MYOCARDIAL CAPILLARY DIFFUSION CAPACITY IN RAT HEARTS WITH CARDIAC-HYPERTROPHY DUE TO PRESSURE AND VOLUME OVERLOAD

Citation
H. Wahlander et al., MYOCARDIAL CAPILLARY DIFFUSION CAPACITY IN RAT HEARTS WITH CARDIAC-HYPERTROPHY DUE TO PRESSURE AND VOLUME OVERLOAD, The American journal of physiology, 265(1), 1993, pp. 80000061-80000068
Citations number
45
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
265
Issue
1
Year of publication
1993
Part
2
Pages
80000061 - 80000068
Database
ISI
SICI code
0002-9513(1993)265:1<80000061:MCDCIR>2.0.ZU;2-P
Abstract
The functional adaptation of the myocardial capillary bed in response to cardiac hypertrophy was studied in one volume overload (aortocaval fistula, ACF) and in one pressure overload model [left renal arterial stenosis, two-kidney, one-clip (2K,1C)]. Furthermore, a group where re nal hypertention was reversed 1 wk before experimentation (UC-2K,1C) a nd a sham-operated (Sham) group were studied. Functional estimations o f myocardial capillary diffusion capacity in terms of permeability sur face area products (PS) per 100 g of myocardium were obtained by the s ingle-injection indicator dilution technique in a Langendorff preparat ion. After 4 wk, ACF hearts, with 72% hypertrophy and normal minimal c oronary vascular resistance (CVR), displayed an unchanged diffusion ca pacity, i.e., PS for Cr-EDTA and vitamin B-12. This indicates a struct ural outgrowth of the coronary vascular bed to match the increased dem and of the tissue. 2K,1C hearts with marked elevations of minimal coro nary vascular resistance and left ventricular hypertrophy (65%) showed higher PS values than Sham, implying that diffusion capacity was enha nced despite structural coronary vascular changes. These changes were completely reversed in UC-2K,1C. Thus the present data imply that myoc ardial capillary diffusion capacity was well maintained in volume over loaded cardiac hypertrophy and in contrast with earlier morphometric e stimations, even enhanced in pressure overload hypertrophy.