Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were designed to test autologous rectus sheath as a replacement for the thoracic aorta in the growing dog. Adequacy of graft function was determined by angiography at 4 month intervals; stress-strain measurements and microscopic examination were made at the time of autopsy. A 3 cm tubular graft of rectus sheath tissue was employed as an aortic graft in 13 mongrel puppies. Nine puppies (70%) were long-term survivors and were put to death between 6 and 22 months postoperatively. No deaths were due to graft failure. Angiographic studies demonstrated patency of the graft without development of pressure gradients. An increase in diameter of the aorta (21.25%) and the rectus sheath graft %22.87%) were demonstrated in all cases. During the time of observation, the compliance of the growing aorta (93,120 dynes/cm2) decreased to one fourth that of the control aortic tissue (24,800 dynes/cm2), whereas the compliance of the rectus sheath graft (547,1000 dynes/cm2) decreased to only one eighth that of the control rectus sheath (47,400 dynes/cm2). Tensile strength is maintained in both the growing aorta (4.5 x 10(7) dynes/cm2) and the rectus sheath graft (4.7 x 10(7) dynes/cm2; p less than 0.05). Microscopic examination showed no calcification, thinning, or weakness. Vascularization of the graft had occurred, with cellular proliferation and development of more than 30 lamellar-like units in the media and an adventitia-like surface.
J Thorac Cardiovasc Surg 1979 Nov
PMID:Autologous rectus sheath grafts. V. Growth in aortic grafts. 15 82

CI-959, a cell-activation inhibitor that prevents the formation of oxygen-derived free radicals by inflammatory cells, was studied to determine its effects on myocardial infarct size and subsequent scar formation in dogs. The left circumflex coronary artery was occluded for 90 min, followed by 6 h of reperfusion. Drug infusion was started 15 min before reperfusion at a loading dose of 8 mg/kg i.v., followed immediately by 2 mg/kg i.v. infused over 80 min. The infarct size, assessed by TTC staining techniques, was significantly reduced in 12 dogs treated with CI-959 (23.3 +/- 3.6% of the area at risk) when compared to 11 vehicle-treated animals (35.5 +/- 4% of the area at risk, p less than 0.05). This reduction in infarct size was not attributed to changes in regional myocardial blood flow, as measured by radioactive microspheres, or to a reduction in myocardial oxygen demand, as estimated by changes in the rate-pressure product. The scar thickness, measured after a 6-week recovery period in 9 animals treated with CI-959, was not significantly reduced in comparison with 11 controls. In vitro, CI-959 effectively inhibited oxygen free radical formation by canine neutrophils. The results of this study show that CI-959 significantly reduces the myocardial infarct size without causing scar thinning, which might lead to ventricular aneurysm, and suggests the most likely mechanism for its beneficial action is the prevention of formation of toxic oxygen radicals.
J Cardiovasc Pharmacol 1992 Oct
PMID:Reduction of canine myocardial infarct size by CI-959, an inhibitor of inflammatory cell activation. 128 Jul 19

We have previously described a new surgical technique for control of arrhythmogenic foci in patients with recurrent ventricular tachycardia that we call balloon electric shock ablation. With this method sequential shocks are delivered to a grid of electrodes on a balloon that can be introduced across the mitral valve into the intact ventricle. A series of experiments was undertaken to investigate possible deleterious effects of balloon electric shock ablation when shocks are delivered directly to the mitral valve apparatus. In six animals shocks totaling 1200 joules were given through a closely spaced electrode grid applied to the area of the mitral valve. Nine to 12 weeks later, left ventricular and mitral valve function were assessed. Balloon electric shock ablation in the basilar portion of the ventricle was associated with decreased myocardial performance, as evidenced by ejection phase indices. In five of six animals balloon ablation led to minor thickening of the valve leaflets and chordal attachments plus necrosis of adjacent myocardium, including papillary muscles. In these animals there was no significant dysfunction of the valve observed. In the remaining animal, however, ablation was centered on the posterior papillary muscle and resulted not only in necrosis of the base of the papillary muscle but also in full-thickness scarring and thinning of the adjacent left ventricular wall. In this dog, mitral regurgitation was seen on long-term follow-up. We conclude that when balloon electric shock ablation is used to destroy a localized area of myocardium in the basilar portion of the intact ventricle, the procedure results in decreased myocardial performance. When shocks were directly applied to the mitral valve apparatus in five of six animals, ablation did not result in significant negative effects on the structure and function of the valve. In the sixth dog, however, shock delivery resulted in transmural necrosis and thinning at the site of papillary muscle insertion and was associated with severe mitral regurgitation with volume loading. Therefore caution should be used when considering clinical application of this technique if the area to be ablated is in the basal portion of the heart.
J Thorac Cardiovasc Surg 1992 Apr
PMID:Surgical treatment of ventricular tachycardia by balloon electric shock ablation. Potential effects on the mitral valve apparatus. 154 4

This study attempted to evaluate the efficacy of chronic extra-aortic counterpulsation with a latissimus dorsi neuro vascular flap. Five dogs had a preliminary procedure consisting of the creation of a latissimus dorsi flap and a thoracotomy in which the flap was wrapped around the descending aorta just distal to the left subclavian artery. An epicardial lead was placed on the left ventricle and a nerve stimulating lead placed around the thoraco-dorsal nerve. Three weeks later, both leads were connected to a cardiomyostimulator programmed to function in a counterpulsation mode with a 1:2 assist frequency. Hemodynamic measurements were made at 6 and 8 and 10 and 12 weeks and the dogs were sacrificed. Three dogs had all sets of hemodynamic measurements made. Two of the three dogs demonstrated diastolic augmentation at 6 and 8 and 10 and 12 weeks average 20 to 25 mmHg. The third dog failed to demonstrate any change. All dogs were sacrificed at 12 weeks and specimens were submitted for histologic evaluation. The muscle flap was preserved in all animals. The aorta subjacent to the flap showed, (1) normal intima with no evidence of disruption or thrombus in all animals, (2) in the animals in whom counterpulsation was observed, there appeared to be thinning of the media in the aorta subjacent to the muscle flap, and (3) no evidence of distal emboli. This study demonstrated that chronic counterpulsation can be obtained with a latissimus dorsi flap. The actual hemodynamic benefits are not determined from this study. The medial thinning in the aortic wall may limit the long-term benefit of this procedure.
J Cardiovasc Surg (Torino)
PMID:Physiologic and pathologic evaluation of chronic extra-aortic counterpulsation with latissimus dorsi flap. Preliminary results. 186 78

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.
J Thorac Cardiovasc Surg 1990 Nov
PMID:Simulated left ventricular aneurysm and aneurysm repair in swine. 223 42

An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and uninfarcted regions of the myocardium are equally involved in the process. The remodeling process comprises left ventricular wall thinning (mainly due to cell slippage), chamber dilatation, and compensatory hypertrophy of the uninfarcted segment of the myocardium. The hypertrophy may initially be physiologic but may ultimately become a pathologic process, and thereby contribute to pump dysfunction. The possible reasons why the ventricular hypertrophy may ultimately be dysfunctional include alterations in local architecture and their sequelae alone or in concert with local changes in the beta-adrenergic, alpha-adrenergic, or renin angiotensin systems. At the present time, there are encouraging data to suggest that nitroglycerin, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process.
Cardiovasc Drugs Ther 1990 Oct
PMID:Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. 214 59

Ketanserin is a serotonin antagonist with age-related antihypertensive efficacy. Its effects on left ventricular (LV) function and hypertrophy have not been adequately reported. We studied noninvasively 54 elderly hypertensives before and 6 months after ketanserin monotherapy. Mean blood pressure was controlled (174/101 to 145/86 mmHg, p less than 0.0001) with no heart rate changes. LV dimensions and volumes remained unchanged, as did all LV ejection indices, thus preserving LV output (p = ns). Total peripheral resistances fell (from means of 1986 to 1615 dynes, cm.s-5, p less than 0.0001), as did LV systolic wall stresses. Mean LV mass was reduced (248 to 237 g, p less than 0.0001), mainly due to interventricular septum thinning (11.8 to 11.1 mm, p less than 0.0001), resulting in a decrease in mean LV cross-sectional area (21.3 to 20.5 cm2, p less than 0.0001) and mass/volume ratio (2.14 to 2.01 p = 0.0001). Thus, LV hypertrophy regression did not affect contractility (LV mass index relation to stress/end-systolic volume index, r = -0.558 before and r = -0.564 after ketanserin therapy). It is concluded that ketanserin is an effective antihypertensive agent in the elderly that reduces LV hypertrophy indices and maintains cardiac output, with no concomitant burdening on LV hemodynamics.
Cardiovasc Drugs Ther 1990 Jan
PMID:Left ventricular hypertrophy regression and function changes with ketanserin in elderly hypertensives. 214 17

Although the perfluorochemical Fluosol-DA 20% has been shown to reduce myocardial infarct size, its effect on the evolution of infarct healing has not been determined. Rabbits (n = 91) were randomized to ether-oxygenated Fluosol-DA (20 ml/kg) administered intravenously at the time of reperfusion after 30 min of coronary occlusion or no intervention. Animals were sacrificed at 1, 3, 7, and 14 days after infarction. Infarct size was significantly reduced in Fluosol-DA treated animals when compared with controls at one and three days. Infarct thinning was observed at one and three days in both groups. Left ventricular wall thickness in the infarcted area was greater with Fluosol-DA than control at 7 and 14 days. Increasing amounts of foamy macrophages containing perfluorochemical particles were noted in treated animals at 7 and 14 days. No differences were noted in hydroxyproline content between groups. These studies suggest that Fluosol-DA results in persistence of foamy macrophages without significantly altering infarct topography in the temporary occlusion rabbit model.
Am J Cardiovasc Pathol 1990
PMID:The effect of perfluorochemical fluosol-DA (20%) on myocardial infarct healing in the rabbit. 233 63

Despite the rat heart having very low collateral flow, there are many reports of pharmacological limitation of infarct size in rats with permanent coronary occlusion. Investigating possible artefacts, cardiac function was measured in isolated rat hearts (n = 12/group) 1, 2, 4, 6, 12, 18, 24, or 48 h after permanent coronary occlusion. In sham operated controls, cardiac output was 63.8 +/- 3.8 ml/min; in rats with occlusion this fell to 37.7 +/- 3.3 ml/min after 1 h of occlusion and did not increase during the 48 h of study. Lumen areas, areas of underperfusion, and minimum wall thickness were unchanged after 4 h of occlusion. Between 4 and 12 h, substantial wall thinning occurred (midinfarct wall thickness decreased from 3.69 +/- 0.24 mm to 2.01 +/- 0.16 mm). After 12 h of occlusion, wall thinning and expansion of the infarct increased lumen volume by three- to fourfold. Wall thinning resulted in a progressive decrease in the volume of the zone of underperfusion (which decreased by almost 30% over 48 h). Tetrazolium negative tissue was not evident in the first 4 h of occlusion but by 12 h, 85.0 +/- 2.6% of the underperfused tissue was necrotic. Gross examination of sections often indicated apparently tetrazolium positive tissue within the zone of underperfusion. Microscopic examination of histological sections revealed this tissue to be necrotic but, in contrast to the tetrazolium negative tissue within the zone of underperfusion, not yet subject to white cell infiltration. "Apparent" infarct size limitation in the rat heart might be due to: (1) incorrect designation of tissue as tetrazolium positive within the severely ischaemic zone of underperfusion; (2) inappropriately equating the zone of underperfusion (measured at the end of ischaemia) to the risk zone (measured at the onset of ischaemia); (3) the possibility that some drugs might affect white cell infiltration, tetrazolium staining characteristics, wall thinning, and tissue remodelling.
J Cardiovasc Pharmacol 1988 Jun
PMID:Evolving myocardial infarction in the rat in vivo: an inappropriate model for the investigation of drug-induced infarct size limitation during sustained regional ischaemia. 245 66

Thinning and dilatation (expansion) of the infarct region and complete rupture of the ventricular wall are significant complications of acute transmural myocardial infarction associated with increased morbidity and mortality. The pathogenesis of these related events is unknown. Recent studies of myocardial connective tissue have delineated an extensive array of intercellular and pericellular structures which serve as a skeletal framework and which may modulate contractile activity. We have employed a modified silver impregnation method to visualize the connective tissue components by light microscopy. To explore whether the skeletal framework is altered in acute myocardial infarction with and without ventricular rupture, we studied 9 human hearts at autopsy, and 4 canine infarcts of known duration. The human infarctions included 4 nonruptured cases with infarcts 1-5 days old, and 5 ruptured cases with infarcts 3-10 days old. Sections from normal, lateral, and central infarct or ventricular rupture sites were stained with silver. The normal tissue from each heart served as a control. Silver staining was moderately decreased in the lateral infarct zones, and markedly decreased in the central non-ruptured infarct zones. In the 5 ventricular rupture cases, the rupture site had no silver staining. A similar pattern was observed in the 4 canine infarcts. Thus, we conclude that the skeletal framework is markedly altered in the central zone of acute myocardial infarction. The acute changes of silver stained connective tissue may contribute significantly to the development of infarct expansion or ventricular wall rupture.
Am J Cardiovasc Pathol 1987 Jan
PMID:Alterations of the myocardial skeletal framework in acute myocardial infarction with and without ventricular rupture. A preliminary report. 245 17


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