Capillary perfusion patterns in reperfused ischemic subendocardial myocardium: Experimental study using fluorescent dextran

Camilléri, J P; Nlom, M. Ossondo; Joseph, Danielle; Michel, Jean‐Baptiste; Barres, D; Mignot, J

doi:10.1016/0014-4800(83)90043-6

Cited by 10 publications

(6 citation statements)

References 22 publications

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“…Functional capillary density is known to decrease as early as 20 min after coronary artery clamping followed by short reperfusion [ 39 ]. In our study we don’t see a decrease of capillary density after 30 minutes of ischemia.…”

Section: Discussionmentioning

confidence: 99%

Dissecting the Effects of Ischemia and Reperfusion on the Coronary Microcirculation in a Rat Model of Acute Myocardial Infarction

et al. 2016

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BackgroundMicrovascular injury (MVI) after coronary ischemia-reperfusion is associated with high morbidity and mortality. Both ischemia and reperfusion are involved in MVI, but to what degree these phases contribute is unknown. Understanding the etiology is essential for the development of new potential therapies.Methods and FindingsRats were divided into 3 groups receiving either 30 minutes ischemia, 90 minutes ischemia or 30 minutes ischemia followed by 60 minutes reperfusion. Subsequently hearts were ex-vivo perfused in a Langendorff-model. Fluorescence and electron microscopy was used for analysis of capillary density, vascular permeability and ultrastructure. Most MVI was observed after 30 minutes ischemia followed by 60 minutes reperfusion. In comparison to the 30’ and 90’ ischemia group, wall thickness decreased (207.0±74 vs 407.8±75 and 407.5±71, p = 0.02). Endothelial nuclei in the 30’-60’ group showed irreversible damage and decreased chromatin density variation (50.5±9.4, 35.4±7.1 and 23.7±3.8, p = 0.03). Cell junction density was lowest in the 30’-60’ group (0.15±0.02 vs 2.5±0.6 and 1.8±0.7, p<0.01). Microsphere extravasation was increased in both the 90’ ischemia and 30’-60’ group.ConclusionsIschemia alone for 90 minutes induces mild morphological changes to the coronary microcirculation, with increased vascular permeability. Ischemia for 30 minutes, followed by 60 minutes of reperfusion, induces massive MVI. This shows the direct consequences of reperfusion on the coronary microcirculation. These data imply that a therapeutic window exists to protect the microcirculation directly upon coronary revascularization.

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Section: Discussionmentioning

confidence: 99%

Dissecting the Effects of Ischemia and Reperfusion on the Coronary Microcirculation in a Rat Model of Acute Myocardial Infarction

et al. 2016

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“…The introduction of this polysaccharide as a plasmatic tracer appeared to be useful for microcirculation studies (25). Methods for localizing this tracer in tissue section have been proved to be reliable, particularly for studying the microcirculation in heart (22) as in the brain (21). This marker labelled the lumen of capillaries and permitted some functional approach.…”

Section: H Effect Of Cardiac Hypertrophy On the Capillary Bedmentioning

confidence: 98%

“…Fluoresceinisothiocyanate labelled dextran (FITC-D) (molecular weight 150,000), was injected into a peripheral vein (femoral or penis vein) as a bolus of 20 rag/100 g of body weight (BW) diluted in 0.5 ml of 150 mM sodium chloride (22,25). Five minutes after FITC-D injection, diastolic arrest was induced by i.v.…”

Section: Cardiac Hypertrophymentioning

confidence: 99%

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Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy

et al. 1986

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In order to investigate the consequences of different types of cardiac hypertrophy on myocardial capillary and fibrosis density in rats we describe here, in the same hearts, the pattern of capillary bed density visualized by fluorescein isothiocyanate dextran (FITC-dextran) and the pattern of fibrosis density as determined by automated image analysis. Pressure overload was induced by clipping one renal artery in rats (one-clip, two-kidney Goldblatt hypertension, RHV). Volume overload was induced by creation of an arteriovenous shunt between the abdominal aorta and the vena cava (aorto-caval fistula model ACF). Animals were sacrified at 1, 3 and 6 months following surgical procedure. Immediately prior to sacrifice, FITC-dextran (MW 150,000) was injected with the animal under ether anesthesia. Five minutes later, cardiac diastolic arrest was induced by the i.v. injection of potassium chloride. The heart was rapidly excised and placed in a formaldehyde solution. The degree of cardiac hypertrophy was calculated after measurement of cardiac weight. Left ventricular wall thickness and cavity area were measured by microscopic methods. Capillary density and geometry were determined by morphometric methods, under ultraviolet light microscopy, using a graphic tablet connected to a microcomputer. The degree of myocardial fibrosis, visualized with Sirius Red, was estimated by the use of automated image analysis using light microscopy. In renovascular hypertension, cardiac hypertrophy was maximum at one month (36%) and persisted through the six months of the study. This increase in cardiac mass was concentric, due to a significant increase in ventricular wall thickness and was associated with a marked increase in fibrosis and a significant decrease in subendocardial capillary density. These effects existed already one month and did not change with time. In the aorto-caval fistula model, cardiac hypertrophy was also maximum at one month (+56%), but this eccentric increase in cardiac mass was associated with no significant change in left ventricular wall thickness, but rather with a significant increase in the surface area of the left ventricular cavity. This volume overload hypertrophy was associated with a decrease in subendocardial capillary density which was negatively correlated with time. In contrast to concentric hypertrophy there was no increase in the fibrosis density compared to the sham-operated groups. Despite the identical degrees of hypertrophy, pressure and volume cardiac overload differed in a significant manner in both left ventricular wall thickness and cavity surface area.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…In reperfused myocardium, experimental findings consistent with these observations include a reduction in FCD26 and an increase in arteriovenous shunting 27. Evidence of myocyte injury upon reperfusion following a relatively brief (20 mins) coronary occlusion was seen only in regions with poor capillary flow within heterogeneous microvascular flow patterns 26…”

Section: Introductionmentioning

confidence: 60%

<p>Reperfusion Microvascular Ischemia After Prolonged Coronary Occlusion: Implications And Treatment With Local Supersaturated Oxygen Delivery</p>

Spears¹

2019

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Following a prolonged coronary arterial occlusion, heterogeneously scattered, focal regions of low erythrocyte flow are commonly found throughout the reperfused myocardium. Experimental studies have also demonstrated the presence of widespread, focally patchy regions of microvascular ischemia during reperfusion (RMI). However, the potential contribution of RMI to tissue viability and function has received little attention in the absence of practical clinical methods for its detection. In this review, the anatomic/functional basis of RMI is summarized, along with the evidence for its presence in reperfused myocardium. Advances in microcirculation research related to obstructive responses of vascular endothelial cells and blood elements to the effects of hypoxia and low shear stress are discussed, and a potential cycle of intensification of RMI from such responses and progressive loss of functional capillary density is presented. In capillaries with impaired erythrocyte flow, compensatory increases in the delivery of oxygen, because of its low solubility in plasma, are effective only at high partial pressures. As discussed herein, attenuation of the cycle with oxygen at hyperbaric levels in plasma is, very likely, responsible for improved tissue level perfusion noted experimentally. Observed clinical benefits from intracoronary SuperSaturated oxygen (SSO2) delivery, including infarct size reduction, can be attributed to attenuation of RMI with improvement in microvascular blood flow.

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Capillary perfusion patterns in reperfused ischemic subendocardial myocardium: Experimental study using fluorescent dextran

Cited by 10 publications

References 22 publications

Dissecting the Effects of Ischemia and Reperfusion on the Coronary Microcirculation in a Rat Model of Acute Myocardial Infarction

Dissecting the Effects of Ischemia and Reperfusion on the Coronary Microcirculation in a Rat Model of Acute Myocardial Infarction

Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy

<p>Reperfusion Microvascular Ischemia After Prolonged Coronary Occlusion: Implications And Treatment With Local Supersaturated Oxygen Delivery</p>

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