Intrarenal arterial collateral circulation.

In three cases of intrarenal arterial collateral circulation the collateral channels developed between interlobar arteries in diseased kidneys. Probably these originated in hypertrophied spiral vessels that had arisen from the interlobar arteries in the area of the minor calyces. This form of collateral circulation will undoubtedly be recognized more frequently with the increased use of magnification radiography.     

Effect of multiple arterial haemorrhage on the coronary circulation

In the open-chest anesthetized dog, multiple arterial haemorrhage induces a reduction of the mean coronary flow, an absote or relative increase of the phasic flow during the early ventricular ejection phase and a decrease during the remaining phases of the cardiac cycle. When blood pressure falls sharply during the haemorrhage, coronary vascular resistance increases, whereas it does not change or decreases when blood pressure falls slowly. Moreover, coronary vascular resistance decreases transiently after the stoppage of the haemorrhage.     

Wave propagation in a model of the arterial circulation

The propagation of the arterial pulse wave in the large systemic arteries has been calculated using a linearised method of characteristics analysis to follow the waves generated by the heart. The model includes anatomical and physiological data for the 55 largest arteries adjusted so that the bifurcating tree of arteries is well matched for forward travelling waves. The peripheral arteries in the model are terminated by resistance elements which are adjusted to produce a physiologically reasonable distribution of mean blood flow. In the model, the pressure and velocity wave generated by the contraction of the left ventricle propagates to the periphery where it is reflected. These reflected waves are re-reflected by each of the bifurcations that they encounter and a very complex pattern of waves is generated. The results of the calculations exhibit many of the features of the systemic arteries, including the increase of the pulse pressure with distance away from the heart as well as the initial decrease and then the large increase in the magnitude of back flow during late systole going from the ascending aorta to the abdominal aorta to the arteries of the leg. The model is then used to study the effects of the reflection or absorption of waves by the heart and the mechanisms leading to the incisura are investigated. Calculations are carried out with the total occlusion of different arterial segments in order to model experiments in which the effects of the occlusion of different arteries on pressure and flow in the ascending aorta were measured. Finally, the effects of changes in peripheral resistance on pressure and velocity waveforms are also studied. We conclude from these calculations that the complex pattern of wave propagation in the large arteries may be the most important determinant of arterial haemodynamics.     

Effect of changes in arterial oxygen content on circulation and physical performance.

To evaluate the effect of different levels of arterial oxygen content on hemodynamic parameters during exercise nine subjects performed submaximal bicycle or treadmill exercise and maximal treadmill exercise under three different experimental conditions: 1) breathing room air (control); 2) breathing 50% oxygen (hyperoxia); 3) after rebreathing a carbon monoxide gas mixture (hypoxia). Maximal oxygen consumption (Vo2 max) was significantly higher in hyperoxia (4.99 1/min) and significantly lower in hypoxia (3.80 1/min) than in the control experiment (4.43 1/min). Physical performance changes in parallel with Vo2 max. Maximal cardiac output (Qmax) was similar in hyperoxia as in control but was significantly lower in hypoxia mainly due to a decreased stroke volume. A correlation was found between Vo2 max and transported oxygen, i.e., Cao2 times Amax, thus suggesting that central circulation is an important limiting factor for human maximal aerobic power. During submaximal work HR was decreased in hyperoxia and increased in hypoxia. Corresponding Q values were unchanged except for a reduction during high submaximal exercise in hyperoxia.     

Abnormal arterial flows by a distributed model of the fetal circulation

Modeling the propagation of blood pressure and flow along the fetoplacental arterial tree may improve interpretation of abnormal flow velocity waveforms in fetuses. The current models, however, either do not include a wide range of gestational ages or do not account for variation in anatomical, vascular, or rheological parameters. We developed a mathematical model of the pulsating fetoumbilical arterial circulation using Womersley's oscillatory flow theory and viscoelastic arterial wall properties. Arterial flow waves are calculated at different arterial locations from which the pulsatility index (PI) can be determined. We varied blood viscosity, placental and brain resistances, placental compliance, heart rate, stiffness of the arterial wall, and length of the umbilical arteries. The PI increases in the umbilical artery and decreases in the cerebral arteries, as a result of increasing placental resistance or decreasing brain resistance. Both changes in resistance decrease the flow through the placenta. An increased arterial stiffness increases the PIs in the entire fetoplacental circulation. Blood viscosity and peripheral bed compliance have limited influence on the flow profiles. Bradycardia and tachycardia increase and decrease the PI in all arteries, respectively. Umbilical arterial length has limited influence on the PI but affects the mean arterial pressure at the placental cord insertion. The model may improve the interpretation of arterial flow pulsations and thus may advance both the understanding of pathophysiological processes and clinical management.     

Numerical simulation of blood flow and pressure drop in the pulmonary arterial and venous circulation

A novel multiscale mathematical and computational model of the pulmonary circulation is presented and used to analyse both arterial and venous pressure and flow. This work is a major advance over previous studies by Olufsen et al. (Ann Biomed Eng 28:1281–1299, 2012) which only considered the arterial circulation. For the first three generations of vessels within the pulmonary circulation, geometry is specified from patient-specific measurements obtained using magnetic resonance imaging (MRI). Blood flow and pressure in the larger arteries and veins are predicted using a nonlinear, cross-sectional-area-averaged system of equations for a Newtonian fluid in an elastic tube. Inflow into the main pulmonary artery is obtained from MRI measurements, while pressure entering the left atrium from the main pulmonary vein is kept constant at the normal mean value of 2 mmHg. Each terminal vessel in the network of ‘large’ arteries is connected to its corresponding terminal vein via a network of vessels representing the vascular bed of smaller arteries and veins. We develop and implement an algorithm to calculate the admittance of each vascular bed, using bifurcating structured trees and recursion. The structured-tree models take into account the geometry and material properties of the ‘smaller’ arteries and veins of radii \(\ge \) 50  \(\upmu \) m. We study the effects on flow and pressure associated with three classes of pulmonary hypertension expressed via stiffening of larger and smaller vessels, and vascular rarefaction. The results of simulating these pathological conditions are in agreement with clinical observations, showing that the model has potential for assisting with diagnosis and treatment for circulatory diseases within the lung.     

Insignificant response of the fetal placental circulation to arterial hypotension in sheep

Infusion of the angiotensin-converting enzyme inhibitor enalaprilat into fetal sheep caused a profound arterial hypotension within days. Five fetal lambs were infused with enalaprilat for 8 days starting at day 128 of gestation. Total accumulated dose was 0.30 ± 0.11 mg/kg. Arterial pressure decreased from 43.6 to 25.6 mmHg; venous pressure did not change. Biventricular output was not statistically significantly changed; placental blood flow decreased almost in proportion to the decrease in pressure but the increase in somatic flow was not statistically significant. There were no significant changes in pressure 30 min after the initial 50-μg loading dose of enalaprilat. However, the arterial pressure responses to test doses of ANG I were largely abolished. After 1 day, however, there was a significant decrease in somatic vascular resistance, which became stronger with time, but almost no decrease in the placental resistance. We conclude that the fetal somatic circulation exhibits a slow but strong decrease in resistance but that the response to hypotension is weak or absent in the fetal placenta, possibly because it is already fully relaxed.