McAllister R M, Laughlin M H, Musch T I
Department of Veterinary Biomedical Sciences, University of Missouri, Columbia 65211.
Am J Physiol. 1993 Mar;264(3 Pt 2):H686-91. doi: 10.1152/ajpheart.1993.264.3.H686.
The purpose of this study was to determine the effects of chronic heart failure (HF) on the vascular transport capacity of rat skeletal muscle. A large myocardial infarction (MI) was surgically produced in rats by ligating the left main coronary artery (n = 10). Sham operations were performed in control animals (Sham, n = 4). The vascular transport capacity of each animal's hindquarters was determined 8-9 mo post-MI to ensure that each rat was in a chronic state of left ventricular (LV) dysfunction and HF. With the use of an isolated, maximally vasodilated hindquarters preparation, we found that perfusion pressures, capillary pressures, capillary filtration coefficients, and precapillary vascular resistances were similar for the two groups under isogravimetric conditions. In contrast, postcapillary resistance was elevated (Sham, 0.9 +/- 0.2; MI, 1.5 +/- 0.2 mmHg.ml-1 x min x 100 g; P = 0.03), and flow to the hindquarters was reduced for rats in chronic HF compared with controls (Sham, 16.1 +/- 2.3; MI, 12.1 +/- 0.9 ml.min-1 x 100 g-1; P = 0.07). Vascular flow capacity (VFC) for the hindquarters was similar for control rats and rats with chronic HF across a wide range of perfusion pressures (20-60 mmHg). However, regional flow capacities were reduced in soleus and red gastrocnemius but not in white gastrocnemius muscles of rats in chronic HF compared with controls. These results suggest that the VFC of muscle comprised primarily of high oxidative fibers is selectively reduced in rats with chronic HF.(ABSTRACT TRUNCATED AT 250 WORDS)
