Influence of Vessel Distension and Myogenic Tone on Pulmonary Arterial Input Impedance. A Study using a Computer Model of Rabbit Lung

A computer model of the pulmonary arterial (PA) bed of rabbit lungs was designed in order to test experimental observations of changes in PA input impedance and pulsatile hydraulic power (cap.) during increased PA pressure. The computer model was based on a simple 3-component analog representation of single vessels (i.e. resistance, inertance and compliance). 16 generations of arterial vessels, from PA to 60 μm diameter, were combined to calculate PA input impedance. Input impedance was found to mimic closely that observed experimentally. Both venous pressure elevation and arteriolar constriction was found to reduce input impedance and Wp. By combining arteriolar constriction with increased myogenic tone of the larger arteries, Wp was found to show a minimum level at a certain PA pressure, dependent on the degree of arterial stiffening. Wp was found to follow changes in arterial volume and resistance during simulated vasoconstriction. Wp dissipation in arterial vessels was calculated to approx. 50% of total input Wp at physiological pressure conditions, and could be reduced by one half after PA pressure increase from 20 to 50 cm H₂O, despite a concurrent halving of arterial compliance. Arterial vessels smaller than 200 pm diameter were found to have negligible direct influence on PA input impedance.     

Responses of cerebral arteries and arterioles to acute hypotension and hypertension

The responses of cerebral precapillary vessels to changes in arterial blood pressure were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation of the parietal cortex. Vessel responses were found to be size dependent. Between mean arterial pressures of 110 and 160 mmHg autoregulatory adjustments in caliber, e.g., constriction when the pressure rose and dilation when the pressure decreased, occurred only in vessels larger than 200 micron in diameter. Small arterioles, less than 100 micron in diameter, dilated only at pressures equal to or less than 90 mmHg; below 70 mmHg their dilation exceeded that of the larger vessels. When pressure rose to 170- 200 mmHg, small vessels dilated while the larger vessels remained constricted. At very high pressures (greater than 200 mmHg) forced dilation was frequently irreversible and was accompanied by loss of responsiveness to hypocapnia. Measurement of the pressure differences across various segments of the cerebral vascular bed showed that the larger surface cerebral vessels, extending from the circle of Willis to pial arteries 200 micron in diameter, were primarily responsible for the adjustments in flow over most of the pressure range.     

Some Physical Properties of the Pulmonary Arterial Bed Deduced from Pulsatile Arterial Flow and Pressure

This study aimed to quantify changes of vascular compliance and resistance of the proximal and the peripheral pulmonary arterial vessels when vascular smooth muscle was stimulated. These above vascular characteristics were derived from registrations of pulsatile pressure and flow in the pulmonary artery (PA). An in situ cat lung preparation was used, with the right heart by-passed by a pulsatile blood pump. Vascular input impedance was derived from PA pulsatile pressure and flow recordings, and impedance characteristics were used for calculation of the variables of a simple lumped analog representation of the arterial bed. PA smooth muscle was stimulated by infusions of collagen suspension, by general hypoxia and by nor-adrenaline injections. Collagen caused 40% reduction of vascular compliance (C), no changes in proximal arterial resistance (Rl) and 18076 increase in peripheral vascular resistance (R2). Hypoxia caused 5096 reduced C, 20% increased R1 and 70% increased R2. Noradrenaline caused 20:6 reduced C and 30 % increased R1 and R2. These results, together with results derived from simulation of the observed impedance changes in a computer model of the lung arterial bed, indicated that collagen infusion elicited contraction of small and medium-sized arteries, with increased arterial volume as result of increased distending pressure. Hypoxia and noradrenaline, seemed both to cause contraction of the total arterial bed. This effect being most pronounced during hypoxia.     

Dynamic pressure-flow diagrams and impedance in experimental arterial stenosis and in stenotic atherosclerosis

Dynamic pressure-flow diagrams were generated by plotting instantaneous pulsatile pressure versus pulsatile flow measured 2 to 3 cm proximal to a graded arterial stenosis in the dog femoral artery. The slope of the major axis of the diagram was defined as the pulse impedance (Z _P).Z _p under steady-state and vasodilated conditions was linearly related to the large vessel impedance (Z _l) calculated independently as the average vascular input impedance modulus from 3 to 19 Hz, and linearly related to the hydraulic resistance of the stenosis. In a separate study,Z _p andZ _l each were shown to be greater in patients with severe femoral artery stenotic atherosclerosis than in control patents, and unchanged during vasodilation. In addition,Z _p andZ _l were reduced following femoral-to-popliteal bypass procedures. In summary, dynamic pressure-flow diagrams provide an easy-to-obtain index of the effective vascular hydraulic input impedance in stenotic arteries, and an index of the severity of distal arterial stenosis. This research has been supported in part by the North Carolina Heart Association (Grant-in-Aid 1974-75-A-62) and the Environmental Protection Agency, Chapel Hill, North Carolina.     

Loci of Neurogenic and Metabolic Effects on Precapillary Vessels of Skeletal Muscle

Folkow , B., R. R. Sonnenschein , and D. L. Wright , Loci of neurogenic and metabolic effects on precapillary vessels of skeletal muscle. Acta physiol. scand. 1971. 81. 459–471. By cannulation of a branch of the proximally clamped sural artery of the anesthetized cat, distal arterial pressure (DAP) in the gastrocnemius muscle was recorded. Measurement of blood flow, femoral arterial pressure and DAP allowed calculation of total resistance (R_t) and its partition into a distal component (R_d) which included precapillary sphincters and the smaller arterioles, and a proximal component (R_P) which included the larger arteries. With sympathetic vasoconstriction, the initial increase in R_t was accounted for mainly by constriction of the distal vessels which then tended to relax; progressive constriction of proximal vessels accounted for most of the elevated R_t during the steady state; subsequent reactive hyperemia mainly involved distal vessels. R_t was less affected by sympathetic stimulation during exercise than when the muscle was at rest; constriction of distal vessels was more markedly reduced than that of proximal vessels. Ascending dilatation was evident during exercise. Sympathetic cholinergic vasodilatation mainly involved vessels more proximal to those which were dilated early in exercise. The findings are compatible with the concept that capillary flow distribution, as a function of terminal arterioles and precapillary sphincters, is adjusted by local factors towards an optimum for the prevailing metabolic level of the tissue.     

The Influence of Pulmonary Blood Flow Rate on Vascular Input Impedance and Hydraulic Power in the Sympathetically and Noradrenaline Stimulated Cat Lung

This study was designed to evaluate the influence of sympathetic nerve stimulation (NS) and α-adrenergic receptor stimulation (αS) on the pulmonary vascular input impedance and hydraulic power output of the right heart during variations of cardiac output (CO). An open chest cat preparation was used and pulsatile pressure and flow in the pulmonary artery were measured by high frequency response transducers. Calculations showed that vascular resistance (VR) was inversely dependent on CO, hut input impedance of the unstimulated lung was not influenced by CO variations. NS or αS increased VR and input impedance significantly, and the relation pulsatile hydraulic power/total hydraulic power (W_p/W_t) increased 40%, indicating that such stimulation has larger relative influence on impedance than on resistance. The reduction of arterial compliance during NS (maximal stimulus) was calculated to be 60%, independent of CO. Input impedance during NS or αS was reduced by CO elevations, probably because the concomitant distension of the arterial bed reduced arterial resistance and inertance. The ratio W_p/CO, which expresses the fraction of pulsatile hydraulic power lost per ml mean arterial flow, was found to be flow dependent both in control and stimulated conditions: W_p/CO was positively correlated to CO in control condition and weakly negatively correlated to CO during stimulation. At high CO the arterial vessels could he stimulated and stiffened without much extra load on the right heart.     

Correlation of the directly observed responses of mesenteric vessels of the rat to nerve stimulation and noradrenaline with the distribution of adrenergic nerves

1. The effects of nerve stimulation and of the topical application of noradrenaline on arteries, capillaries and veins of the mesentery of the anaesthetized rat were examined by direct observation under a microscope. The distribution of adrenergic nerves to the vessels of the mesentery was studied using the fluorescence histochemical method.

2. Principal arteries, small arteries and terminal arterioles were all innervated by a network of adrenergic fibres and they all constricted in response to the stimulation of paravascular nerves and to exogenous noradrenaline. Few adrenergic fibres accompanied the smaller, precapillary arterioles; these vessels did not respond to nerve stimulation, although they were constricted by concentrations of noradrenaline as low as 10^-10 g/ml.

3. The capillaries did not respond to nerve stimulation or to applied noradrenaline. All veins were constricted by noradrenaline, but only those veins greater than about 30 μm in internal diameter responded to nerve stimulation.

4. At stimulus frequencies greater than 4 Hz the flow of blood through the microvasculature usually ceased, although there was never complete closure of these vessels. The maximum constriction observed in principal arteries was usually between 50 and 70% of the control internal diameter, and in small arteries and terminal arterioles was between 40 and 65% of the control internal diameter.

5. It is concluded that the principal arteries and small arteries of the mesenteric vasculature are important in the control of blood flow through this vascular bed during sympathetic stimulation and following topical application of noradrenaline, and that the precapillary arterioles are important vessels determining the rate of blood flow through the capillary bed under resting conditions.

     

Contractile Responses to Noradrenaline: Varying Dependence on External Calcium of Consecutive Vascular Segments of Perfused Rat Hindquarters

To study the dependency of vascular smooth muscle contractions, produced by noradrenaline, on the concentration of extracellular calcium, experiments were performed on adult male Wistar rats. The hemodynamic characteristics of the isolated, perfused hindquarters were investigated from maximal dilatation up to maximal, noradrenaline-induced constriction under constant flow conditions. Pressor responses to noradrenaline in the consecutive segments of the vascular bed (“proximal” and “distal” precapillary resistance vessels and postcapillary resistance vessels) were determined at low (0.2 mM) and at normal (1.5-2.0 mM) Ca⁺⁺ concentrations in the perfusate. Dependence on external calcium is much greater peripherally. The smallest pre- and postcapillary resistance vessels are the most dependent while the larger, “proximal” precapillary resistance vessels are the least dependent on the availability of external calcium. The results illustrate the considerable differentiation of smooth muscle, depencling on its location along the vascular circuit. They further indicate that it is likely that the hemodynamically so important microvessels are highly dependent on extrinsic Ca⁺⁺ sources not only concerning their involvement of remote adrenergic control, but also in their maintenance of normally pronounced “myogenic” tone.     

A compartmental model for oxygen transport in brain microcirculation

A compartmental model is formulated for oxygen transport in the cerebrovascular bed of the brain. The model considers the arteriolar, capillary and venular vessels. The vascular bed is represented as a series of compartments on the basis of blood vessel diameter. The formulation takes into account such parameters as hematocrit, vascular diameter, blood viscosity, blood flow, metabolic rate, the nonlinear oxygen dissociation curve, arterial PO₂, P₅₀ (oxygen tension at 50% hemoglobin saturation with O₂) and carbon monoxide concentration. The countercurrent diffusional exchange between paired arterioles and venules is incorporated into the model. The model predicts significant longitudinal PO₂ gradients in the precapillary vessels. However, gradients of hemoglobin saturation with oxygen remain fairly small. The longitudinal PO₂ gradients in the postcapillary vessels are found to be very small. The effect of the following variables on tissue PO₂ is studied: blood flow, PO₂ in the arterial blood, hematocrit, P₅₀, concentration of carbon monoxide, metabolic rate, arterial diameter, and the number of perfused capillaries. The qualitative features of PO₂ distrbution in the vascular network are not altered with moderate variation of these parameters. Finally, the various types of hypoxia, namely hypoxic, anemic and carbon monoxide hypoxia, are discussed in light of the above sensitivity analysis.     

Patient-Specific Modeling of Blood Flow and Pressure in Human Coronary Arteries

Coronary flow is different from the flow in other parts of the arterial system because it is influenced by the contraction and relaxation of the heart. To model coronary flow realistically, the compressive force of the heart acting on the coronary vessels needs to be included. In this study, we developed a method that predicts coronary flow and pressure of three-dimensional epicardial coronary arteries by considering models of the heart and arterial system and the interactions between the two models. For each coronary outlet, a lumped parameter coronary vascular bed model was assigned to represent the impedance of the downstream coronary vascular networks absent in the computational domain. The intramyocardial pressure was represented with either the left or right ventricular pressure depending on the location of the coronary arteries. The left and right ventricular pressure were solved from the lumped parameter heart models coupled to a closed loop system comprising a three-dimensional model of the aorta, three-element Windkessel models of the rest of the systemic circulation and the pulmonary circulation, and lumped parameter models for the left and right sides of the heart. The computed coronary flow and pressure and the aortic flow and pressure waveforms were realistic as compared to literature data.     

Effect of compliance on a time-domain estimate of the characteristic impedance of the pulmonary artery during acute pulmonary hypertension

In 11 pigs under general endotracheal anaesthesia, the time-domain method of determining the pulmonary arterial input impedance was compared with the frequency-domain equivalent under normal conditions as well as acute pulmonary hypertension induced by glass microspheres. The time-domain methods of determining the pulmonary arterial compliance C and pulmonary vascular bed resistance R_p compared favourably with the frequency-domain equivalent (r=0·744, n=60, p<0·001 and r=0·906, n=60, p<0·001, respectively), even at mean pulmonary artery pressures (MPAP) of 35 mmHg and above. A consistent and everincreasing difference between characteristic impedance Z_o(ω), estimated by averaging input impedance modulus values over a selected frequency range, and its time domain equivalent R_o with increasing MPAP was shown to be the cause of the poor fit between the measured and remodelled pulmonary blood flow. By analysing a time-domain estimate of the pulmonary characteristic impedance R_o(C, R_p, t), it was demonstrated that the characteristic impedance was dependent on C. R_o is therefore not an accurate representation of the characteristic impedance, especially under conditions of acute pulmonary hypertension. R_o (C, R_p, t) should therefore be calculated instead.     

Influence of Moderate Vasoconstriction on the Wave Reflection Properties of the Pulmonary Arterial Bed

Increased transmural pressure in the pulmonary arterial bed may reduce vascular input impedance and reduce hydraulic power linked to pulsatile blood flow. Vascular impedance and pulsatile hydraulic power (Wp) levels of isolated perfused rabbit lungs were compared after similar rises of pulmonary arterial pressure (PAp), induced either by vasoconstriction or by left atrial pressure (LAp) elevation. Resulting Wp levels were significantly smaller after vasoconstriction than LAp elevation. Wp showed a minimum level at physiologic PAp (about 20 cm H₂O) irrespective of the cause of PAp elevation. Pressure pulse wave reflection coefficient (Γ) was calculated for control and test situations, and was found to be approximately doubled after vasoconstriction. Only minor changes in Γ were found after LAP elevation. Accordingly, moderate vasoconstriction (resulting PAp?20 cm H₂O) caused a backward traveling pressure wave of high amplitude, appearing in counter-phase to the forward pressure wave at the input site. The total pressure wave amplitude was thereby markedly lowered, resulting in a reduced Wp level. We assume that this effect of moderate vasoconstriction may be one reason for the existence of vascular smooth muscles in the pulmonary arteries.     

Sympathetic a-adrenergic control of large-bore arterial vessels,arterioles and veins,and of capillary pressure and fluid exchange in whole-organ cat skeletal muscle

The sympathetic nervous control of the vascular bed of cat gastrocnemius muscle was studied with a new whole-organ technique which permits simultaneous, continuous and quantitative measurements of capillary pressure (P_c), capillary fluid exchange and resistance reactions in the whole vascular bed and in its three consecutive sections: large-bore arterial vessels (> 25 μm), arterioles (< 25 μm) and veins. The results demonstrated a distinct neural control of all three consecutive vascular sections, graded in relation to the rate of nerve excitation up to maximum at 16 Hz. Stimulation at high rates, which in the steady state caused an average rise of overall regional resistance from 15.3 to 120 PRU (7.8-fold increase), thus raised large-bore arterial vessel resistance from 8.8 to 64 PRU (7.3-fold increase), arteriolar resistance from 4.5 to 49 PRU (10.9-fold increase) and venous resistance from 2.0 to 7 PRU (3.5-fold increase). The rate of resistance development (PRU s^-1) of the sympathetic constrictor response was much higher in the arteriolar than in the other sections, which indicates that the neural control is especially prompt and efficient in the arterioles. A passive component was shown to contribute to the described responses only on the venous side, but in no case by more than 10% of the total sympathetic venous resistance response, which thus is mainly active. Of special functional importance was that the new technique provided information about the adrenergic control of P_c, in absolute figures. From the control value of 19 mmHg, graded sympathetic stimulation caused a graded decline in P_c, at maximum constriction by about 7 mmHg. This resulted in marked net transcapillary fluid absorption, in turn increasing plasma volume.     

Respiratory input impedance measurement: Forced oscillation methods

The paper reviews how forced oscillation techniques (FOT) for measuring respiratory input impedance Z_{rs, in} have recently been used in clinical applications. Z_{rs, in} is clinically relevant, as it provides data on both the resistive, R_rs, and nonresistive, X_rs, components of the respiratory system. Additionally, when excitatory test signals extending into low- (<4 Hz) or high-frequency (>100 Hz) ranges are used, reliable partitioning of lung tissue from airway components is feasible. Adult and paediatric studies examining the use of Z_{rs, in} for routine lung-function assessment, sleep and mechanical ventilation are reviewed. For clinicians, Z_{rs, in} is repeatable and sensitive to airway resistance. It is helpful for assessing unco-operative and severely obstructed patients, for monotoring mechanics during artificial ventilation and for tracking airway closure during sleep studies. For paediatricians, longitudinal studies of the growth and development of the respiratory system can also be made using Z_{rs, in}. Forced oscillation techniques, however, require further standardisation, and Z_{rs, in} is limited by upper-airway shunt artifacts. In conclusion, measurement of Z_{rs, in} using FOT is an important and sophisticated non-invasive lung-function test, showing good potential for future clinical applications.     

Augmented vasoconstrictor response to changes in vascular transmural pressure in patients with essential arterial hypertension

The vasoconstrictor response to increase in venous transmural pressure in subcutaneous tissue was studied in 9 patients with essential arterial hypertension. Subcutaneous blood flow was measured on the distal part of the forearm and at the lateral malleolus by the local ¹³³Xe washout technique. Increase in venous transmural pressure was obtained by lowering the area under study 40cm below midaxillary line in the recumbent subject. Average mean arterial pressure ± 1 S.E. was 133 ± 6 mmHg. The fractional increase in vascular resistance induced by arteriolar constriction was more pronounced in the hypertensive patients than in a normotensive control group. “Minimal vascular resistance” in the papaverine relaxed vascular bed was higher in the hypertensive patients than in the controls. Distensibility of the papaverine relaxed resistance vessels was diminished in the patients. Follow-up studies after 6–18 months of anti-hypertensive treatment indicate that the vasoconstrictor response as well as “minimal vascular resistance” are normalized, whereas the distensibility of the papaverine relaxed arterioles remained unaltered in the hypertensive patients. The results indicate that the arteriolar smooth muscle cells of hypertensive patients are subjected to reversible hypertrophy whereas the reduced distensibility of the resistance vessels is due to irreversible structural changes.     

Correlation of the directly observed responses of mesenteric vessles of the rat to nerve stimulation and noradrenaline with the distribution of adrenergic nerves

1. The effects of nerve stimulation and of the topical application of noradrenaline on arteries, capillaries and veins of the mesentery of the anaesthetized rat were examined by direct observation under a microscope. The distribution of adrenergic nerves to the vessels of the mesentery was studied using the fluorescence histochemical method.2. Principal arteries, small arteries and terminal arterioles were all innervated by a network of adrenergic fibres and they all constricted in response to the stimulation of paravascular nerves and to exogenous noradrenaline. Few adrenergic fibres accompanied the smaller, precapillary arterioles; these vessels did not respond to nerve stimulation, although they were constricted by concentrations of noradrenaline as low as 10(-10) g/ml.3. The capillaries did not respond to nerve stimulation or to applied noradrenaline. All veins were constricted by noradrenaline, but only those veins greater than about 30 mum in internal diameter responded to nerve stimulation.4. At stimulus frequencies greater than 4 Hz the flow of blood through the microvasculature usually ceased, although there was never complete closure of these vessels. The maximum constriction observed in principal arteries was usually between 50 and 70% of the control internal diameter, and in small arteries and terminal arterioles was between 40 and 65% of the control internal diameter.5. It is concluded that the principal arteries and small arteries of the mesenteric vasculature are important in the control of blood flow through this vascular bed during sympathetic stimulation and following topical application of noradrenaline, and that the precapillary arterioles are important vessels determining the rate of blood flow through the capillary bed under resting conditions.     

Mathematical model for interpretation of doppler velocity waveform indices

Various empirical indices such as the pulsatility index (PI) are widely used for quantitative analysis of Doppler ultrasound velocity waveforms. The physical interpretation of these indices was studied using a mathematical model. Although the method has more general applicability, this particular study was concerned with the umbilical-placental circulation. A lumped element electrical circuit equivalent was used, with each arterial branch represented by a resistor and a capacitor. The placental villous bed was modelled by a two-step parallel branching structure. Placental vascular disease was modelled either as obliteration of a fraction of the terminal branches, or as a fractional decrease in the radius of the vessels. The main features of both normal and abnormal umbilical artery waveforms can be reproduced by this simple model. Theoretical relationships between the velocity waveform indices and the lumped resistances and capacitance of the system were obtained for different input pressure functions. Over a wide range of physically reasonable conditions, the umbilical artery PI is approximately proportional to the ratio of the placental resistance to the umbilial artery resistance. The PI also depends on the pulsatility of the input pressure waveform. The Fourier pulsatility index was evaluated for an arbitrary pressure function, and shown to behave like (PI)² for the umbilical artery waveform.     

Endogenous nitric oxide as a physiological regulator of vascular tone in cat skeletal muscle during haemorrhage

The problem whether endogenous nitric oxide (NO) may serve as a true physiological regulator of vascular tone in vivo was approached by testing its role during graded acute haemorrhage with the aid of the nitric oxide synthase (NOS) inhibitor l -NAME. The study was performed on the vascular bed of cat skeletal muscle with a technique permitting quantitative recordings of vascular resistance in the whole vascular bed (R_T) and in its consecutive sections, the proximal arterial resistance (‘feeder’) vessels (>25 μm; R_a,prox), the small arterioles (<25 μm) and the veins. NO blockade by close-arterial l -NAME infusion in the control situation increased R_T from 16.3 to 33.0 PRU (+102%), because of a selective increase in R_a,prox by 16.7 PRU. A 35% blood loss per se raised R_T from 13.6 to 21.7 PRU. Superimposed NO blockade in this state caused a much stronger vasoconstriction than in the control situation, increasing R_T to 60.9 PRU (+181%) and R_a,prox by 40.5 PRU, which indicated an ～2.4-fold increase (P< 0.001) in the NO dilator influence in the R_a,prox section above control. The effect was independent of autonomic nerves. The increased NO dilator influence during haemorrhage most likely was caused by an increased production of endothelium-derived nitric oxide (EDNO). The constrictor response to l -NAME was graded in relation to the blood loss (17.5 vs. 35%). The results indicate that EDNO functions as a physiological regulator of vascular tone in the arterial ‘feeder’ vessels during haemorrhage, serving to counterbalance to a significant extent the concomitant adrenergic constriction, and thereby preventing critical reduction of blood flow and untoward heterogeneous flow distribution within the tissue.     

Effects of angiotensin-converting enzyme inhibition on arterial,venous and capillary functions in cat skeletal muscle in vivo

The aim of the present study was to analyse quantitatively, on a cat gastrocnemius muscle preparation in vivo, the effects of local angiotensin-converting enzyme (ACE) inhibition by enalaprilat on total regional vascular resistance (tone) and its distribution to the large-bore arterial resistance vessels (>25 μm), the small arterioles (<25 μm) and the veins. Associated effects on capillary pressure and fluid exchange were also studied. Close-arterial infusion of enalaprilat (0.05–0.20 mg kg muscle tissue min^-1) elicited a moderate dilator response in all three consecutive sections of the muscle vascular bed, an increase in capillary pressure and transcapillary fluid filtration. This dilation could be abolished by the selective bradykinin B₂-receptor antagonist Hoe 140 (2 mg kg^-1 min^-1, i.a.), indicating that the dilator mechanism of ACE inhibition was an increased local concentration of bradykinin, and hardly at all a decreased concentration of angiotensin (AT) II. The generalized dilator response to ACE inhibition along the vascular bed suggested a relatively uniform distribution of ACE from artery to vein and this was further supported by the finding that a close-arterial infusion of AT I (0.04–0.32 μg kg^-1 min^-1), which was vasoactive only after conversion to AT II by local ACE, elicited a generalized constrictor response in all three vascular sections. In contrast, infused AT II (0.01–0.16 μg kg^-1 min^-1) constricted almost selectively the large-bore arterial vessels. The specific angiotensin AT₁-receptor antagonist losartan (2 mg kg^-1 min^-1, i.a.) abolished the constrictor response to AT II but did not affect vascular tone under control conditions, indicating that AT II is not involved in the initiation of basal vascular tone in muscle. These results, taken together, indicate that under basal conditions vascular ACE contributes to the local control of vascular tone in skeletal muscle by degrading the endogenous dilator bradykinin, and not by converting AT I into vasoconstrictor AT II.     

基于电网络模型的动脉树输入阻抗递归计算及参数分析

目的 通过提出一种计算人体动脉树输入阻抗的递归算法,分析动脉树各参数对输入阻抗的影响,为动脉树生理和病理变化分析提供参考。方法 利用由大动脉和主要外周动脉构成的55段人体动脉树建立分布式电网络模型,通过设定电网络模型外周阻力,建立动脉树单向数据链表,采用递归算法计算动脉树升主动脉的输入阻抗。在此基础上比较不同动脉顺应性、外周阻力和动脉长度、内径、壁厚等参数对输入阻抗的影响。结果 计算结果与实验数据和其他模型结果相一致,验证了该方法的有效性。不同参数对动脉树输入阻抗的影响有较大差异且呈现各自特征。结论 输入阻抗能有效地反映动脉树血液动力学参数的变化情况,是人体动脉树生理病理诊断的重要参考。