Biomechanics and vasoreactivity of female intramural coronaries in angiotensin II induced hypertension

Hypertension causes small vessel remodeling, vasomotor alterations. We investigated diameter, tone and mechanics of intramural small coronaries of female rats that received chronic angiotensin treatment to induce hypertension.Angiotensin II infusion (AII, 100 ng/bwkg/min, sc.) was used to establish hypertension in 10 female rats. Other 10 rats served as controls. Following 4 weeks of treatment, side branches of the left anterior descendant coronary (diameter∼200 μm) were isolated, cannulated and pressure-diameter curves were registered between 2–90 mmHg. Changes in vessel diameter were measured in Krebs solution, in the presence of thromboxane A2 receptor agonist (U46619, 10-6M), bradykinin (BK, 10-6M), and finally at complete relaxation (in Ca2+-free solution).Chronic AII treatment raised the mean arterial pressure (130±5 mmHg vs. 96±2 mmHg, average ±SEM) significantly. Wall thickness of the AII group was significantly greater (40.2±4.2 μm vs. 31.4±2.7 μm at 50 mmHg in Ca2+-free solution), but cross-section of the vessel wall did not differ. Tangentional wall stress and elastic modulus decreased significantly in hypertensive animals. Constrictions in the presence of U46619 were greater in the AII group (24.4± 5.6% vs. 14.5±3.3% at 50 mmHg).In hypertension, intramural small coronaries showed inward eutrophic remodeling, as a morphological adaptation following AII treatment enhanced thromboxane A2 — induced tone

Aortic root dynamics and surgery: from craft to science

Since the fifteenth century beginning with Leonardo da Vinci's studies, the precise structure and functional dynamics of the aortic root throughout the cardiac cycle continues to elude investigators. The last five decades of experimental work have contributed substantially to our current understanding of aortic root dynamics. In this article, we review and summarize the relevant structural analyses, using radiopaque markers and sonomicrometric crystals, concerning aortic root three-dimensional deformations and describe aortic root dynamics in detail throughout the cardiac cycle. We then compare data between different studies and discuss the mechanisms responsible for the modes of aortic root deformation, including the haemodynamics, anatomical and temporal determinants of those deformations. These modes of aortic root deformation are closely coupled to maximize ejection, optimize transvalvular ejection haemodynamics and—perhaps most importantly—reduce stress on the aortic valve cusps by optimal diastolic load sharing and minimizing transvalvular turbulence throughout the cardiac cycle. This more comprehensive understanding of aortic root mechanics and physiology will contribute to improved medical and surgical treatment methods, enhanced therapeutic decision making and better post-intervention care of patients. With a better understanding of aortic root physiology, future research on aortic valve repair and replacement should take into account the integrated structural and functional asymmetry of aortic root dynamics to minimize stress on the aortic cusps in order to prevent premature structural valve deterioration