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Endothelial membrane (EnM) at the coronary vessels is a key element in the pathway involved in the coronary ischemia/reperfusion injury (cIRI). We demonstrated the presence of the mannose receptor (MR) in the coronary EnM. MR mediates a positive (+) inotropic and dromotropic effects in isolated guinea pig hearts. We used mannose polymer (Man‐pol) that has + charge, this polymer was synthesized with a high MW dextran, divinyl sulfone (DVS) as linker for mannose and ethylene diamine to inactivate unbound DVS residues. EnM glycocalyx (Gcx) has been involved in the pathway of the IRI, and its homeostasis is required to down modulate the cIRI. + Charged macromolecules damage the Gcx and exacerbates IRI. Therefore, we evaluated the effect of the +Man‐pol on in vivo cIRI models. We determinate myocardial viability on rat hearts 4 hrs after the cIRI with tetrazolium, and reported as ratio between infarcted area (IA) and total area (TA). +Man‐pol treated hearts 15 min prior reperfusion, significantly increases the damage induced by the cIRI when compared with vehicle treated hearts, IA/TA was 1.7 fold. Detrimental effect of the + charge on the Man‐pol suggests the role of the Gcx on the response against the cIRI. On the other hand, uncharged Man‐pol treated hearts decreased IA/TA by half when compared with vehicle treated hearts; this effect could be induced by the beneficial interaction between Gcx and MR. CONACyT # 46187‐A.