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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

The dynamic geometry of the left ventricle was assessed with the use of chronically implanted pulse-transit ultrasonic dimension transducers. The orientation of the transducers allowed the measurement of left ventricular minor and major axis diameters and equatorial wall thickness in the conscious dog. The left ventricle was modeled as a three-dimensional, prolate ellipsoidal shell. Left ventricular and pleural pressures were measured with high fidelity micromanometers. Aortic blood flow was obtained with electromagnetic flow probes. To test the assumptions inherent in this technique, left ventricular mass, internal volume, stroke volume, and peak aortic flow were computed from the dimension data and compared to directly measured values. Correlation coefficients of 0.95 or greater were obtained for each of these comparisons. In addition, the calculated left ventricular mass was constant to within +/- 6% of the mean value throughout the cardiac cycle. We found that the dynamic contraction pattern of the left ventricle was dependent on the physiological state of the dog. Furthermore, in the conscious state, shortening of the minor axis diameter, lengthening of the major axis diameter, and slight thickening or thinning of the wall were noted during isovolumic contraction (isovolumic ellipticalization pattern). In the open-chested, anesthetized state, however, marked rearrangements in geometry were observed during isovolumic contraction manifested by lengthening of the minor axis diameter, and significant thickening of the wall (isovolumic sphericalization pattern). We also observed that left ventricular volume was significantly diminished in the open-chested state. The isovolumic contraction pattern in open-chested dogs could be changed from sphericalization to ellipticalization by increasing end-diastolic volume with the infusion of saline. During a vena caval occlusion in the conscious state, the contraction pattern changed from isovolumic ellipticalization to isovolumic sphericalization as the end-diastolic volume decreased. Thus, the exact pattern of left ventricular contraction was found to be a function of left ventricular volume.
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PMID:The three-dimensional dynamic geometry of the left ventricle in the conscious dog. 78 42

A simple implantable device was applied to the left middle cerebral artery of adult cats. One week later the artery was occluded acutely while the animals were conscious. Forced circling and tonic deviation of the head and neck toward the left were noted within seconds of occlusion. A right hemiparesis developed one to two minutes later. Cerebral angiography confirmed the presence of the middle cerebral artery occlusion when the occluding stylet was inserted. Removal of the stylet resulted in reopening of the artery. Light microscopic examination of the brains revealed severe acute ischemic changes in a large left cortical and subcortical area. Partial loss of endothelial lining and thinning of the media were demonstrated in the compressed segment of the middle cerebral artery.
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PMID:Implanted device for middle cerebral artery occlusion in conscious cats. 84 93

Longitudinal stretch of the rabbit basilar artery produces local injury followed by prolonged circular constriction. After stretching and rapid release in vitro localized constrictions promptly occurred. This could be prevented by prior treatment with cyanide or calcium-free solution. Once produced, constrictions persisted for more than 72 hours. Previously induced constriction was not reversed by treatment for two hours with cyanide or by removing calcium. Histological observation indicated that constricted areas were associated with a discrete circumferential rupture of the internal elastic lamina and disruption and thinning of the underlying media. Specific catecholamine fluorescence at the adventitio-medial junction was unchanged in constricted areas. The relationship between smooth muscle cell length and resting tension of artery segments with and without constrictions was compared. Segments with constrictions had a shorter muscle length for any given resting tension, which confirms that constriction was not due to passive collapse of the vessel wall. These findings suggest that injury of cerebrovascular smooth muscle may result in essentially irreversible vasoconstriction. Such a mechanism could contribute to the pathogenesis of prolonged cerebral vasospasm after SAH or traumatic injury to the cerebrum.
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PMID:An in vitro study of prolonged vasospasm of a rabbit cerebral artery. 126 10

To determine whether modulation of systolic ventricular interaction influences right ventricular performance during right heart ischemia, the effects of septal ischemia and inotropic stimulation were studied in 15 dogs in an open chest preparation. Right coronary branch occlusions led to right ventricular dilation and free wall dyskinesia, reversed septal curvature and reduced left ventricular diastolic volume. In systole, the septum thickened but bulged paradoxically into the right ventricle generating an active but depressed right ventricular systolic pressure (28.9 +/- 5.5 to 22.1 +/- 4.5 mm Hg), with associated decreases in right ventricular stroke work (5.66 +/- 0.94 to 1.92 +/- 0.53 g.m/m2) and left ventricular systolic pressure (123 +/- 11 to 80 +/- 10 mm Hg). Septal ischemia induced systolic septal thinning, left ventricular dilation and decreased left ventricular systolic pressure (80 +/- 10 to 55 +/- 10 mm Hg) and stroke work. Although the extent of paradoxic septal displacement increased, there were further decrements in right ventricular systolic pressure (22.1 +/- 4.5 to 18.7 +/- 4.3 mm Hg) and stroke work (1.92 +/- 0.53 to 0.7 +/- 0.2 g.m/m2). Dopamine infusion augmented left ventricular free wall contraction and increased left ventricular systolic pressure (55 +/- 10 to 172 +/- 17 mm Hg) and stroke work. Although systolic septal thinning persisted, the extent of paradoxic septal displacement increased strikingly and, despite continued right ventricular free wall dyskinesia, right ventricular systolic pressure increased (18.7 +/- 4.3 to 39.6 +/- 6.2 mm Hg) as did right ventricular stroke work (0.7 +/- 0.2 to 7 +/- 1.6 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of left ventricular function and systolic ventricular interaction to right ventricular performance during acute right heart ischemia. 153 32

Patch reconstruction of left ventricular aneurysm may be superior to linear closure, but this hypothesis has not been tested experimentally. Accordingly, six anesthetized domestic pigs were instrumented to measure regional left ventricular wall thickening, stroke volume, systolic left ventricular pressure, and myocardial oxygen consumption. With total bypass and cardioplegia, a 6 by 8 cm Dacron patch was inserted into the anteroapical left ventricle. Simulations were as follows: left ventricular aneurysm, patch open; patch reconstruction, 50% patch plication; standard repair, ventriculotomy edges approximated. Global function, from stroke work (stroke volume x integral of left ventricular pressure)-left ventricular end-diastolic pressure curves, was depressed in all three simulations compared with control. A tendency for stroke work to be greater for standard repair than for left ventricular aneurysm and patch reconstruction at higher preloads was not statistically significant. Mechanical efficiency, from stroke work/myocardial oxygen consumption (joules per milliliter oxygen per beat), was 2.43 +/- 0.52 (mean +/- standard error of the mean) (control), 2.22 +/- 0.94 (standard repair), 1.27 +/- 0.39 (patch reconstruction), and 1.09 +/- 0.37 (left ventricular aneurysm) (no significant differences). Regional work was calculated as regional left ventricular wall thickening x integral of left ventricular pressure. The slope of the regional work-end-diastolic wall thickness relation decreased in the posterior wall 14.0 +/- 2.9 (control) versus 8.4 +/- 2.0 (left ventricular aneurysm), 6.9 +/- 1.4 (patch reconstruction), and 7.4 +/- 1.4 (standard repair) (p less than 0.05). In the anterior wall, contractility did not change significantly (7.4 +/- 1.2, control; 7.8 +/- 2.7, left ventricular aneurysm; 5.0 +/- 0.4, patch reconstruction; and 5.3 +/- 0.4, standard repair). Decreased end-diastolic wall thinning anteriorly suggested tethering. These results in the normal left ventricle suggest that patch ventriculoplasty is of no greater benefit than linear repair. Either repair may impede function of adjacent myocardium through restriction of regional diastolic lengthening.
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PMID:Simulated left ventricular aneurysm and aneurysm repair in swine. 223 42

There is a distinct inverse relationship between the force and the extent or velocity of muscle shortening in isolated muscle at a constant resting muscle length or in the intact heart with the preload and inotropic state held constant. In the normal ventricle, however, preload is usually allowed to increase as the aortic pressure is augmented, and the stroke volume tends to be maintained constant. Such complex interaction between increases in preload and afterload can be analyzed by a two dimensional framework in terms of the appropriateness of the matching between afterload and the level of inotropic state as modulated by preload. The initial response to chronic volume overload consists of near maximum use of the Frank-Starling mechanism. An increase in afterload due to the wall thinning and increased chamber size does not produce a fall of wall shortening. As an eccentric hypertrophy develops with series addition of sarcomeres, a delivery of much larger stroke volume is attained without any further use of the Frank-Starling mechanism, with a optimal extent of wall shortening per unit of circumference. Acute severe pressure overloading causes an acute afterload mismatch despite the maximum use of preload reserve. Subsequently, chronic adaptation takes place with development of concentric hypertrophy which returns the ventricle to the control force-velocity curve. As wall thickening accomplishes a decrease in wall stress, wall shortening also becomes normal. Thus, chronic mechanical overload is initially adjusted by an adequate hypertrophy to correct afterload mismatch. Inadequate hypertrophy results in an elevation of wall stress and produces a decrease in stroke volume with the expenditure of the preload.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac hypertrophy as early adjustments to a chronically sustained mechanical overload. 315 60

Moyamoya disease was originally defined as a characteristic syndrome of recurrent headaches, occlusion of the distal internal carotid arteries and the foggy (moyamoya) clusters of collateral vessels at the base of the brain as demonstrated by cerebral angiography. The etiology is unknown and pathobiology is poorly understood. We examined the intracranial arteries in 3 patients to demonstrate characteristic changes and to obtain a better understanding of the basis mechanisms of the disease. Controls were obtained from 3 normotensive patients who died as a result of cancer. Occluded internal carotid arteries were characterized by severe thickening of the intima with a dense luminal array of smooth muscle cells, a deeper less cellular zone, pronounced tortuosity of the internal elastica and thinning of the media. Collateral vessels were arterial in structure and were affected by similar proliferative changes in the intima, thinning of the media, and contorted internal elastica. Stainable lipids were not part of the typical components. Severe contortion of the internal elastica, medial damage and intimal proliferation may result from recurrent and sustained spasticity of the cerebral arteries. The distal lenticulostriate arteries showed severe medial damage similar to what is termed as a moth-eaten change in hypertensive patients dying of massive cerebral hemorrhage.
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PMID:Ultrastructural studies of cerebral arteries and collateral vessels in moyamoya disease. 646 67

The geometry of arterial bifurcations appears to play a significant role in the development of vascular disease. We have investigated the changes in bifurcation geometry with changes in distending pressure over the range 0.0 to 190.0 mm Hg. Five cerebral arterial bifurcations from human subjects were studied. The investigation focussed on the shape and on changes in the shape of the leading edge of the flow divider (internal apical curve). The curve outline at each transmural pressure increment (each 10.0 mm Hg) was photographed and digitized. The curves were plotted serially on an expanded scale. Visual comparison of the curves indicated flattening in the central region and broadening of the shoulders of the curves with increasing transmural pressure. Regression analysis using second order polynomials was used to obtain coefficients for equations defining short, overlapping segments of each curve. Twenty-four coordinates were used for each successive regression. Each curve was characterized by 85 to 100 digitized coordinates. The regression equations for each curve were used to calculate the curvature parameter, K, and the radius of curvature, R. Three of the five bifurcations demonstrated a negative correlation of K with increasing transmural pressure (p less than .001). This result supports the visual observation that the internal apical curve flattens with increasing transmural pressure. Flattening of the internal apical curve together with thinning of the arterial wall with increasing transmural pressure would contribute to a stress concentration at the apex of a cerebral bifurcation. This stress concentration would be more pronounced in the presence of a medial gap at the apex of the bifurcation. It is on or near this region of stress concentration that aneurysms develop.
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PMID:Shape changes at the apex of isolated human cerebral bifurcations with changes in transmural pressure. 682 89

The effects of step-wise reduction in left circumflex coronary blood flow on: 1) posteroinferior wall dynamics; 2) normally-perfused anterior wall dynamics; and 3) cavity function were assessed simultaneously by roentgen videometric analysis of left ventricular angiograms in open-chest dogs during normal and increased afterload. At control coronary flow with normal afterload, peak rates of systolic thickening and diastolic thinning of the posteroinferior and anterior walls were similar. Step-wise reduction in circumflex coronary flow resulted in a progressive fall in systolic and diastolic posteroinferior wall dynamics. Increased LV afterload resulted in a decrease in posteroinferior wall dynamics even at control coronary flow, and reduction in flow resulted in even greater deterioration than occurred with normal afterload. The decrease in posteroinferior wall dynamics with reduction in circumflex coronary flow was accompanied by an increase in peak rates of systolic thickening and diastolic thinning of the normally perfused anterior wall. The level of coronary blood flow at which this increase in anterior wall dynamics occurred, varied with LV loading conditions, occurring earlier when afterload was increased. There was no earlier or greater decrease in diastolic than systolic wall dynamics with progressive reduction in coronary flow with either normal or increased afterload. Left ventricular end-diastolic volume, end-diastolic pressure and ejection fraction changed little until coronary blood flow was reduced to 50% of control; by contrast, stroke-work was exquisitely sensitive to changes in coronary flow. There was no correlation between changes in regional and cavity systolic or diastolic function. The delay in onset of LV cavity dysfunction with ischemia may have been partly due to the "compensatory increase" in anterior wall dynamics, counterbalancing the impaired posteroinferior wall dynamics.
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PMID:Effects of progressive reduction in coronary blood flow on regional and global left ventricular contraction and relaxation during normal and increased afterload: a roentgen videometric study. 717 76


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