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PubMed1993

The anatomy of the atrioventricular bundle in the heart of camels (Camelus dromedarius).

The anatomy and histology of the atrioventricular bundle (AVB) was studied in the heart of six camels (Camelus dromedarius). The trunk of the atrioventricular bundle (bundle of His) was a direct continuation of the atrioventricular (AV) node with no sharp line of demarcation between the node and the bundle. The atrioventricular bundle ran through the fibrous trigone and entered the lower part of the interventricular membranous septum, beneath the right endocardium, then lay over or slightly to the side of the centre of the muscular interventricular crest. The AVB of camels measured 4.12 +/- 1.00 mm in length, 3.66 +/- 1.13 mm in width and 1.13 +/- 1.85 mm in thickness, its maximum sectional area being 12.68 +/- 6.13 mm2. Histologically, the AVB in the heart of camels comprised multiple strands of Purkinje cells separated by collagen fibres and surrounded by connective tissue. It resembled that in human beings and dogs except that, in camels, intercalated discs were present at the intercellular connections in the AVB.

Animals↗
PubMedDate not supplied

Tissue edema and loss of tracer microspheres in infarcted myocardium.

Microsphere loss from the ischemic myocardium was studied in a canine model after 2 and 7 days coronary occlusion. 10 million tracer microspheres (TM) of 7-10 micrograms diameter were injected into the left atrium before and 15 minutes after left anterior descending coronary artery (LAD) occlusion. To determine the tissue water content, dried tissue weight was measured after desiccation. TM content in the nonoccluded left circumflex coronary artery (LCX) area was unchanged before and after coronary occlusion. In the infarcted area, microsphere loss was maximum at the low flow endocardial region averaging 27% and 42% in 2 and 7 days occlusion, respectively. An inverse linear correlation between TM loss and regional blood flow in 2 (r = -0.82, p less than 0.05) and 7 (r = -0.96, p less than 0.01) days coronary occlusion was noted. Water content was increased in the ischemic endocardium by 4.1 and 5.7% in 2 and 7 days occlusion, thus approximately 17% of TM loss was attributed to tissue edema. These results suggest that there is an ischemia-dependent reduction of TM in the ischemic myocardium and that microsphere migration participates in the major part of TM loss. Thus flow measurements by TM may be invalid when this compound is injected during the active phase of microsphere migration or during water content alterations.

Animals↗
PubMedDate not supplied

Model of the coronary circulation based on pressure dependence of coronary resistance and compliance.

The effect of pressure-dependent changes in vascular volume, resistance and capacitance in the coronary micro-circulation, has been studied by a distributed mathematical model of the coronary micro-vasculature in the left ventricular wall. The model does not include regulation of coronary blood flow and is evaluated only for the fully dilated coronary vasculature. The left ventricular wall was thought to consist of eight parallel layers, each of them with an arteriolar, capillary and venular compartment. The resistance of each vessel was thought to depend on the inverse of squared volume, according to Poiseuille's Law for tubes with constant length. Tissue pressure has been assumed to be equal to left ventricular cavity pressure at the endocardium and to decrease linearly to atmospheric level at the epicardium. The pressure-volume relation of the vessel compartments were assumed to be sigmoidal. There is a rest volume at transmural pressure zero and delta V/delta P decreases with increasing transmural pressure. Simulation of experimental protocols described by other authors yielded results which were similar to the experimental outcomes, illustrated by: (1) a parallel shift to the flow axis of the pressure-flow curves due to cardiac arrest (2) steady-state endo/epi ratio of flow as a function of heart rate. It is concluded that interpretation of transients in coronary flow and/or pressure by models containing fixed resistance and capacitance may seriously underestimate intramyocardial capacitative effects and characteristic time constants for pressure-induced resistance changes.

Blood Pressure↗
PubMedDate not supplied

Physiological hypotheses--intramyocardial pressure. A new concept, suggestions for measurement.

Intramyocardial pressure is supposed to play a major role in systolic coronary flow impediment. Via its assumed relation with radial wall stress it is supposed to be similar to ventricular pressure at the endocardium and decreases linearly to negligible values epicardially. Many attempts to measure intramyocardial pressure have been reported in the literature with rather different results. For instance, with most of the various methods, intramyocardial pressures both higher and lower than left ventricular pressure have been obtained and intramyocardial pressures of more than 125 mm Hg have been found in low-loaded isobaric beats (negligible pressure development in systole). In this "physiological hypotheses paper" I suggest left ventricular pressure and intramyocardial pressure both to result from the varying stiffness of cardiac muscle over the heart cycle. For any intramuscular cavity a time varying pressure-volume (P-V) relation results from the changes in muscle stiffness, the so-called time varying elastance defined as E(t) = P(t)/V(t), and with maximal or systolic elastance called Emax. For a constant contractile state the time varying elastance (E(t)) is suggested to be almost independent of preload and afterload. This concept has been well established for the ventricular cavities, but is here proposed to hold for the interstitial space as well. If a cavity is subject to isovolumic conditions the pressure will be high, but when volume in systole decreases (ventricular ejection or squeezing out of interstitial fluid) pressures will be lower. Thus for constant load on the interstitial cavities, but different loads on the ventricle, left ventricular pressure will vary while intramyocardial pressure remains the same. For low-loaded isobaric beats where left ventricular pressure is minimal intramyocardial pressure will remain the same as during normal ventricular loads and isovolumic beats. Augmented contractility will increase Emax and this will increase left ventricular and intramyocardial pressure only by the same amount if loading conditions of both cavities remain the same. Both ventricular pressure and intramyocardial pressure arise from varying stiffness of cardiac muscle and intramyocardial pressure does not result from left ventricular pressure. A proportionality of left ventricular and intramyocardial pressure is therefore not to be expected. The results on intramyocardial pressure obtained by the different methods used in the literature should be re-interpreted taking this concept into account.

Animals↗
PubMedDate not supplied

Coronary collateral reserve during exercise induced ischemia in swine.

We determined coronary collateral vasodilator reserve during exercise-induced ischemia in 17 mini-swine. We induced coronary collateral development in the left circumflex bed by placing an ameroid occluder on that artery. Four weeks later we studied the animals at rest and during exercise (EX) eliciting heart rates (HR) of 240 and 265 beats/min. We measured myocardial blood flow with microspheres and myocardial function by wall thickness sonomicrometry gauges. At matched exercise HRs we treated the animals with nifedipine (10 micrograms/kg IV) (EXN 10), nifedipine (100 micrograms/kg IV), (EXN 100), and adenosine infusion (1.2 mg/min/kg) EXAD. EXN 10 did not significantly alter hemodynamics compared to EX but EXN 100 and EXAD both decreased blood pressure significantly (p less than 0.05). Ischemic endocardial/nonischemic endocardial flow ratios and collateral resistance served as indices of vasodilator reserve. In the ischemic zone exercise reduced vasodilator reserve to 24 +/- 3% in the endocardium and 64 +/- 7% in the epicardium. Neither EXN 10 nor EXAD improved exercise-induced ischemia measured either as flow or function. However EXN 100 improved function during exercise-induced ischemia without improving coronary collateral flow. We conclude there is no additional coronary flow reserve during exercise-induced ischemia in the collateral dependent bed of the pig a few days after occlusion that can be recruited. Large doses of nifedipine improve function by direct action on the myocardium or by reducing afterload. The lack of development and deep myocardial distribution of the coronary collateral vessels in the pig may be an important factor of why these nifedipine responses differ from those reported in species which have primarily large epicardial coronary collaterals.

Adenosine↗
PubMedDate not supplied

Left ventricular wall stress distribution in chronic pressure and volume overload: effect of normal and depressed contractility on regional stress-velocity relations.

Regional stress-velocity relations were determined in a first group of patients (n = 15) with normal (five controls, five patients with aortic stenosis, and five patients with aortic insufficiency) and a second group of patients (n = 10) with depressed contractility (five patients with aortic stenosis and five with aortic insufficiency). LV circumferential wall stress was calculated from high-fidelity pressure and frame-by-frame angiocardiographic data using the Wong thick-wall model. Regional wall stress and shortening velocity were calculated from the endo- to the epicardium, and from the equator to the apex at 35 points. Regional LV wall stress was in all patients lower at the epi- than the endocardium, and lower at the apex than the equator. Regional stress-velocity relations were downward shifted from the endo- to the epicardium and from the equator to the apex (family of curves) in both groups. At corresponding LV regions stress-velocity relations showed significantly smaller slopes and intercepts (downward depression) in group 2 than in group 1. Thus, wall stress distribution is inhomogeneous in the normal, as well as in the pressure and volume overloaded left ventricle. Regional differences in stress-velocity relations within groups (family of curves) are probably related to changes in preload rather than to changes in regional contractility. Downward depression of the regional stress-velocity relations in group 2 is caused by depressed myocardial contractility.

Adult↗
PubMedDate not supplied

Morphological changes accompanying physiological changes in atrial stretch receptors.

A shunt connecting the descending aorta and posterior vena cava was established surgically in six mongrel dogs. All animals subsequently developed hemodynamic and clinical signs of congestive heart failure at which time the shunt was closed. Six to seven weeks after ligation of the shunt, activity of the left atrial stretch receptors was recorded and found to be similar to that of sham-operated dogs. Methylene blue-stained sections of left atrial endocardium indicated that approximately one-third of the receptors were normal in histological appearance. The remaining two-thirds were fragmented and degenerate. Evidence is presented which indicates that structural changes in these receptors parallel their changes in physiological activity.

Animals↗
PubMedDate not supplied

Effects of recurrent ischemia on myocardial high energy phosphate content in canine hearts.

Successive ischemic episodes are commonly seen in clinical and experimental cardiology. Although prolonged abnormalities of the canine myocardium have been described following a single ischemic episode, it is not known whether myocardial injury is cumulative following multiple ischemic episodes. Dogs were subjected to three 15-min left anterior descending coronary artery occlusions, each followed by 30 min of reperfusion. In vivo biopsies were obtained for biochemical analysis before and during the first occlusion and 30 min into each reperfusion period. ATP and creatine phosphate (CP) fell in the endocardium during occlusion by 24% and by 69% respectively (both p less than .0001). While CP recovered during each reperfusion period, ATP remained significantly depressed. Loss of membrane-permeable purine nucleotide synthesis precursors occurred with the first reperfusion period but not with the second and third reperfusion periods. Therefore, reperfusion following one 15-min coronary occlusion is associated with severe depression of myocardial high energy phosphates; however, two additional occlusions do not cause a further decrease of these substances when intermittent reperfusion is allowed for 30 min.

Adenine Nucleotides↗
PubMedDate not supplied

The effects of ventricular hypertrophy on the coronary circulation.

Recent animal studies suggest that cardiac hypertrophy compromises the coronary circulation. Although flow per gram of ventricle in most animal models of hypertrophy is normal, coronary vasodilator responses to pharmacological or physiological stimuli are mildly impaired. Studies of regional perfusion indicate that the limitation of coronary vasodilator capacity in hypertrophied ventricles primarily affects the endocardium. In contrast to studies in animals, measurements of coronary reactive hyperemia in man suggest that coronary dilator responses are profoundly depressed in patients with severe left ventricular hypertrophy secondary to aortic stenosis. These studies in man demonstrate that alterations in the coronary circulation secondary to cardiac hypertrophy are of sufficient magnitude to contribute to the development of angina and heart failure (secondary to endocardial fibrosis) in patients with aortic stenosis.

Animals↗
PubMedDate not supplied

Editorial: Myocardial sarcomeres and the functioning mammalian heart.

Previously the length-tension properties of the isolated papillary muscle have been related to myocardial sarcomere lengths. Though past studies have relied upon fixed material, recentlly, living muscles have been used. Sarcomere lengths have now been measured on the same specimens in both living and fixed material and the sarcomere length at optimum muscle length established. These lengths are extremely uniform. Studies on the sarcomere lengths through the wall of the left ventricle have also been carried out. Surprisingly sarcomere lengths were relatively uniform from endocardium to epicardium over a wide range of intraventricular pressures. Furthermore, enddiastolic sacarcomere lengths were 91% to 94% of optimum sarcomere length over a physiologic pressure range. Since the papillary muscle in function has been shown to shorten by 23% (to 70% of optimum sarcomere length), these results suggest that the papillary muscle uses the entire ascending limb of the length-tension curve during function.

Animals↗
PubMedDate not supplied

Myocardial blood flow distribution in miniature pigs during exercise.

Total and regional myocardial blood flow was measured in miniature pigs at rest and during two levels of treadmill exercise, including maximal exercise. Exercise increased the myocardial blood flow in a linear manner with heart rate (r = 0.87). At rest the endocardial/epicardial blood flow ratio was significantly greater than unity with flow favoring the endocardium. Exercise failed to appreciably alter the distribution of coronary blood flow. Thus the myocardium was capable of further dilatation and perfusion of blood without compromising endocardial flow even during the most severe level of exercise when maximal heart rates were attained.

Animals↗
PubMedDate not supplied

The effects of intracoronary Renografin injection on coronary flow and distribution in dogs following coronary occlusion.

To study the effects of a contrast agent commonly used in coronary angiography (Renografin) on myocardial flow distribution, the main left coronary arteries of 9 dogs were cannulated and perfused from the carotid arteries. The left anterior descending coronary artery (LAD) was ligated and cannulated to monitor peripheral coronary pressure (PCP). Myocardial blood flow and distribution were determined with radioactive microspheres before Renografin administration and after resolution of the brief period of hypotension following injection of 2-3.5 cm3 of the contrast agent directly into the coronary perfusion tubing. Renografin significantly increased blood flow to normal myocardial regions (0.90 to 1.51 cm3 . g-1 . min-1, p less than 0.001). Despite this flow augmentation and normal aortic and coronary perfusion pressures. PCP decreased from 28.0 +/- 3.4 to 24.4 +/- 2.8 mm Hg (p less than 0.001), and myocardial blood flow to the central ischemic LAD area halved from 0.17 +/- 0.04 to 0.09 +/- 0.03 cm3 . g-1 . min-1 (p less than 0.025). The inner/outer left ventricular wall blood flow ratio in the central ischemic region increased from 0.28 to 0.39 (p less than 0.05). Thus the contrast agent causes a coronary steal or redistribution of coronary flow away from already ischemic regions, and the endocardium appears to be less affected than the epicardium.

Animals↗
PubMed1990

Lyme carditis in immunodeficient mice during experimental infection of Borrelia burgdorferi.

Recently, we described the severe combined immunodeficiency (scid) mouse as a laboratory model for B. burgdorferi infection. Scid mice inoculated with the virulent low-passage tick isolate Borrelia burgdorferi ZS7 developed a severe pancarditis involving endocardium, myocardium and epicardium in the absence of functional B- or T-cells. Soon after inoculation perivascular infiltration was observed, later diffuse infiltration of the interstitium of the subendocardial and subepicardial areas was seen. The infiltrate was mainly mononuclear and predominantly composed of Mac-1+ cells. Concomitantly, fibroblast proliferation and augmented collagen deposition occurred in the interstitium. This was associated with the presence of B. burgdorferi organisms. The histopathological and ultrastructural findings observed in scid mice resemble those observed in human Lyme carditis. The data emphasize the suitability of the scid mouse as a model in which to study the role of the immune system in the pathogenesis of Lyme carditis.

Animals↗
PubMedDate not supplied

Autonomic influences on regional cardiac [14C]2-deoxyglucose uptake in paced dog heart.

Sixteen dogs were anesthetized with pentobarbital sodium and placed on positive pressure ventilation. Twelve animals were cardiac paced and four animals were non-paced controls. In four of the paced animals, the left cut peripheral end of the cervical vagus was stimulated electrically. In another four animals, the decentralized left stellate ganglion was stimulated efferently. The four remaining paced animals were controls. The animals were injected i.v. with a single bolus of [14C]2-deoxyglucose, 100 microCi/kg. After 45 minutes of periodic stimulation, the hearts were removed, sectioned and prepared for autoradiography. Cardiac pacing significantly (p less than 0.02) decreased systolic blood pressure, and significantly increased (p less than 0.05) glucose utilization by all regions of the heart, with the exception of the left ventricular endocardium and the left ventricular papillary muscles. Vagal efferent stimulation elicited significant (p less than 0.05) decreases in glucose utilization in both the right atrium and right ventricle. Conversely, efferent stellate ganglion stimulation had no effect on the glucose utilization of any regions of the myocardium studied. This study demonstrates that both cardiac pacing and cardiac vagal efferent neuronal stimulation can produce distinct changes in regional myocardial glucose utilization.

Animals↗
PubMed1996

The extracellular matrix proteins fibulin-1 and fibulin-2 in the early human embryo.

Fibulin-1 and fibulin-2, two recently identified extracellular matrix proteins with a homologous domain structure, are known to bind various extracellular ligands and calcium. In this study, they have been localized at the light microscopical level in human embryos of gestational weeks 4-10, using polyclonal antibodies. Identical localization patterns were observed for the two fibulins in most of the tissues. In the heart, the endocardial cushion tissue and endocardium, but not the myocardium, were stained, as were the basement membrane zones and adventitia of blood vessels. Staining was also observed in the perichondrium and calcifying regions of developing bones. Moreover, reactions occurred with the gut subepithelium and epithelial basement membranes of the skin. Differences in staining patterns, however, were observed in various neural structures. Fibulin-1 was prominent in the matrix of the leptomeningeal anlage, in basement membranes of the neuroepithelium and the perineurium of peripheral nerves. Fibulin-2 was detected primarily within the neuropithelium, spinal ganglia and peripheral nerves. The early embryonic expression of both fibulins indicates specific roles during organ development and, in particular, involvements in the differentiation of heart, skeletal and neuronal structures.

Animals↗
PubMed1987

3-D ventricular myocardial electrical excitation: a minimal orthogonal pathways model.

This study is part of our attempt to develop a fast-responding interactive computer simulator of the left ventricle (LV) which describes the spatial and temporal myocardial characteristics and the global performance of the LV, accounting for the continuous interactions between the electrical activation sequence, fiber mechanics, blood perfusion and transmural metabolism and oxygen demand. Here, the activation propagation front throughout the healthy 3-dimensional LV myocardium is simulated in a macro global level by utilizing an analytical model based on the principle of the propagation of the electric activation signal along minimal pathways in an elliptically assumed LV geometry. The Purkinje network dominates the propagation at the endocardial layer while three orthogonal directions of propagation are assumed within the myocardium. The shortest path consists of the geodetic line at the endocardial layer and the normal that connects the endocardium with the point considered. The generated three-dimensional propagation front maps are in fair agreement with reported experimental data. The study thus presents a new approach that permits a quick reconstruction of the 3-D isochrons in a relatively simple but useful model of the normal heart.

Computer Simulation↗
PubMed1992

A conical model to describe the nonuniformity of the left ventricular twisting motion.

The systolic contraction and fiber shortening in the left ventricle (LV) produces torsional moments in the myocardium, resulting in a gradient of angular displacements about the long axis. This is manifested as a counterclockwise rotation of the apex relative to the base, when viewed from the apex. Recent studies with magnetic resonance imaging (MRI), using noninvasive magnetic tags, have revealed three important properties of the LV twist: (a) The angle of twist (i.e., the angular rotation of a slice relative to the basal slice) is consistently higher at the endocardium as compared to the epicardium; (b) The twist increases towards the apex; and (c) Straight MRI-tagged radial lines at end-diastole (ED) are slightly curved at end-systole (ES), implying a nonlinear transmural variation of the twist. The present study suggests that the geometry of the LV at ES can be represented by a thick-walled hollow cone, and that the transmural twist patterns from ED to ES can be described using the continuum mechanics approach and a small strain analysis of an isotropic cone subjected to external torque. The predicted results are compared with the noninvasive MRI measurements of transmural twist in eight human volunteers. Given the epicardial angles of twist of each slice, the predicted endocardial angles of twist are in good correlation with the experimental findings (r = 0.86, slope = 1.09, SEE = 4.1 degrees). In addition, the model reliably describes the changes in the twist magnitude from apex to base (no significant difference from experimental values, P = 0.2), and predicts the curvilinear pattern at ES of the originally straight ED radial lines. Thus, the conical model with uniform properties of the LV, reliably predicts the nonuniformity of the twist patterns, implying that the LV twist is strongly affected by LV geometry.

Adult↗
PubMedDate not supplied

Coronary flow patterns in normal and ischemic hearts: transmyocardial and artery to vein distribution.

The dynamics of the transmyocardial coronary flow patterns during normal and ischemic conditions are complex and relatively inaccessible to measurements. Therefore, theoretical analyses are needed to help in understanding these phenomena. The proposed model employs compartmental division to three layers, each with four vessel-size compartments which are characterized by resistance and compliance. These compartments are subjected to the extravascular compressive pressure (ECP) generated by cardiac contraction, which by modifying the transmural pressure causes changes in cross-sectional area of the vessels in each compartment continuously determining the resistance and capacitance values. Autoregulation and collaterals are also included in order to simulate the flow patterns during regional ischemia. Using these features, the model predicts the typical out of phase arterial and venous flow patterns. Systolic collapse of the large intramyocardial veins during the normal cycle, as well as systolic arteriolar collapse during ischemia are predicted. The transmural flow during ischemia is characterized by alternating flows between the layers. The ECP is considered here is two ways: (a) as a function of left ventricle (LV) pressure, decreasing linearly from endocardium to epicardium and (b) as the interstitial fluid pressure, employing a multilayer muscle-collagen model of the LV. While both of these approaches can describe the dynamics of coronary flow under normal conditions, only the second approach predicts the large compressive effects due to high ECP obtained at very low cavity pressure, resulting from significant muscle shortening and radial collagen stretch. This approach, combining a detailed description of transmural coronary circulation interacting with the contracting myocardium agrees with many observations on the dynamics of coronary flow and suggests that the type of LV mechanical model is important for that interaction.

Animals↗