscle cells, and that this injury persists beyond myocardial stunning. Thus, endothelial-dependent dysfunction can still impair vasodilatation while ventricular dysfunction has already resolved.
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