On deriving lumped models for blood flow and pressure in the systemic arteries

Author(s):  
Mette S. Olufsen ◽  
Ali Nadim
1996 ◽  
Vol 199 (6) ◽  
pp. 1435-1446 ◽  
Author(s):  
J W Hicks ◽  
A Ishimatsu ◽  
S Molloi ◽  
A Erskin ◽  
N Heisler

The mechanism of cardiac shunting in reptiles is controversial. Recent evidence suggests that a right-to-left shunt in turtles results primarily from a washout mechanism. The mechanism that accounts for left-to-right (L-R) shunting is unresolved. This study used haemodynamic analysis and digital subtraction angiography to determine the mechanism of L-R cardiac shunting in the turtle Trachemys (Pseudemys) scripta. Animals were instrumented with ultrasonic blood flow probes (Transonic Systems, Inc.) for the measurement of total pulmonary blood flow and total systemic blood flow. In addition, catheters were inserted into the common pulmonary artery (PA), the systemic arteries, the left atrium and right atrium. These catheters were used for the measurement of blood pressure or for the infusion of radio-opaque material. Haemodynamic conditions were altered by electrical stimulation of the afferent (VAF) or efferent vagal nerves or by infusion of vasoactive drugs. Under control conditions, the peak systolic pressure in the systemic arteries was slightly higher than that in the PA (30.6 versus 28.3 mmHg; 4.08 versus 3.77 kPa), whereas diastolic pressure in the PA was significantly less than that in the systemic arteries (9.8 versus 24.4 mmHg; 1.31 versus 3.25 kPa). During VAF stimulation, the peak systolic pressures in the PA and aortae almost doubled. Diastolic pressure in the systemic arteries also doubled, but it increased by only 45% in the PA. Ejection of blood into the PA preceded that into the left aorta by 53 ms under control conditions. This difference increased (by as much as 200 ms) as the difference in the diastolic pressures between the two circulations increased during VAF stimulation. This resulted in the development of a large net L-R shunt. Under these conditions, digital subtraction angiography showed that the L-R shunt resulted from a combination of both washout and pressure mechanisms.


1982 ◽  
Vol 53 (1) ◽  
pp. 272-279 ◽  
Author(s):  
M. G. Magno ◽  
A. P. Fishman

This anatomical-physiological study was undertaken to determine the suitability of the sheep for studies of the bronchial circulation. We designated the terminal portion of the bronchoesophageal artery, which runs to the trachea at the carina, as the “carinal” artery. Postmortem injections of india ink (9 sheep) and Batson's solution (4 sheep) into the carinal artery showed that the carinal artery supplied the bronchi of all lobes except the right apical lobe; the mass of the lung containing bronchi perfused represented 88 +/- 1% of total lung mass. Communications were also found between branches of the carinal artery and branches of the systemic arteries supplying the visceral pleura. In three of six sheep, the carinal artery wedge pressure measured in vivo indicated that patent collaterals were present, but that their incidence is variable. In additional postmortem casts of the aorta made in four sheep after ligation of the carinal artery, the bronchial microcirculation was not entered by the perfusing medium. These data indicate that the collaterals do not contribute significantly to bronchial blood flow and that the carinal artery is the major source of bronchial blood flow in the sheep. In 19 sheep, carinal artery flow, measured electromagnetically, was 0.46 +2- 0.09 ml . min-1 . kg body wt-1. Bronchial blood flow normalized for the weight of the lobes in which bronchi perfused by the carinal artery were located was 3.97 +/- 0.48 ml . min-1 . 100 g lung-1 (n = 11); carinal artery blood flow was 0.39 +/- 0.03% of cardiac output (n = 5). During the 90 min of observation, at normal aortic blood pressure (103 +/- 3.4 Torr), carinal artery blood flow was stable. In conclusion, determination of carinal artery blood flow affords a reliable approach to the bronchial circulation in the sheep.


1999 ◽  
Vol 276 (1) ◽  
pp. H257-H268 ◽  
Author(s):  
Mette S. Olufsen

A central problem in modeling blood flow and pressure in the larger systemic arteries is determining a physiologically based boundary condition so that the arterial tree can be truncated after a few generations. We have used a structured tree attached to the terminal branches of the truncated arterial tree in which the root impedance is estimated using a semianalytical approach based on a linearization of the viscous axisymmetric Navier-Stokes equations. This provides a dynamic boundary condition that maintains the phase lag between blood flow and pressure as well as the high-frequency oscillations present in the impedance spectra. Furthermore, it accommodates the wave propagation effects for the entire systemic arterial tree. The result is a model that is physiologically adequate as well as computationally feasible. For validation, we have compared the structured tree model with a pure resistance and a windkessel model as well as with measured data.


PEDIATRICS ◽  
1953 ◽  
Vol 12 (3) ◽  
pp. 307-325
Author(s):  
J. FRANCIS DAMMANN ◽  
WILLIAM H. MULLER

In the normal human being systemic blood pressure is maintained at a high level by means of the high resistance offered to the flow of blood by the smaller systemic arteries and arterioles. In contrast, pressure in the pulmonary circulation is maintained at a low level because of the relatively large size of the pulmonary vessels. In the fetal and newborn period pulmonary arteries resemble systemic arteries in that they have a small lumen and thick media. In this period pulmonary pressure and resistance are high. As these vessels gradually thin out and enlarge, resistance to pulmonary blood flow falls and consequently pulmonary blood pressure falls. There is evidence to suggest that the fetal state of thick-walled, thin-lumened pulmonary arteries is retained in instances where the two circulations are joined, such as in patients with a single ventricle, large ventricular defect, aortic septal defect or large patent ductus arteriosus. As the patient grows, resistance to pulmonary blood flow may: (1) decrease. If the small pulmonary arteries develop normally and become thin-walled and large-lumened, pulmonary resistance will fall. More and more blood will be shunted into the lungs and the patient will develop the signs and symptoms of cardiac decompensation. (2) remain the same. If the small pulmonary arteries retain their fetal characteristics, pulmonary resistance will remain elevated. A balance between systemic and pulmonary blood flow will be maintained compatible with a relatively normal life. (3) increase. If, because of secondary intimal changes, the pulmonary arteries become thicker-walled and smaller-lumened, pulmonary resistance will increase. Progressively less blood will be shunted to the lungs and finally the shunt will reverse and become predominantly venous arterial. The patient will develop the signs and symptoms of pulmonary stenosis with increasing dyspnea and cyanosis. Data from two groups of patients are presented to illustrate the importance of the pulmonary vascular bed. In the first group, early and severe symptoms of cardiac failure necessitated closure of a large patent ductus arteriosus early in life. The ductus was large, comparable to the size of the aorta, pressures from the aorta and pulmonary artery were similar and a study of the lung biopsies demonstrated that the lumens of the small pulmonary arteries were decreased in size and the media were abnormally thick. In each instance closure of the ductus resulted in a cure. In the second group the two circulations were joined by either a large ventricular defect or a single ventricle. Three patients were in cardiac failure due to excessive pulmonary blood flow. Pulmonary blood flow was decreased by the creation of pulmonary stenosis, the main pulmonary artery being narrowed 60 to 80%. The postoperative course in these three patients illustrates the value of the creation of pulmonary stenosis in instances where the two circulations are joined by a large communication between the ventricles or great vessels.


1998 ◽  
Vol 275 (5) ◽  
pp. H1845-H1856 ◽  
Author(s):  
Karen E. Vagnoni ◽  
Cynthia E. Shaw ◽  
Terrance M. Phernetton ◽  
Beth M. Meglin ◽  
Ian M. Bird ◽  
...  

During the follicular phase of the ovarian cycle, when the local estrogen-to-progesterone ratio is elevated, uterine blood flow is elevated. This vasodilatory response is reproduced by exogenous 17β-estradiol (E2β) administration via a nitric oxide (NO)-mediated mechanism. We hypothesized that endogenous ovarian estrogen and exogenous E2β treatment elevate expression of endothelial cell-derived NO synthase (eNOS) in uterine, but not in systemic, arteries. Uterine, mammary, and systemic (renal and/or omental) arteries were collected from 1) ewes synchronized to the follicular ( day −1 to day 0) or luteal ( day 10) phases of the ovarian cycle ( n = 4 per phase), 2) ovariectomized ewes 120 min after systemic vehicle or E2β (5 μg/kg iv) treatment, and 3) ovariectomized ewes on days 0, 3, 6, 8, and 10 of E2β (5 μg/kg iv, followed by 6 μg/kg per day) treatment. Expression of eNOS was localized primarily to the endothelium rather than vascular smooth muscle (VSM) in all arteries examined by immunohistochemistry and Western analysis; inducible NOS was not detected in either endothelium or VSM. Expression of eNOS protein was greater ( P < 0.05) in uterine, but not in systemic, artery endothelium-isolated protein collected from follicular versus luteal phase ewes. Acute systemic E2β treatment of ovariectomized ewes increased ( P < 0.05) eNOS protein levels in uterine artery endothelium. Prolonged E2β administration progressively increased uterine, but not systemic, artery endothelial eNOS protein expression. Therefore, the increased local estrogen-to-progesterone ratio during the follicular phase locally elevates eNOS expression, which possibly elevates uterine blood flow. These responses can be partly reproduced with E2β administration.


Author(s):  
John L. Beggs ◽  
Peter C. Johnson ◽  
Astrid G. Olafsen ◽  
C. Jane Watkins

The blood supply (vasa nervorum) to peripheral nerves is composed of an interconnected dual circulation. The endoneurium of nerve fascicles is maintained by the intrinsic circulation which is composed of microvessels primarily of capillary caliber. Transperineurial arterioles link the intrinsic circulation with the extrinsic arterial supply located in the epineurium. Blood flow in the vasa nervorum is neurogenically influenced (1,2). Although a recent hypothesis proposes that endoneurial blood flow is controlled by the action of autonomic nerve fibers associated with epineurial arterioles (2), our recent studies (3) show that in addition to epineurial arterioles other segments of the vasa nervorum are also innervated. In this study, we examine blood vessels of the endoneurium for possible innervation.


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