Summary
I. Myocardial hypertrophy, for instance in patients with hypertensive heart disease, is characterized by a reduction of coronary vascular reserve, even in the presence of normal coronary arteries. In hypertensive animals, on the microcirculatory level functional changes can be observed before the onset of any structural rarefications.
In 10 rats with renal hypertension and pressure-induced left ventricular hypertrophy (LVH), the microcirulation of the left ventricular myocardium was studied using in vivo fluorescence microscopy and morphometric analysis. Renal hypertension was provoked by clipping of the left renal artery. After 8 weeks, systolic blood pressure in LVH rats averaged 172 ± 8 mm Hg, compared to 91 ± 2 mmHg in 10 normotensive (NT) rats. In LVH rats, distances of plasma-perfused capillaries were significantly increased (NT = 17.7; LVH = 20 μm;p < 0.001). Volume density, surface density, and length density of capillaries in LVH rats were reduced by 20% compared to NT rats. Capillary red cell content as measured by the ratio of capillaries filled with red cells to those containing plasma alone (Q) in LVH animals exceeded that in NT rats (LVH: Q = 0.83 ± 0.04; NT Q = 0.77 ± 0.04;p < 0.025). During hypoxia (H, 5% 02) capillary red cell recruitment in LVH rats (Q: control c = 0.83; H = 0.95) was diminished by 33% as compared to NT rats (Q: c = 0.77; H = 0.95). Thus, in addition to the decreased capillary density, the reduction of capillary red cell recruitment may be responsible for chest pain in patients with LVH and normal coronary arteries.
2. In 11 rats, the microcirculation of the repeatedly ischemic (stunned) left ventricular myocardium (SM) was studied using in vivo fluorescence microscopy. Stunning was provoked by 6 subsequent 10 minute ligations of the left anterior descending coronary artery, each of them followed by a 20 min reperfusion period.
In the SM showing hypokinetic wall motion mean capillary blood flow velocity was markedly reduced (control c =1312; SM = 694 μm/sec;p < 0.001): myocardial blood flow (hydrogen clearance) in the SM dropped by 55%. In SM, leukocytes often appeared in slow-flow capillaries plugging capillary branches: the percentage of capillaries and postcapillary venules with adherent leukocytes was markedly increased (c = 3%; SM = 68%). In close link to leukocyte adherence, a rise of microvascular permeability was documented by extravascular clouds of fluorescent dextran. The ratio of capillaries filled with red cells to those containing plasma alone was diminished in SM (c = 0.77; SM = 0.65;p < 0.001). In the SM there are microcirculatory disturbances which occur before the onset of detectable structural alterations of both the microvasculature and the myocyte.
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Tillmanns, H., Neumann, F.J., Parekh, N. et al. Microcirculation in the hypertrophic and ischemic heart. Eur J Clin Pharmacol 39, S9–S12 (1990). https://doi.org/10.1007/BF01409200
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DOI: https://doi.org/10.1007/BF01409200