Straight Arteries Research Articles

Observations on the vascular pattern of the septum of normal and hypertrophied human hearts.

The arterial vascular pattern of the myocardium of the interventricular septum of normal and hypertrophied human hearts was studied by post-mortem injection of a radio-opaque medium, Colourpaque, and the taking of microradiographs of transverse ventricular slices using the immersion technique. There were large penetrating septal arteries arising from the anterior and posterior descending coronary arteries. The arterial vascular pattern on each side of the septum closely resembled the respective patterns in the right and left ventricular free walls. In the hypertrophied hearts the branching and straight type arteries were of smaller calibre compared to normal hearts and were smallest in the greatly hypertrophied hearts and hearts with asymmetrical left ventricular hypertrophy. The role of the septal intercoronary anastomosis in coronary artery disease is discussed.

Observations on the vascular pattern of the left ventricular freewall in normal and hypertrophied hearts.

The arterial vascular pattern of the myocardium of the left ventricular freewall of normal and hypertrophied human hearts was studied by post mortem injection of a radio-opaque medium Colourpaque, and the taking of microradiographs of transverse ventricular slices using the immersion technique. The branching type arteries supplied the myocardial wall including the subendocardial zone, the straight type arteries supplied the papillary muscles and the trabeculae carnae. The branching and straight type arteries in the hypertrophied hearts were of smaller calibre than normal hearts. The vascular pattern in the freewall of hearts with concentric left ventricular hypertrophy was similar to those of hearts with asymmetrical left ventricular hypertrophy.

Vascular smooth muscle orientation in straight portions of human cerebral arteries.

A technique of embedding, sectioning and analysis has been developed for studying the orientation and proportional composition of smooth muscle in the straight portions of human major cerebral arteries. Various distortions, which occurred during processing and sectioning, were measured quantitatively. Nerve fibres were implanted as a reference frame within the paraffin block containing an arterial bifurcation. The nuclei of smooth muscle have been treated as three-dimensional vectors of cellular orientation. The projected length in the plane of the section and the section thickness were used to define section pitch. To relate these vectors to the overall geometry of cerebral arteries they were transformed such that the resultant pitch would be the same as that observed if the sections were cut normal to the arterial longitudinal axis. Matrix transformations of nuclear vectors were of the expansion and Eulerian forms. The average pitch for the five sections from three straight portions was -0.22 degrees +/- 2.36 (SD of five means) with a range between -2,8 degrees and 3.2 degrees. Because this pitch is small it is possible to use 6.9 micrometers thick longitudinal and mid-plane sections of straight arteries to obtain estimates of proportional composition. Stereological point counting was used to determine that smooth muscle comprised 72.0% +/- 4.76 (SD for ten segments) of the tunica media in cerebral arteries.

Ethical aspects of plans to combat Huntington's disease--a response.

<h3>Rationale</h3> The role of hypertension in cerebral small vessel disease is poorly understood. At the base of the brain (the ‘vascular centrencephalon’), short straight arteries transmit blood pressure directly to small resistance vessels; the cerebral convexity is supplied by long arteries with many branches, resulting in a drop in blood pressure. Hypertensive small vessel disease (lipohyalinosis) causes the classically described lacunar infarctions at the base of the brain; however, periventricular white matter intensities (WMIs) seen on MRI and WMI in subcortical areas over the convexity, which are often also called ‘lacunes’, probably have different aetiologies. <h3>Objectives</h3> We studied pressure gradients from proximal to distal regions of the cerebral vasculature by mathematical modelling. <h3>Methods and results</h3> Blood flow/pressure equations were solved in an Anatomically Detailed Arterial Network (ADAN) model, considering a normotensive and a hypertensive case. Model parameters were suitably modified to account for structural changes in arterial vessels in the hypertensive scenario. Computations predict a marked drop in blood pressure from large and medium-sized cerebral vessels to cerebral peripheral beds. When blood pressure in the brachial artery is 192/113 mm Hg, the pressure in the small arterioles of the posterior parietal artery bed would be only 117/68 mm Hg. In the normotensive case, with blood pressure in the brachial artery of 117/75 mm Hg, the pressure in small parietal arterioles would be only 59/38 mm Hg. <h3>Conclusion</h3> These findings have important implications for understanding small vessel disease. The marked pressure gradient across cerebral arteries should be taken into account when evaluating the pathogenesis of small WMIs on MRI. Hypertensive small vessel disease, affecting the arterioles at the base of the brain should be distinguished from small vessel disease in subcortical regions of the convexity and venous disease in the periventricular white matter.

Studies on the microvasculature of human myocardium.

The microvasculature of human myocardium was examined stereoscopically after the injection of Silicone rubber. Material were 40 normal hearts, three of infants, one of child, and 36 of adults, ranging in age from 27 to 79 years. Three types of arteries, subepicardial, branching, and straight type arteries, were confirmed. The microvascular pattern of left ventricular free wall, the posterior wall of the left ventricle, interventricular septum, right ventricular free wall, papillary muscles, trabeculae carneae, infant heart, and aged heart were also examined. The present study revealed that the inner one-third zone was supplied by the terminal branches of both branching and straight type arteries. In infant heart, the inner zone was wider than that of the adult. In the aged cases, reduction in filling with patchy deficit often appeared in this inner zone. The finding of the aged change was probably caused by the characteristic microvascular pattern, and this suggested that the same anatomical mechanism might commit myocardial infarction.

Plasmatic arterionecrosis and its thrombotic occlusion

The vascular lesions directly responsible for hypertensive intracerebral hemorrhage were studied in autopsy cases, associated with some animal experiments. The immediate cause of the hemorrhage was the rupture of the intracerebral microaneurysms resulted from plasmatic arterionecrosis. At the beginning of the morphogenesis of the arterionecrosis, medial smooth muscle cells of the intracerebral arteries underwent necrosis and disappeared. Subsequently the lumen became somewhat dilated, followed by slight intimal thickening with fibrous tissue. In such intima occurred blood plasma insudation, which induced not only histolysis of the intimal tissue, but also intimal deposition of fibrinoid substance consisting mainly of fibrin. In the striate and thalamic arteries in the basal ganglia, the arterionecrosis and consequent microaneurysms occurred preferably at the bifurcations or in the somewhat distal segments from them. In the medullary arteries in the cortices, however, most of the microaneurysms were found in the just proximal segments from the rectangular bends at the cortico-medullary junction. But they were rarely seen in the straight medullary arteries without bending. These findings suggested the possible role of hemodynamics in the pathogenesis of the arterial lesions. The arterionecrosis was accompanied or not accompanied with the deposition of fibrinoid substance in the intima. In the latter occurred also histolysis due to blood plasma insudation and consequent microaneurysms. The intimal fibrinoid deposition, that is, fibrin deposition, could be considered, like mural thrombi, to have a biological significance of reinforcing the arterial wall that had been affected with marked histolysis. It seemed that microaneurysms most liable to rupture were those revealing the arterionecrosis with neither thrombosis nor dense deposition of abundant fibrin in the intima. The microaneurysms were sometimes occluded by thrombi and saved from rupture. The occluded lesions, however, were one of the causes of cerebral infarction. Twenty-six % of infarcts in the basal ganglia were caused by the occluded microaneurysms. The microaneurysms in the cortices were more liable to be occluded by thrombi than those in the basal ganglia, presumably because of the lower blood pressure in the former according to the law of Hagen-Poiseuille.

Reevaluation of arterial constitutive relations. A finite-deformation approach.

The purpose of this investigation was to use the finite-deformation theory of elasticity to interpret pressure-diameter data for in situ canine aortas and other arterial response data reported in the literature. A meaningful mechanical property for arterial tissue was identified as ∂ W 1 /∂ I , the partial derivative of the strain-energy density function with respect to the first strain invariant. An exponential function was found to characterize the mechanical property ∂W 1 /∂I for all arteries considered. Thin-walled tube stress approximations were found to result in inaccurate values for arterial stresses and incremental elastic mechanical properties. Wave speeds calculated using ∂ W 1 /∂ I for these arterial tissues agreed well with experimental measurements of wave speeds reported in the literature. Elevated values for strain-energy density were found in the inner arterial tissue layers. These high values for strain energy may contribute to atherogenesis in relatively straight arteries (e.g., the abdominal aorta) subjected to hypertension.

Urinary Oxygen Pressure in Renal Parenchymal and Vascular Disease

Sarre,¹in 1938, observed a consistently lower oxygen pressure (Po₂) in the urine than in renal-vein blood. Twenty years later, this finding was confirmed by Reeves et al²who attributed the disparity to the cell-separation, plasma-skimming mechanism proposed by Pappenheimer and Kinter.³According to this concept, the urinary oxygen pressure (Puo₂) is controlled by renal hemodynamic factors. The rapid blood flow through the long straight interlobular arteries results in a midstream concentration of red blood cells and a marginal sheath of low-hematocrit plasma. The afferent glomerular arterioles, which take off at right angles from the interlobular arteries, are fed from the periphery of the stream. Thus each tier of glomeruli, from the deep to the outer cortex, receives blood of increasingly higher hematocrit. The renal medulla, which derives its blood supply from the efferent arterioles of the juxtamedullary glomeruli (the vasa recta), therefore receives cell-poor,