Arterial expansive remodeling induced by high flow rates

The effects of chronic increase in aortic blood flow on arterial wall remodeling were investigated in vivo with the use of an aortocaval fistula (ACF) model in rats. Phasic hemodynamics and aortic wall structure upstream and downstream in 30 male Wistar rats with ACF and 30 sham-operated rats were compared immediately and 2 mo after the ACF was opened in anesthetized rats. Opening the ACF upstream acutely decreased aortic pressure (-30%, P < 0.001) and increased aortic blood velocity (x12, P < 0.001), blood flow (x9, P < 0.001), wall shear stress (x10, P < 0.001) and guanosine 3',5'-cyclic monophosphate (cGMP) wall content (+50%, P < 0.01). After 2 mo, aortic pressure decreased (-22%, P < 0.001) and aortic blood velocity, diameter, and blood flow increased (+114%, P < 0.001; +60%, P < 0.001; and +250%, P < 0.001; respectively) compared with the control group. Aortic wall shear stress and cGMP wall content dropped over time and tended to recover control values; aortic wall tensile stress was higher than in the control group (P < 0.05). Medial cross-sectional area and elastin and collagen contents increased (+38%, P < 0.01; +50%, P < 0.01; and +30%, P < 0.05, respectively) and were associated with smooth muscle cell hypertrophy) (+23%, P < 0.05), despite a decrease in arterial wall thickness (-13%, P < 0.01). Opening the ACF downstream acutely decreased aortic pressure (-30%, P < 0.001) without any change in aortic blood velocity, diameter, blood flow, shear stress, and cGMP wall content. After 2 mo, pressure, blood velocity, shear stress, and cGMP wall content decreased (-22%, P < 0.001; -31%, P < 0.01; -46%, P < 0.02; and -50%, P < 0.05; respectively) and diameter and blood flow were unchanged; smooth muscle cell hypertrophy and hypoplasia were the only observed changes in the aortic wall structure. These results suggest that both shear and tensile stresses are involved in the aortic wall remodeling. Increase in shear stress likely induces expansive remodeling in relation to flow-dependent vasodilation, whereas increase in tensile stress is responsible for medial hypertrophy and fibrosis.

Noninvasive measurement of ascending aortic blood velocity in mice

Mice are useful models in numerous research protocols, but monitoring cardiovascular parameters in small animals is difficult. Therefore we evaluated the use of 20-MHz pulsed Doppler ultrasound to measure ascending aortic blood velocity in intact anesthetized mice. Using a 0.5-mm-diameter 20-MHz transducer applied to the right sternal border, we recorded audio Doppler signals from the ascending aorta of 31 mice [24.4 +/- 1.5 (SD) g body wt]. The signals were played back at speed into a fast Fourier transform analyzer from which we measured heart rate (453 +/- 96 beats/min), ejection time (38 +/- 3%), peak velocity (90 +/- 11 cm/s), mean velocity (23 +/- 4 cm/s), rise time (7.3 +/- 2 ms), stroke distance (29 +/- 7 mm), and acceleration (163 +/- 63 m/s2) from the spectral envelopes. We determined aortic diameter (1.2 +/- 0.2 mm) and Doppler angle (0–20 degrees) in six mice by molding the aortic root and major systemic vessels with casting resin infused at 100 mmHg pressure. For an aortic diameter of 1.2 mm, cardiac output was estimated to be 14.8 ml/min and stroke volume to be 33 microliters. To verify the origin of the signals and to test responsiveness to known stimuli, we measured velocity signals from the aorta and other nearby vessels and varied heart rate and aortic velocity by warming or by infusion of isoproterenol in three open-chest animals. For the noninvasive applications, acoustic coupling was adequate through the moistened fur, and aortic velocity signals were obtained in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Preliminary observations on blood flow in the coronary arteries of two school sharks (Galeorhinus australis)

Coronary arterial blood flow and pressure, intraventricular blood pressure, and ventral aortic blood velocity were measured in two anaesthetized school sharks (Galeorhinus australis) in order to examine the phasic relationships between these flows and pressures. Maximum instantaneous flow recorded in the ventral coronary artery was 0.37 mL∙min−1∙kg−1 body mass (estimated 0.63 mL∙min−1∙g−1 ventricular mass). The average mean coronary blood flow was estimated as 0.28 mL∙min−1∙g−1 ventricular mass during periods of high coronary blood flow. On average, 86% of coronary flow occurred during diastole. Coronary arterial flow began during the last quarter of ventricular systole. Coronary blood flow peaked when intraventricular pressure fell to just below zero immediately after ventricular systole. Coronary blood flow fell slightly as diastole continued and reflected the small fall in coronary arterial pressure. Coronary flow reversed briefly during isovolumic ventricular contraction. Increases in the proportion of the cardiac cycle occupied by ventricular diastole, which occur during hypoxic bradycardia, have the potential to more than double coronary blood flow provided coronary arterial pressure is maintained.

Heart rate perturbation in the stage 17-27 chick embryo: effect on stroke volume and aortic flow

Heart rate (HR), stroke volume (SV), and aortic flow increase linearly between developmental stages 17 and 27, as the embryonic chick heart progresses from a bent tube to a rudimentary four-chambered structure and cardiac mass increases fourfold. We hypothesized that HR perturbation, expressed as percent of intrinsic HR (%HR), would have a developmentally dependent effect on flow and SV. HR was transiently perturbed to 40–250% of intrinsic rate with a 1-mm cooled or heated steel probe applied to the sinus venosus of 81 embryos. Aortic blood velocity, cross-sectional area, and HR were used to calculate flow and SV. At each stage, flow was maximal at intrinsic HR. The %HR vs. SV relationship was linear, inverse, and developmentally dependent. In spite of a tremendous change in ventricular shape, mass, and volume, HR control during development of the preinnervated heart maximizes blood flow to the developing embryo.