Adipocyte blood flow in four distinct adipose tissue depots has been measured in conscious, unrestrained, male Sprague-Dawley rats by using the microsphere technique together with cellularity determinations. Blood flow was determined in young rats (90 days old, 387 g mean body wt), spontaneously obese rats (450 days old, 713 g mean body wt), and long-term calorically restricted rats (450 days old, 390 g mean body wt), therefore allowing the comparison of the relative effects of age and fat mass on adipose tissue blood flow. Results of these experiments indicate that while cardiac index remained constant, cardiac output increased in only the obese group, concomitant with increased body fat mass. Spontaneously obese rats exhibited increased adipose tissue depot weight, fat cell lipid, and fat cell size compared with young and restricted groups. Despite significant differences in cell volume, blood flow per cell was remarkably similar between young and obese rats. Long-term caloric restriction, however, was associated with decreased flow per cell. Interdepot comparisons of flow per unit surface area (mm2) or per unit volume (pl) indicate that mesenteric cells receive significantly more blood than cells of the other depots. Our results suggest that adipocyte blood flow is dependent in part on anatomic location, may be further influenced by age or dietary manipulation, and is not a limiting factor in the enlargement of adipocytes during the development of spontaneous obesity.

The effect of defined increments of weight loss on hemodynamics has been investigated in conscious, unrestrained, spontaneously obese rats. Obese rats were subjected to a calorically restricted diet and were used for experimentation on achieving a 10, 20, or 30% reduction in body weight. After monitoring resting blood pressure and heart rate, radioactive microspheres were infused for determination of blood flow distribution. Of 10 organs sample, only heart, liver, kidneys, and 2 adipose tissue depots exhibited significant decreases in weight associated with body weight reduction. Mean arterial blood pressure remained unchanged, while stroke volume, left ventricular work, and cardiac output decreased significantly. Blood flow decreased to kidneys, testes, and adipose tissue through a 30% reduction in body weight, but the fractional distribution of cardiac output decreased only to adipose tissue. Therefore the large decreases in renal and adipose tissue blood flow during weight reduction may contribute to the associated decrease in cardiac output. Of those vascular beds examined, however, both absolute and relative blood flow decreased only to adipose tissue, thus denoting the influence of fat mass on hemodynamics during obesity.

No abstract

To determine the biochemical and hemodynamic responses to aortic ligation, and to assess the survival rate after the induction of hypertension, 90 normotensive rats were subjected to surgical constriction of the abdominal aorta. Mortality, left ventricular hemodynamics, myocardial biochemical assays, and plasma renin assays were determined 1 week, 1 month, 3 months, or 1 year later. Mortality was greatest between 1 week and 3 months after aortic ligation, during which plasma renin activity was significantly elevated. The rate of left ventricular pressure rise, contractile index, and myocardial alpha-adrenoceptor number were increased at 1 month, but were comparatively depressed at 3 months after the operation, suggesting that the heart was in failure at this time. At 1 year after ligation, hemodynamic and biochemical parameters continued toward normalization. Our data suggest that, in this rodent model, cardiac pump failure occurs through a combination of time-dependent, pressure-induced mechanical adaptations and myocardial biochemical changes that involve both the renin-angiotensin and sympathetic nervous systems. The observed relationship between mortality, myocardial hemodynamics, and biochemical parameters may be used for additional basic research investigations concerning the early periods of cardiac failure.

Direct quantitation of blood flow with radioactive microspheres in conscious spontaneously obese rats indicated that the development of obesity was associated with an elevated cardiac output and stroke volume, a normotensive blood pressure, and a reduced total peripheral resistance when directly comparing obese rats with their lean counterparts. Obesity was also associated with increased blood flow and decreased regional vascular resistance in a variety of vascular beds, whereas cardiac index and total peripheral resistance per unit of body weight were similar between groups. When corrected for tissue weight, unique alterations in flow and resistance were observed in the adipose tissue. When expressed as resistance per organ, the greatest relative alterations in vascular resistance with the development of obesity also occurred in the adipose tissue. Furthermore, localized adipose tissue expansion through cellular hypertrophy was consistently associated with a different pattern of blood flow and vascular resistance than adipose tissue that expanded through both cellular hypertrophy and hyperplasia, implying an association between depot cellularity and its hemodynamic profile.