Development of the cardioprotective drugs class based on pathophysiology of myocardial infarction: A comprehensive review.

The cardiovascular system is mainly responsible for the transport of substances necessary to cellular metabolism. However, for the good performance of this function, there is need for adequate control of blood pressure levels of tissue perfusion and systemic arterial. Acute myocardial infarction is one of the complications of the cardiovascular system, that most affects the population around the world. This condition can be defined as a disease generated by an imbalance of oxygen concentrations used in cardiovascular metabolism, this change usually occurs because coronary occlusion, which prevents myocardial blood flow. The diagnosis is based on the set of clinical and laboratory investigations, which are in the release of cardiac enzyme biomarkers, cardiovascular and hemodynamic changes and cardiac accommodations. The treatment consists in the use of concomitant cardiovascular drugs, such as: antihypertensive, antiplatelet and hypolipidemic. Despite improvements in clinical and pharmacological management, acute myocardial infarction remains the leading cause of death worldwide. This finding encourages the scientific research of new drugs for the treatment of myocardial infarction or supporting therapies aimed at reducing the levels of deaths and comorbities generated by cardiovascular diseases.

Alpha-terpineol prevents myocardial damage against isoproterenol-MI induced in Wistar-Kyoto rats: new possible to promote cardiovascular integrity.

Alpha-terpineol (TPN) is one of the major components of the resin obtained from Protium heptaphyllum. This plant has been utilized as medicine by Brazilian indigenous tribes to treat cardiovascular diseases. Scientific reports have shown that the TPN possesses vasorelaxant and antihypertensive effects. This study was conducted to assess the cardioprotective action of TPN against isoproterenol (ISO)-induced cardiotoxicity. Wistar rats were randomly divided into six groups. Rats were orally administered with TPN (25, 50, and 75 mg/kg, respectively) for 15 days, and ISO was administered (85 mg/kg, subcutaneously) on the 14th and 15th days. At the end of the experiment, the hemodynamic, baroreflex test, ECG, biochemical, histological, and morphometric changes were monitored from control and experimental groups, i.e., on the 15th day. ISO-induced myocardial infarcted rats showed an increase in mortality rates, cardiac marker enzymes, tachycardia, hypertrophy, myocardium necrosis, edema, hemorrhagic areas, infiltration of inflammatory cells like lymphocytes, and increased myocardial infarct size. However, pretreatment with TPN significantly inhibited these effects of ISO. The histopathological findings obtained for the myocardium further confirmed the biochemical results. Thus, the present study provides evidence for the efficacy of TPN against ISO-induced myocardial infarction in rats.

Cardioprotective effects induced by hydroalcoholic extract of leaves of Alpinia zerumbet on myocardial infarction in rats.

ETHNOPHARMACOLOGY RELEVANCE: The leaves of Alpinia zerumbet is used in folk medicine in Brazil to treat hypertension. However, the cardioprotective effect of this plant has not been studied yet. AIM OF THIS STUDY: To evaluate the cardioprotective effects of the hydroalcoholic extract of the leaves of Alpinia zerumbet (AZE) against isoproterenol (ISO)-induced myocardial infarction in rats. MATERIAL AND METHODS: Rats were pretreated orally with AZE (300 mg/kg) for 30 days prior to ISO-induced myocardial infarction. The rats were sacrificed and hearts were collected and homogenized for biochemical analysis. At the end of the experiment, cardiac marker enzyme levels, histological and morphometric parameters, and hemodynamic measurements were assessed. Phytochemical compounds were verified by gas chromatography-mass spectrometry (GC-MS). RESULTS: Rats administered with ISO showed a significant increase in cardiac marker enzymes, i.e., in creatine kinase-NAC (CK-NAC) and CK-MB. Triphenyltetrazolium chloride (TTC) staining exhibited an increase in infarct areas. In the animals treated with ISO induced a significant increase in heart rate. Pretreatment with AZE significantly inhibited these effects of ISO. Moreover, biochemical findings were supported by histopathological observations. The GC-MS analyses of AZE identified volatile oils, kavalactones, and phytosterols. CONCLUSIONS: Haemodynamic, biochemical alteration and histopathological results suggest a cardioprotective protective effect of oral administration of AZE in isoproterenol induced cardiotoxicity.

Antihypertensive and vasorelaxant effects of ethanol extract of stem barks from Zanthoxylum rhoifolium Lam. in rats.

Administration of ethanol extract of stem bark from Z. rhoifolium (EEtOH-ZR) induced hypotension associated with a dual effect in heart rate in normotensive rats. This response was highlighted in spontaneously hypertensive rats (SHR). In rat superior mesenteric artery rings, the cumulative addition of EEtOH-ZR (0.1-750 microg/mL) on a phenylephrine-induced pre-contraction (10(-5) M) promoted a vasorelaxant effect by a concentration-dependent manner and independent of vascular endothelium. A similar effect was obtained on KCl-induced pre-contractions (80 mM). EEtOH-ZR attenuated contractions induced by cumulative addition of CaCl2 (10(-6)-3 x 10(-2) M) in depolarizing medium without Ca2+ only at 500 or 750 microg/mL. Likewise, on S-(-)-Bay K 8644-induced pre-contractions (10(-7) M), the EEtOH-ZR-induced vasorelaxant effect was attenuated. EEtOH-ZR (27, 81, 243 or 500 microg/mL) inhibited contractions induced by cumulative addition of phenylephrine (10(-9) - 10(-5) M) in endothelium-denuded preparations or by a single concentration (10(-5) M) in a Ca(2+)-free medium. The involvement of K+ channels was evaluated by tetraethylammonium (3 mM); the EEtOH-ZR-induced vasorelaxation was not attenuated. Thus, calcium influx blockade through voltage-operated calcium channels (CavL) and inhibition of calcium release from intracellular stores are probably underlying EEtOH-ZR-induced cardiovascular effects.