Increased Wall Tension Research Articles

Spontaneous Bladder Rupture Following Augmentation Enterocystoplasty

Spontaneous bladder rupture following enterocystoplasty has been reported recently. The etiology remains unclear but appears to be multifactorial. The common factors among the reported patients are a high outlet resistance with total urinary continence and the presence of an augmented, dysfunctional native bladder. This combination may result in the development of high intravesical pressures or increased wall tension through several mechanisms, including over-filling and active contraction in the bowel or detrusor. The presence of an abnormal detrusor may cause the wall tension to be unevenly distributed toward the bowel segment. Diagnosis requires a high degree of suspicion and prompt laparotomy with closure of the defect. Prevention depends on maintaining low bladder volumes and, thus, pressures.

Mechanism of long-term degeneration of arterialized vein grafts

This study examined long-term changes in the morphology and cellular kinetics of rabbit vein grafts transplanted into the carotid artery. Six grafts were studied 1 year after implantation. Although the circumference and thickness of the wall were not different than at 12 weeks, degenerative changes occurred. The endothelial lining of the graft appeared intact, but large segments of the graft surface no longer excluded Evans blue dye, suggesting increased permeability. Collections of red blood cells were noted within the intima. Several grafts had extensive subendothelial fibrin deposits, often associated with foam cells, and evidence of previous hemorrhage, but these changes did not stimulate significant smooth muscle cell proliferation. Increased permeability with entrance of proteins and erythrocytes into the intima may result from increased wall tension or from low shear rates at the wall. Similar changes may lead to atherosclerosis in human vein grafts at late times.

Effect of chronic ibuprofen therapy on early healing of experimentally induced acute myocardial infarction in dogs

Anecdotal evidence has suggested that ibuprofen therapy for concomitant pericarditis may be associated with an increased clinical incidence of ventricular septal rupture after acute myocardial infarction. 1 Decreased tensile strength and increased wall tension in the necrotic region have both been proposed as possible pathogenic factors in cardiac rupture. 2,3 Thus, ibuprofen may “weaken” the myocardium—perhaps by altering the integrity of the native collagen fibroskeleton—and thereby predispose the heart to early postinfarction rupture. This study assesses the effect of chronic pretreatment with high-dose ibuprofen on tensile strength of isolated myocardial samples, left ventricular wall thickness and myocardial collagen content during the initial hours after coronary artery occlusion in an anesthetized dog model of acute myocardial infarction.

Brain-gut interactions: brain stem neuronal response to local gastric effects of substance P

Single-unit activity that responded to phasic gastric distension was recorded extracellularly from neurons in brain stem of anesthetized cats during local substance P chemically induced changes in wall tension. Local gastric intra-arterial administration of substance P via splenic artery often produced a triphasic gastric response. Gastric changes were characterized by 1) an initial brief increase in distension of corpus immediately after peptide and 2) a subsequent contraction that gave way to 3) a prolonged late increase in distension exceeding control levels. The contraction phase was atropine sensitive, suggesting that one mechanism of action during this phase was linked to cholinergic enteric nerves. Distension phases were unaffected by atropine, suggesting a different mechanism of action. Increase in gastric wall tension after peptide resulted in 1) onset of or enhanced activity of brain stem unit during nondistending phase and 2) greater spike discharge per unit change in volume during distending phase in many neurons. Some neurons showed a brief flurry of tonic activity during distending and nondistending phases of the cycle after local gastric injection of peptide with no observable change in wall tension. This suggests that the peptide may also act on chemoreceptors served by vagal primary afferents, which impinge on this neuronal population in the brain stem. Less than 10% of the neurons showed no change in discharge rate after a significant increase in wall tension, which occurred after local gastric injection of substance P, suggesting a mechanism of action involving input from primary vagal afferent fibers serving mucosal receptors unaffected by this level of change in wall tension.(ABSTRACT TRUNCATED AT 250 WORDS)

Preload Dependence of Right Ventricular Blood How: I. The Normal Right Ventricle

Right ventricular (RV) failure is commonly treated with intravascular volume expansion to increase the RV–left atrial pressure gradient and improve left-sided filling. As RV pressure rises, chamber distention occurs and wall tension increases. These studies were designed to determine if increased wall tension might impede RV myocardial blood flow in the normal canine right ventricle and thus contribute to RV failure. Hemodynamic data, the septal–RV free wall dimension, and RV myocardial blood flow were obtained at low and high levels of preload and in both the autoregulated and vasodilated (adenosine, 2 mg per kilogram of body weight per minute) states. Elevated filling pressure decreased RV myocardial blood flow in both the autoregulated (0.85 ± 0.18 to 0.67 ± 0.15 ml/min/gm; p < .05) and vasodilated (2.25 ± 0.50 to 0.85 ± 0.25 ml/min/gm; p < .05) states but did not change the transmural distribution of blood flow to the right ventricle. Vasodilator reserve was markedly impaired in the high-preload state. These observations suggest that preload is an important determinant of RV myocardial blood flow. Volume loading to treat RV dysfunction may be limited by impairment of RV myocardial blood flow.

Shear stress regulation of artery lumen diameter in experimental atherogenesis

We studied the adaptive response of the arterial wall and intimal thickening under conditions of increased flow in an atherogenic model. Blood flow was increased by construction of an arteriovenous fistula between the right iliac artery and vein in six cynomolgus monkeys fed a diet containing 2% cholesterol and 25% peanut oil. The left iliac artery served as the control. Serum cholesterol increased from 135 ± 22 mg/dl to 880 ± 129 mg/dl during the experiment. After 6 months, blood flow in the right iliac artery (420 ± 95 ml/min) was 10 times greater than in the left iliac artery (44 ± 9 ml/min, p < 0.005). Flow velocity in the right iliac artery (31 ± 6 cm/sec) was more than twofold greater than in the left (12 ± 1 cm/sec, p < 0.05). Despite the marked difference in blood flow and flow velocity, calculated wall shear stress was the same in both the right (16 ± 4 dynes/cm2) and left iliac vessels (15 ± 2 dynes/cm2) because of a twofold increase in lumen diameter (p < 0.001) of the right iliac artery. Shear stress in the aorta was also normal (12 ± 2 dynes/cm2). There was no difference in plaque deposition or mean intimal thickness between the right and left iliac arteries. In the right iliac artery there was a twofold increase in media cross-sectional area (p < 0.001) but no change in media thickness or total wall thickness. Tangential wall tension and tangential wall stress were two times greater on the right than on the left (p < 0.001). These results suggest that increased blood flow results in arterial dilatation and normalization of wall shear stress and that shear stress may serve to regulate artery lumen diameter. Increased blood flow and increased flow velocity do not enhance atherosclerotic plaque deposition under these experimental conditions. Arterial enlargement resulting in an increase in wall tension without artery wall thickening or compensatory changes in wall composition may explain the aneurysmal dilatation seen in chronic arteriovenous fistulas and high flow autogenous grafts in human beings.

Local changes in myosin types in diseased human atrial myocardium: a quantitative immunofluorescence study.

Two monoclonal antibody groups were prepared from adult human atrial and ventricular myosin heavy chains. Using these two groups, we were able to identify two myosin variants in human atria and to classify human atrial fibers into alpha-, mixed, or beta-fibers according to the reactivity of the two monoclonal antibody groups to alpha- and beta-myosin heavy chains of normal young and hypothyroid rat ventricles, respectively. The alpha-fiber percentage of the left atria in two normal human hearts was 15% higher than in the right atria. The auricles contained two to three times more alpha-fibers than beta-fibers, whereas the proportion was reversed in the crista terminalis. The mean fiber diameter of the alpha- and beta-fibers was 13.6 +/- 3 micron. A complete alpha- to beta-fiber transition was observed in all atrial regions of two hearts with severe ventricular myocardial infarction; a moderate alpha- to beta-fiber transition was observed only in the left atria of two hearts with primary congestive cardiomyopathy. The mean diameters of the two fiber types were significantly increased in all diseased hearts (19 +/- 3.8 micron). We hypothesize that pressure overload and increased wall tension successively induce an enlargement of the fiber diameter and an alpha- to beta-myosin transition.

Pathophysiology of congestive heart failure

Congestive heart failure is a syndrome that can be caused by a variety of abnormalities, including pressure and volume overload, loss of muscle, primary muscle disease or excessive peripheral demands such as high output failure. In the usual form of heart failure, the heart muscle has reduced contractility. This produces a reduction in cardiac output, which then becomes inadequate to meet the peripheral demands of the body. The 4 primary determinants of left ventricular (LV) performance are generally altered as follows: (1) There is an intrinsic decrease in muscle contractility. (2) Preload or left atrial filling pressure is increased, resulting in pulmonary congestion and dyspnea. (3) Although systemic blood pressure is often reduced, there is an increase in systemic vascular resistance (afterload), which can further reduce cardiac output. (4) Heart rate is generally increased as part of a compensatory mechanism associated with an increase in sympathetic tone and circulating catecholamines. In patients with coronary disease, there is often an imbalance between myocardial oxygen supply and demand. An increase in heart size may be particularly deleterious by increasing wall tension because of the Laplace relation and increasing myocardial oxygen consumption. Intrinsic compensatory mechanisms include an increase in catecholamines, which increase contractility and heart rate in an attempt to maintain cardiac output; cardiac muscle hypertrophy, which helps maintain cardiac function; a rise in LV filling pressure, which can optimize performance according to the Frank-Starling mechanism; and an increase in peripheral arterial-venous oxygen extraction so as to maximize the oxygen delivered for a given cardiac output. Although these compensatory mechanisms are initially helpful, many of them may actually be excessive, such as an increase in catecholamines and systemic vascular resistance.

Conformational stress and anastomotic hyperplasia

Late failure of synthetic vascular grafts to small-diameter arteries (≤4 mm) is commonly due to anastomotic hyperplasia. Theoretic analysis suggests that conformational changes at the anastomosis lead to high localized arterial wall stress caused by increases in radius of curvature of the artery (law of Laplace: tension = pressure × radius). Nine 3 kg rabbits had a plastic insert implanted into the infrarenal aorta. The insert was designed to recreate the conformational changes caused by the anastomosis of a synthetic graft to a small-diameter artery, without significantly altering blood flow. The increase in arterial wall tension created by the insert was calculated to be 80% to 100% over baseline values. Aortography, real-time ultrasound, and computed tomography (CT) scanning were done to confirm the absence of luminal thrombus formation or migration of the insert. Ultrasound and CT scans also confirmed the desired conformational changes in the aorta at the site of the insert. Aortas, with the inserts in place, were removed from 3 days to 6 months after implantation. Implantation times of 1 to 6 months resulted in a hyperplastic subintimal lesion characterized by fibrous tissue deposition, spindle cells (which may have been fibroblasts), and/or smooth muscle cells covered by endothelium. In contrast, two rabbits that had the insert placed and then removed at 1 minute and were allowed to survive for 37 and 72 days, respectively, demonstrated complete healing of the aorta without anastomotic hyperplasia. The arterial wall conformational changes induced in this experiment led to the formation of a lesion consistent with anastomotic hyperplasia. An increase in wall tension may have been the stimulus for this response. Prevention of anastomotic hyperplasia may require a means of uniting a graft to an artery without increasing wall tension.

Optimal postoperative volume loading

Intravenous infusions are required to maintain ventricular preload after uneventful coronary bypass operation. During the early postoperative period, when myocardial metabolic recovery is incomplete, volume loading is intended to stabilize ventricular function and metabolism and to prevent progressive ischemic injury. This study attempts to define the optimal preload for both metabolism and performance. Thirty-seven patients recovering from elective coronary bypass operations and cold potassium cardioplegia underwent volume loading with whole plasma. The initial response (VLA) from a low left atrial pressure (LAP = 7.3 +/- 3.3 mm Hg) was compared with the subsequent response (VLB) from a higher filling pressure (LAP = 10.9 +/- 2.7 mm Hg). Both VLA and VLB produced a similar increase in cardiac index, stroke work index, and end-diastolic volume index (EDVI), and a decrease in ejection fraction (measured by nuclear angiography). Myocardial lactate extraction increased with VLA, but myocardial lactate production resulted with VLB. A careful analysis of these volume loading studies suggested that myocardial performance and compliance were not altered in the early postoperative period. The decrease in ejection fraction with volume loading may have resulted from a combination of increased wall tension and decreased inotropic stimulation. After uneventful coronary bypass surgery, an LAP between 5 and 12 mm Hg corresponded to an EDVI between 30 and 80 ml/m2 and produced adequate cardiac index, stroke work index, and lactate extraction. A lower or higher preload did not improve function and resulted in abnormal metabolism.

Noninvasive Assessment of Changes in Left Ventricular Function Induced by Graded Isometric Exercise in Healthy subjects

This study was designed to characterize the changes in left ventricular performance induced by graded isometric exercise. Fourteen healthy subjects (12 men and 2 women), aged 19 to 27, performed handgrip isometric exercise at 20, 40, and 60 percent of their maximal voluntary contraction (MVC) with three minutes of rest interval between each contraction. Left ventricular performance was assessed by M-mode echocardiography at rest and during each isometric contraction. Left ventricular end-diastolic and end-systolic dimensions did not change significantly. Heart rate and blood pressure increased significantly during each level of isometric contraction. Left ventricular posterior wall thickness fell from 8.6 +/- .4 (mean +/- SE) to 7.1 +/- .5 (P less than 0.01) and 6.5 +/- .4 mm (P less than 0.001) in response to 40 and 60 percent of MVC, respectively. Left ventricular wall thickness to radius ratio decreased progressively as systolic blood pressure increased which suggests increased wall tension. Fractional shortening remained unchanged during graded isometric exercise. However, mean velocity of circumferential fiber shortening (mVcf) increased from 1.08 +/- 0.4 to 1.24 +/- .05 circ/sec (P less than 0.005) in response to 60 percent of MVC. We conclude that the effect of isometric exercise on left ventricular performance depends, to some extent, on the relative strength of muscle contraction. In healthy subjects, isometric exercise of low intensity (less 40 percent of MVC) does not generally result in depression of left ventricular function. Higher levels of isometric exercise may modestly enhance left ventricular performance despite a sudden increase in blood pressure.

Proline and thymidine uptake in rabbit ear artery segments in vitro increased by chronic tangential load.

Indices of structural change were examined in blood vessel walls subjected to increased tangential load in a new, in vitro model system. Ring segments of rabbit ear artery were maintained in organ culture medium for times up to 9 days. Tangential load was chronically applied with small, intraluminal springs made of 0.010 in. diameter stainless steel wire. the applied load was considered to produce levels of circumferential wall tension corresponding to those induced by a range of levels of blood pressure. The indices of structural change examined were the uptake of radioactively-labelled proline and thymidine, which indicate protein synthesis and cell division respectively. Increased uptake of both proline and thymidine was noted in artery segments under elevated mechanical tension after a latency of 3 to 4 days. The degree of uptake was related to the degree of calculated wall tension elevation. The work indicated that cell division and protein synthesis can be induced in the blood vessel wall by increased wall tension alone, in vitro.

Norepinephrine sensitivity, tension development and neuronal uptake in resistance arteries from spontaneously hypertensive and normotensive rats.

Intact segments of mesenteric resistance arteries (200 micron) from 5-month-old spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats were tested for norepinephrine (NE) sensitivity. Dose-response curves were obtained both before and after adrenergic denervation produced by short-term, in vitro, 6-hydroxydopamine (6-OHDA) treatment. NE sensitivities of innervated vessels were the same in SHR and WKY rats, however, after 6-OHDA, not only did both ED50s show significant decreases (8.7- and 3.8-fold, respectively), but the ED50 of SHR vessels was half that of WKY (NE sensitivity increased twofold). In addition there was a 33% increase in wall tension generated in response to maximum NE stimulation, and a 44% increase in neuronal NE uptake in the SHR vessels. These results show that several important alterations have occurred in resistance vessels from SHR rats in the established phase of hypertension. The relationship of the increase in neuronal uptake to the increased total peripheral resistance and increased vascular reactivity commonly seen in SHR perfused beds and whole animals is unknown. However, the increase in NE sensitivity and in maximum NE wall tension could contribute to increase in both of these characteristics.

Is a Left Ventricular Vent Necessary During Cardiopulmonary Bypass?

This study evaluated the coronary flow and the internal diameter, pressure, and metabolism of the left ventricle using four different cardiopulmonary bypass techniques. Conditioned dogs underwent a 30-minute stabilizing period on cardiopulmonary bypass with a beating, empty heart (normothermia and a flow of 80 ml/kg/min). They were then fibrillated and subjected to four experiments: Group A (7 dogs)—left ventricular vent, caval tapes open; group B (7 dogs)—left ventricular vent, caval tapes closed; group C (7 dogs)—no vent, caval tapes open; group D (4 dogs)—no vent, caval tapes closed. There was no major difference in any of these variables among Groups A and B (both ventricles vented). Group D (no vent, tapes closed) had significantly increased wall tension, decreased coronary flow, decreased subendocardial flow, and ischemia. In contrast, Group C dogs (no vent, tapes open) had only a slight increase in left ventricular diameter and pressure, with no change from Group A and B dogs in coronary flow, lactate extraction, hydrogen ion production, or potassium difference. Therefore, venting the fibrillating ventricle, either with or without snaring of the caval tapes, is probably the best method to use during the distal anastomosis in a coronary artery bypass operation. However, if a vent is not used, the caval tapes should be left open to allow complete diversion of the venous blood and decompression of the left ventricle.

Effects of Conventional Hypothermic Ischemic Arrest and Pharmacological Arrest on Myocardial Supply/Demand Balance During Aortic Cross-Clamping

Aortic cross-clamping may produce ischemic damage due to a discrepancy between supply and demand. Supply is determined by noncoronary collateral flow and substrate stores, and demand by electromechanical activity, wall tension, and temperature. The effects of 60 minutes of conventional hypothermic ischemic arrest were compared to those of pharmacological arrest. Noncoronary collateral blood supply was comparable in both groups during cross-clamping. With ischemic arrest, mechanical activity and endocardial electrical activity persisted and wall tension fell progressively. With pharmacological arrest, electromechanical activity stopped in less than 1 minute but returned (with increased wall tension) nearly 1 hour. Thirty minutes following reperfusion, coronary flow was redistributed away from subendocardium after ischemic arrest and toward endocardium after pharmacological arrest. Myocardial performance was depressed severely after conventional arrest and only mildly after pharmacological arrest. We conclude that aortic cross-clamping is safer with pharmacological arrest than with ischemic arrest. The cardioplegic solution modifies the supply/demand balance favorably, but it is washed out by noncoronary collateral blood supply.

Right and left ventricular compliance in experimental acute and subacute trypanosomal myocarditis

In order to elucidate the dominance of right ventricular failure in South American trypanosomal myocarditis (Chagas's disease), postmortem ventricular pressure—volume relationships were studied in eight C3H mice with acute experimental myocarditis due to Trypanosoma cruzi and in nine healthy control animals, as well as in seven animals with myocarditis in the subacute stage and eight controls. Pressures and volumes of right and left ventricles, isolated at thoracotomy, were measured within 35 min after death during simultaneous infusion of saline into right and left ventricles. Compliance, defined as the slope of the pressure-volume curve (ΔV/ΔP), was plotted against ventricular pressure over the range from 5 to 20 mm Hg. In the normal and myocarditic C3H mice, right ventricular compliance was always greater than left ventricular compliance. Right ventricular distensibility was maximal during the acute stage of myocarditis and decreased subsequently. Left ventricular distensibility remained unchanged during acute myocarditis, but increased significantly in the subacute stage. It is postulated that the dominance of right ventricular failure in Chagas's disease may be the result of a vicious cycle among inflammation and necrosis, increased compliance with dilatation and increased wall tension in the right ventricle, while the left ventricle remains less compliant.

Long-term effects of hypertension on the rat aortic wall and their relation to concurrent aging changes. Morphological and chemical studies.

The effects of long-term (16 months) hypertension on the thoracic aorta of male rats were compared to previously reported short-term (2.5 months) changes and to concurrent aging changes. Hypertension was produced by clipping a renal artery. Although short-term hypertension was characterized by a disproportionate increase in noncollagenous alkali-soluble proteins, which have been attributed primarily to vascular smooth muscle, with long-term hypertension there was no further increase in these proteins but instead there were striking increases in mural accumulations of elastin and collagen. Chronically elevated wall tension in hypertensive vessels was associated with a progressive increase in wall thickness which resulted in a value for wall stress no different from that of control vessels. Concurrent aging changes were qualitatively similar to, but much less pronounced than, those seen with hypertension and were attributed to an increase in wall tension in controls resulting from a combination of significant increases in diameter and systolic blood pressure with age. This study of the interaction of vessel structure and function has revealed common features of what appears to be a diverse group of vascular alterations.

Partial analysis of segmental resistances in intestinal vessels after endotoxin.

Hemodynamic responses of intestinal vascular segments of the dog to intravenous administration of a lethal dose (1 mg/kg) of E. coli endotoxin were investigated. Pressures were measured in large and small vessels of the intestinal and mesentery (small veins 30–60 µ in radius). Vascular radii of submucosal vessels and blood flow were determined. Changes in total resistance in the intestinal circulation after endotoxin were not uniform during the first few minutes, but there was a significant decrease at 10 min and a subsequent rise to the control value after 1 hr. At both 50 and 60 min, the resistance was increased over control in the arterial segment by 50%, increased 500% in the venous segment, and decreased 40% in the segment from small artery to venule. These circumstances would increase capillary pressure and filtration of edema fluid. Increased wall tension at reduced diameter developed in the venous segment during the secondary shock state, whereas relaxation of wall tension occurred in the arteriolar segment.