Yi-Qi-Fu-Mai (YQFM) is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation (EYQFM), the EYQFM (1.4, 2.8, and 5.5 g·kg(-1)·d(-1)) was assessed for its heart-protective effect in a chronic intermittent hypoxia (CIH) animal model (oxygen pressure 7%-8%, 20 min per day) for 28 days of treatment. Betaloc (0.151 6 g·kg(-1)·d(-1)) was used as a positive control. The histopathological analyses of heart in CIH mice were conducted. Several cardiac state parameters, such as left ventricular ejection fractions (EF), stroke volume (SV), expression of creatine kinase (CK), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. The results showed that treatment with EYQFM markedly reversed swelling of the endothelial cells and vacuolization in the heart when compared with the model group. Further study demonstrated that EYQFM significantly improved ventricular myocardial contractility by increasing EF and SV. In addition, EYQFM inhibited the activity of CK, LDH, decreased the level of MDA and improved SOD activity. The results demonstrated that EYQFM significantly improved the tolerability of myocardium to hypoxia and ameliorated the cardiac damage in the CIH model.
Animals ; Creatine Kinase ; metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Heart ; drug effects ; Heart Injuries ; enzymology ; etiology ; metabolism ; prevention & control ; Humans ; Hypoxia ; complications ; L-Lactate Dehydrogenase ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mice ; Superoxide Dismutase ; metabolism

PURPOSE: It is unknown whether cilostazol pretreatment reduces postprocedural myonecrosis (PPMN). Cilostazol pretreatment reduces PPMN after percutaneous coronary intervention (PCI). MATERIALS AND METHODS: A total of 120 patients with stable angina scheduled for elective PCI were randomly assigned to a 7-day pretreatment with Cilostazol (200 mg/day) or to a control group. Creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) levels were measured at baseline and at 6 and 24 hours after PCI. The primary end-point was the occurrence of PPMN, defined as any CK-MB elevation above the upper normal limit (UNL). Aspirin and clopidogrel were co-administered for 7 days before PCI, and resistance to these agents was then assayed using the VerifyNow System. RESULTS: There was no difference in baseline characteristics between the final analyzable cilostazol (n=54) and the control group (n=56). Despite a significantly greater % inhibition of clopidogrel in the cilostazol group (39+/-23% versus 25+/-22%, p=0.003), the incidence of PPMN was similar between the cilostazol group (24%) and the control group (25%, p=1.000). The rate of CK-MB elevation at > or =3 times UNL was also similar between the two groups (6% versus 5%, p=0.583). The incidence of cTnI increase over the UNL or to 3 times the UNL was not different between the two groups. There was no significant difference in terms of the rate of adverse events during follow-up, although the cilostazol group showed a tendency to have a slightly higher incidence of entry site hematoma. CONCLUSION: This trial demonstrated that adjunctive cilostazol pretreatment might not significantly reduce PPMN after elective PCI in patients with stable angina.
Aged ; Angina, Stable/drug therapy/enzymology/therapy ; Angioplasty, Balloon, Coronary/*adverse effects ; Creatine Kinase, MB Form/blood ; Female ; Heart Injuries/etiology/prevention & control ; Humans ; Male ; Middle Aged ; Myocardium/pathology ; Necrosis ; Phosphodiesterase 3 Inhibitors/*administration & dosage ; Prospective Studies ; Tetrazoles/*administration & dosage