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"Effects of food restriction on mechanical properties of the arterial system in adult and middle-aged rats".

T study by Chang and colleagues, '"Effects of Food Restriction on Mechanical Properties of the Arterial System in Adult and Middle-Aged Rats" in the October 1999 issue of the Journal (pp. B441-B447) addresses some major questions concerning cardiovascular adaptation to reduced food intake and body weight reduction in a rat model. Such studies are very important in light of the recent article by Calle and colleagues published in the New England Journal of Medicine (1) showing a clear association between excess weight and increased mortality in humans. In the article by Chang and colleagues, two age groups, 12 and 18 months, of Long-Evans male rats were studied. Food restriction on alternate days was started in the two groups at ages 6 months and 12 months and was continued for 6 months before collecting hemodynamic data. The 12month-old rats were referred to as adult rats and 18-month-old rats as middle-aged rats. An asymmetric exponentially tapered T-tube model of the cardiovascular system, popularized by Michael O'Rourke (2) and previously used by Chang and colleagues (3,4), was used to analyze pressure and flow waves measured in the ascending aorta of anesthetized open-chest animals. Aortic characteristic impedance, arterial load compliance, and wave transit time were obtained and used to investigate changes in arterial mechanical properties produced by food restriction. Other left ventricular external load components such as pressure wave reflection factor and peripheral vascular resistance were also determined. To our knowledge this is the first study to address specially the effects (if any) of food restriction on ascending aortic pressure-flow relations and mechanical properties of the rat arterial system. Several previous studies have reported decreases in arterial blood pressure in normotensive (5), coarctation hypertensive (6), and spontaneously hypertensive (7,8) rats when food intake was restricted and concluded that the hypotensive affect was due to reduction in sympathetic tone and plasma norepinephrine concentration. Lloyd (9) found that food restriction without malnutrition increased the life span of normotensive and spontaneously hypertensive rats. Histological examination of the heart, kidneys, and brain showed that freely fed hypertensive rats died of end-organ damage associated with hypertension whereas deaths of food-restricted hypertensive rats were due to changes associated with old age. These beneficial affects (reduced end-organ damage) may be due to the observed decrease in systolic and pulse blood pressure observed in food-restriction studies (5-8). Indeed, several prospective epidemiology studies in humans have shown a direct association between systolic and pulse blood pressures and coronary heart disease (10,11), myocardial infarction (12), stroke (13) and cardiovascular mortality (14). Such studies have directed attention toward arterial stiffness as an independent cardiovascular risk factor (15). Arterial stiffening and increased pulse wave velocity cause early return of reflected pressure waves from peripheral reflecting sites, which in turn augments systolic and pulse blood pressure, elevates left ventricular afterload, and increases left ventricular mass (16). Recent studies have suggested that logical treatment for lowering arterial blood pressure should focus not only on arteriolar caliber and peripheral resistance, but also on arterial stiffness and pulse wave reflections (16). These three properties—arterial stiffness, wave reflections, and peripheral resistance—of the rat arterial system constitute total left ventricular afterload and can be obtained from the aortic input impedance spectrum (16). Studies using vasodilator drugs to lower blood pressure have drawn attention to their separate effects on arteries and arterioles (15). Arteriolar vasodilators primarily increase arteriolar caliber, and thereby decrease peripheral resistance and mean arterial pressure, whereas arterial vasodilators primarily relax smooth muscle cells in muscular arteries and thereby decrease wave reflection amplitude and pulse blood pressure (16). Changes in arterial wall properties can alter systolic and pulse pressure in the proximal aorta by two mechanisms depending on whether the change occurs in the central elastic arteries or the peripheral muscular arteries. The early part of the pressure wave with amplitude (PrPd; P: indicates the beginning of the reflected pressure wave and Pd is diastolic pressure) is generated by the left ventricular ejection wave through the "waterhammer" principle, that is, (Pj-Pd) = pVc(l, where p is blood density, V is linear velocity, and c() is pulse wave velocity. For a given flow wave, this forward traveling pressure wave is dependent upon central artery elastance (or characteristic impedance) and is not influenced by wave reflections. The later part of the measured pressure wave with amplitude (Ps-Pj; Ps is systolic pressure) is generated by the reflected wave arriving during systole and adding to the forward pressure wave by the "superposition" principle, that is, pulse pressure = (Pj-Pd) + (PS-P,) = (Ps-Pd). This augmentation of the measured pressure wave is dependent upon the elastic properties of the entire arterial tree, the velocity of the reflected wave, and the distance to the major reflecting site. Arterial vasodilator drugs have their major action on this later part of the pressure wave with less effect on the early part (16). Inhibition of sympathetic tone and decreased