Effects of hawthorn on the progression of heart failure in a rat model of aortic constriction.
OBJECTIVE
To determine the effects of hawthorn (Crataegus oxycantha) on left ventricular remodeling and function in pressure overload-induced heart failure in an animal model.


METHODS
Randomized, parallel, dose-ranging animal study.


METHODS
University research facility.


METHODS
Seventy-four male Sprague-Dawley rats; 44 were included in the final analysis.


METHODS
Rats underwent a sham operation or aortic constriction. Rats subjected to the sham operation were treated with vehicle (10% agar-agar), and those subjected to aortic constriction were treated with vehicle or hawthorn (C. oxycantha special extract WS 1442) 1.3, 13, or 130 mg/kg for 5 months.


RESULTS
Rats and their hearts were weighed, and echocardiographic measurements were performed at baseline and at 2, 3, 4, and 5 months after aortic constriction. Protein expression for markers of fibrosis and for atrial natriuretic factor was also measured. Aortic constriction increased the left ventricular:body weight ratio by 53% in vehicle-treated rats; Hawthorn treatment did not significantly affect the aortic constriction-induced increase in this ratio. Left ventricular volumes and dimensions at systole and diastole significantly increased 5 months after aortic constriction compared with baseline in rats given vehicle (> 20% increase, p<0.05) but not in those given hawthorn 130 mg/kg (< 10% increase). After aortic constriction, the velocity of circumferential shortening significantly decreased in the vehicle group but not in the medium- or high-dose groups. In the aortic constriction-vehicle group, the induced increases in messenger RNA expression for atrial natriuretic factor (approximately 1000%) and fibronectin (approximately 80%) were significantly attenuated by high-dose hawthorn treatment by approximately 80% and 50%, respectively.


CONCLUSIONS
Hawthorn treatment exhibited modest beneficial effects on cardiac remodeling and function during long-term, pressure overload-induced heart failure in rats.
Hwang
Hyun Seok
HS
Division of Kinesiology, Laboratory of Molecular Kinesiology, University of Michigan, Ann Arbor, Michigan, USA.
Boluyt
Marvin O
MO
Converso
Kimber
K
Russell
Mark W
MW
Bleske
Barry E
BE
D000818:Animals; D001011:Aorta / Q000503:physiopathology; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D003251:Constriction, Pathologic / Q000150:complications; D027825:Crataegus / Q000737:chemistry*; D004195:Disease Models, Animal; D018450:Disease Progression; D004305:Dose-Response Relationship, Drug; D004452:Echocardiography; D005353:Fibronectins / Q000378:metabolism*; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy; D008297:Male; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D020257:Ventricular Remodeling / Q000187:drug effects
D015415:Biomarkers; D005353:Fibronectins; D010936:Plant Extracts; D012333:RNA, Messenger; D009320:Atrial Natriuretic Factor