Histological changes in a model of chronic heart failure induced by multiple sequential coronary microembolization in sheep

Schmitto, J; Ortmann, Philipp; Vorkamp, Tobias; Heidrich, Felix M.; Popov, AF; Danner, B; Tirilomis, Theodor; Grossmann, M; Seipelt, R; Schöndube, FA

doi:10.1055/s-0029-1191338

Cited by 11 publications

(19 citation statements)

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“…Schmitto et al used a similar approach in sheep to produce small sequential myocardial lesions, which cumulatively are sufficient to produce CHF but most likely would have been lethal if established in a single intervention [19,20]. An important feature of Schmitto et al's model is the lack of recovery of LV-function after coronary embolizations are completed [25].…”

Section: Coronary Microembolization (Cme)mentioning

confidence: 99%

“…The disadvantages, on the other hand, include fatal arrhythmias despite prophylactic administration of anti-arrhythmic agents, the development of postoperative adhesions and scar tissue, which make subsequent operations more dangerous and difficult, and the need for personnel capable of surgical procedures. In summary, coronary ligation creates a robust, replicable model of ischemic heart failure in several species [31,35] including dogs [32], sheep [19,20,30,33,34], and pigs [36].…”

Section: Coronary Ligationmentioning

confidence: 99%

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Large Animal Models of Chronic Heart Failure (CHF)

Schmitto

Mokashi

Lee

et al. 2011

Journal of Surgical Research

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Section: Coronary Microembolization (Cme)mentioning

confidence: 99%

Section: Coronary Ligationmentioning

confidence: 99%

Large Animal Models of Chronic Heart Failure (CHF)

Schmitto

Mokashi

Lee

et al. 2011

Journal of Surgical Research

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“…After 1 minute, the hearts were removed, atriums and right ventricle were separated from left ventricle, left ventricle was placed in a cutting apparatus (JP40, Shiyuan Science Equipment Co., Shanghai), and sectioned into 10 or 11 cross-sectional slices (each 1 mm in thickness) along long axis. Uneven slices (1,3,5,7,9,11) were irradiated with UV light (365 nm wavelength) to determine the no-flow zone (NF, area not perfused by Thioflavin S). No-flow zone was traced and analyzed using NIH image software.…”

Section: Evaluation the Areas Of No-flow Zonementioning

confidence: 99%

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

Bai

et al. 2010

The American Journal of Pathology

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To establish a model of coronary thrombotic microembolism in rats, either automicrothrombotic particulates (CM group) or saline control (SHAM group) was injected into temporarily clamped aortas of male Sprague-Dawley rats. After automicrothrombotic particulate injection, serum c-troponin I and von Willebrand factor levels, the no-flow area as evaluated by Thioflavin S, myocardial leukocyte infiltration levels, myocardial expressions of tumor necrosis factor ␣ and interleukin-6, the percentage of arterioles obstructed by thrombosis, and myocardial fibrosis were all significantly increased whereas cardiac function as evaluated by echocardiography and hemodynamic measurements were significantly reduced compared with the sham group. Thus, aortic automicrothrombotic particulate injection could induce coronary microembolism in rats, and this model could be of value in improving the understanding of pathophysiology of coronary microembolism. Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndrome and during coronary interventions.1 It does not always result in complete thrombotic occlusion of the epicardial coronary artery with subsequent impending myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation, which has recently been identified as a potential cause of no-reflow phenomenon, myocardium ischemia, and myocardial infarctlet. Atherosclerotic embolization in the microvasculature is associated with adverse prognosis. [1][2][3][4] Research results derived from suitable experimental models of coronary microembolism would help clinicians to understand the underlying pathological mechanisms and to develop effective therapies of coronary microembolism induced by atherosclerotic embolization in the microvasculature.5 Until now, plastic microspheres ranging from 20 to 900 m in diameter were injected into the coronary microcirculation to establish the coronary microembolism models in dog, swine and sheep.6 -11 Experimental models were also made by injecting adenosine-diphosphate or catecholamine to induce platelet aggregation in coronary microcirculation in pigs.12-13 However, injecting microspheres with unique sizing would only occlude respective vessels with comparable sizes, while thrombotic debris in patients might vary greatly in sizing and affect vessels with different diameters. Models using adenosine diphosphate or catecholamine could mimic the platelet aggregation process during coronary microthrombosis but could not reflect the influences of various embolism components of atherosclerotic plaques. Therefore, established coronary microembolism models could only partly mimic the in vivo situation of coronary microthrombosis. In the present study, we showed that coronary microembolism could be induced by intraaortic injection of automicrothrombotic particulates varying in sizing in rats. Increased myocardial inflammatory cells infiltration and fibrosis as well as reduced cardiac function w...

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“…This produced left ventricular-dysfunction, but the mortality was high, however. To create a stable and reproducible animal of chronic heart failure, Schmitto et al 9,10 were the first to describe a novel chronic heart failure model induced by multiple, repetitive, and sequential coronary microembolization in sheep.…”

Section: To the Editormentioning

confidence: 99%

Letter by Schmitto et al Regarding Article “Large Animal Models of Heart Failure: A Critical Link in the Translation of Basic Science to Clinical Practice”

Schmitto

Mokashi

Chen

2010

Circ: Heart Failure

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We read with great interest the review by Dixon and Spinale 1 on "Large animal models of heart failure" and congratulate the authors on a well written and timely article. In addition to those cited in the article, there are several more heart failure animal models in other species that are worth mentioning, including those in calves, goats, or even baboons. [2][3][4] "Coronary microembolizations" is a topic that deserves further elaboration. In addition to the description by Sabbah et al, 5 the feasibility of performing repetitive coronary microembolizations in dogs, many groups have successfully used various approaches to microembolizations, but with different embolic materials. For example, Franciosa et al 6 injected glass beads into the left circumflex coronary artery of dogs to produce chronic left ventriculardysfunction. Weber et al 7 slowly injected latex microspheres into the left main coronary artery in calves. Furthermore, Smiseth et al 8 used a single intracoronary injection of microspheres in dogs to produce acute severe depression of left ventricular-function. With these studies, a single injection of microspheres was used. This produced left ventricular-dysfunction, but the mortality was high, however. To create a stable and reproducible animal of chronic heart failure, Schmitto et al 9,10 were the first to describe a novel chronic heart failure model induced by multiple, repetitive, and sequential coronary microembolization in sheep.We wholeheartedly agree with the authors that "undoubtedly, large animal models of heart failure will continue to play a crucial role . . . in the development and refinement of heart failure therapies." DisclosureNone. Jan

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Histological changes in a model of chronic heart failure induced by multiple sequential coronary microembolization in sheep

Cited by 11 publications

References 0 publications

Large Animal Models of Chronic Heart Failure (CHF)

Large Animal Models of Chronic Heart Failure (CHF)

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

Letter by Schmitto et al Regarding Article “Large Animal Models of Heart Failure: A Critical Link in the Translation of Basic Science to Clinical Practice”

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