Relation of effective arterial elastance to arterial system properties

Effective arterial elastance (E(a)), defined as the ratio of left ventricular (LV) end-systolic pressure and stroke volume, lumps the steady and pulsatile components of the arterial load in a concise way. Combined with E(max), the slope of the LV end-systolic pressure-volume relation, E(a)/E(max) has been used to assess heart-arterial coupling. A mathematical heart-arterial interaction model was used to study the effects of changes in peripheral resistance (R; 0.6-1.8 mmHg x ml(-1) x s) and total arterial compliance (C; 0.5-2.0 ml/mmHg) covering the human pathophysiological range. E(a), E(a)/E(max,) LV stroke work, and hydraulic power were calculated for all conditions. Multiple-linear regression analysis revealed a linear relation between E(a), R/T (where T is cycle length), and 1/C: E(a) = -0.13 + 1.02R/T + 0.31/C, indicating that R/T contributes about three times more to E(a) than arterial stiffness (1/C). It is demonstrated that different pathophysiological combinations of R and C may lead to the same E(a) and E(a)/E(max) but can result in differences of 10% in stroke work and 50% in maximal power.     

Brain stem control of arterial pressure in chronic arterial baroreceptor-denervated rats

Interruption of the baroreceptor reflex by transection of afferent nerves (sinoaortic denervation; SAD) or lesions of nucleus tractus solitarius (NTS) elevates sympathetic nerve activity (SNA) and arterial pressure (AP). However, within 1 wk, mean AP returns to normal despite the absence of baroreflexes. In this study, we examine central mechanisms that control AP in chronic baroreceptor-denervated rats. In urethane-anesthetized rats (1.5 g/kg i.v.) after autonomic ganglionic blockade (5 mg/kg i.v. chlorisondamine), alpha1-adrenergic-mediated pressor responses (1-100 microg/kg i.v. phenylephrine) were not altered by chronic lesions of NTS, indicating vascular reactivity to sympathetic stimulation is normal. Transection of the spinal cord at T1 profoundly decreased AP and was not further reduced by chlorisondamine in control or denervated rats. Inhibition of the rostral ventrolateral medulla (RVLM) by microinjections of muscimol (100 pmol/side) decreased AP to levels not further reduced by chlorisondamine in control rats, rats with SAD, and rats with NTS lesions. Blockade of GABA(A) receptors in the RVLM (50 pmol/side bicuculline) increased AP similarly in control rats and denervated rats. In agreement, inhibition of the caudal ventrolateral medulla (CVLM) by microinjections of muscimol or blockade of glutamatergic inputs (2.7 nmol/side kynurenate) produced comparable increases in AP in control and denervated rats. These data suggest the RVLM continues to drive the SNA that regulates AP in the chronic absence of baroreceptor inputs. In addition, despite the absence of a tonic excitatory input from NTS, in chronic baroreceptor-denervated rats glutamatergic inputs drive the CVLM to tonically inhibit the RVLM. Baroreceptor-independent regulation of the ventrolateral medulla may underlie central mechanisms contributing to the long-term control of AP.     

The subscapular arterial tree as a source of microvascular arterial grafts

The subscapular arterial tree may be used as a source of microvascular grafts to replace damaged or diseased portions of arteries, particularly in the hand and forearm. By studying cadaver dissections, it is possible to estimate the number of branches that may be found at different arterial segment lengths from the origin of the subscapular artery. Fifty-five preserved cadaver subscapular arterial trees were dissected, and the branching patterns were documented. Three major arterial branching patterns of the subscapular artery were observed with one, two, and three major branches to the serratus anterior in 60 percent, 29 percent, and 9 percent of the cases, respectively. The authors determined the number of 1-mm-diameter, 1-cm-long branches arising from each of six 3-cm regions of the arterial tree measured from the origin of the subscapular artery to the end of the longest terminal branch. The probability of finding at least one usable terminal branch that is at least 12.0 cm in length was found to be 98 percent. Typically, there are two to five useful branches at this distance. Such information may help surgeons fine tune their process of selecting an appropriate arterial donor site for a particular arterial defect and supports the use of the subscapular arterial tree as a donor site for microvascular arterial grafts.     

Visualization of arterial and arterial graft patency by intravenous radionuclide angiography

A method of visualizing patency of arteries and arterial grafts by means of intravenous ^99mTc pertechnetate using a Nuclear Chicago Pho/Gamma HP camera is described. Polaroid pictures showing normal arteries in the upper and lower limbs, as well as partial and complete occlusion of arteries and the state of arterial bypass grafts in pre- and postoperative patients are compared with conventional arteriograms. The advantages and limitations of this method are discussed.     

Hydrodynamics of arterial branching--the effect of arterial branching on distal blood supply

A study was conducted to investigate the hydrodynamics of branching flow in relation to the blood supply to the basal part of the brain. A series of measurements of the branching loss-coefficients under laminar steady flow were conducted using model branches with various geometries, and the effect of branching on blood supply to distal areas was described using a lumped-parameter model of the vascular structure. It was revealed that in the blood circulation, branching loss is important where a small artery divides off with a large branching angle from a large trunk. It was also indicated that the effect of such branching on the distal blood supply might become more significant when the peripheral resistance is reduced, thereby increasing the blood velocity in the trunk.     

Computer simulation of arterial flow with applications to arterial and aortic stenoses

A computer model for simulating pressure and flow propagation in the human arterial system is developed. The model is based on the one-dimensional flow equations and includes nonlinearities arising from geometry and material properties. Fifty-five arterial segments, representing the various major arteries, are combined to form the model of the arterial system. Particular attention is paid to the development of peripheral pressure and flow pulses under normal flow conditions and under conditions of arterial and aortic stenoses. Results show that the presence of severe arterial stenoses significantly affects the nature of the distal pressure and flow pulses. Aortic stenoses also have a profound effect on central and peripheral pressure pulse formation. Comparison with the published experimental data suggests that the model is capable of simulating arterial flow under normal flow conditions as well as conditions of stenotic obstructions in a satisfactory manner.     

Determinants of an elevated pulmonary arterial pressure in patients with pulmonary arterial hypertension

Given the difficulty of diagnosing early-stage pulmonary arterial hypertension (PAH) due to the lack of signs and symptoms, and the risk of an open lung biopsy, the precise pathological features of presymptomatic stage lung tissue remain unknown. It has been suggested that the maximum elevation of the mean pulmonary arterial pressure (P_pa) is achieved during the early symptomatic stage, indicating that the elevation of the mean P_pa is primarily driven by the pulmonary vascular tone and/or some degree of pulmonary vascular remodeling completed during this stage. Recently, the examination of a rat model of severe PAH suggested that the severe PAH may be primarily determined by the presence of intimal lesions and/or the vascular tone in the early stage. Human data seem to indicate that intimal lesions are essential for the severely increased pulmonary arterial blood pressure in the late stage of the disease.However, many questions remain. For instance, how does the pulmonary hemodynamics change during the course of the disease, and what drives the development of severe PAH? Although it is generally acknowledged that both pulmonary vascular remodeling and the vascular tone are important determinants of an elevated pulmonary arterial pressure, which is the root cause of the time-dependent progression of the disease? Here we review the recent histopathological concepts of PAH with respect to the progression of the lung vascular disease.     

Heart rate,arterial distensibility,and optimal performance of the arterial tree

In this study we explore the ability of a previously developed model of pulsatile flow for explaining the observed reduction of arterial distensibility with heart rate. The parameters relevant for the analysis are arterial wall distensibility together with permeability and reflection coefficients of the end capillaries. A non-specific artery and the ensemble of tissues supplied by that artery were considered in the model. The blood current within that artery was equalized to the sum of all micro currents in the tissues supplied by that artery. A formula emerged that relates changes in arterial distensibility with heart rate, and also with some particular aspects of microcirculation. Then, that formula was tested with data of distensibilities of the radial and carotid arteries observed at the heart rates of 63, 90, and 110 b.p.m. The formula correctly predicted the trend of decreased distensibility with heart rate for both arteries. Moreover, due to the fact that the carotid artery supplies the brain, and because the Blood–Brain barrier is highly restrictive to colloids in the blood, for the carotid artery the formula predicted a less marked decrease in distensibility than in the case of the radial artery feeding muscle tissue, which has a greater permeability to colloids, a trend that was confirmed by data. It was found that reduction of arterial distensibility with heart rate was greater in arteries that supply end capillaries with high permeability and low reflection coefficients.     

Local geometry of arterial branching

A model of the geometrical structure of arterial bifurcations is proposed in the context of optimality of the bifurcation as a fluid conducting system. Optimality is considered both globally, in terms of the cardiovascular system as a whole, and locally, in terms of the orderliness of the flow in the bifurcation region. It is shown that a bifurcation can be optimal both globally and locally. Typical examples of such bifurcations are given.     

慢性动脉血压调节与原发性高血压病——Ⅰ.慢性动脉血压调节

机体在不同条件下维持动脉血压恒定的机理是不相同的。目前认为,长时程或慢性血压调节的关键器官是肾脏,这种调节与机体的水盐平衡有密切的关系。动脉血压的升高可以导致肾脏排尿量（或排钠量）的升高,即动脉血压与肾脏的排尿量（或排钠量）呈明显的正相关关系,称之为“压力-利尿作用”。当血容量升高时,通过肾脏的压力-利尿作用,可以排出过多的容量,维持动脉血压的恒定。只有在肾脏功能受到损伤的条件下,高血容量才可能引起高血压。