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Biomedical subjects

R D Hogan

Publications and source records attributed to R D Hogan.

At least 19 recordsLinked to original sources
PubMed1990

Echocardiographic definition of the left ventricular centroid. I. Analysis of methods for centroid calculation from a single tomogram.

Quantitation of myocardial contraction requires a frame of reference. Most investigators have sought a single reference frame per image, centered in some manner with respect to the mass of myocardium. Because there is no anatomic marker for the center of the heart, many different approaches have been pursued to identify a centroid of the left ventricle. The issue of whether the reference should be fixed throughout the cardiac cycle or float from image to image has been addressed in previous studies, but the more fundamental question of how a centroid can best be defined has not been answered. This study examines this basic issue by analysis of variance from observer to observer, cycle to cycle, animal to animal and method to method. Both endocardial and epicardial borders were digitized twice by each of two observers at 1/30 s intervals spanning the cardiac cycle for each of three cardiac cycles in six normal dogs. The left ventricular centroid was calculated by six methods: center of endocardial coordinates, center of epicardial coordinates, center of mid-myocardial (average) coordinates, center of endocardial area, center of epicardial area and center of mid-myocardial (average) area. The path of each centroid was correlated between observers and correlation coefficients were transformed for analysis of variance. This analysis indicates a best approach to centroid definition through distinct minimization of the variance: the best of the six methods proved to be center of endocardial area.

Analysis of Variance↗
PubMed1990

Echocardiographic definition of the left ventricular centroid. II. Determination of the optimal centroid during systole in normal and infarcted hearts.

Although two-dimensional echocardiography is widely used in both clinical and experimental evaluations of regional cardiac wall motion, there is no established clinical method for quantitative analysis of the wall motion, not even for the normal radial motion observed in short-axis images. Measurement of radial wall motion requires determination of a centroid from which the radii emanate. Depending on its definition, the centroid is variously affected throughout systole by cardiac translation, regional wall motion and any shift of the subject position or transducer. A floating centroid is defined relative to the ventricular walls frame by frame, whereas a fixed centroid never moves with respect to the transducer. Evaluation of the best approach to definition of a centroid was previously presented (part I, this issue). The next question is how to use the centroid. This study examines which of four centroid applications provides the best reference for quantifying regional wall motion during systole. Method 1 is a floating centroid (defined separately for every image frame), method 2 uses the end-diastolic centroid as a fixed reference for all image frames, method 3 uses the end-systolic centroid as a fixed reference and method 4 uses the average as a fixed reference. Wall motion was measured with respect to each of these centroids by determining radial wall motion from end-diastole to end-systole and correlating radial motion throughout the cardiac cycle with that in normal control hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Evolution of the temporal contraction sequence after acute experimental myocardial infarction.

The effect of infarct maturation on the temporal sequence of contraction within infarct zones has not previously been described. Accordingly, the time-varying pattern of contraction within ischemic/infarct zones was studied with use of cross-sectional echocardiography in 17 dogs at 10 min to 6 weeks after acute experimental myocardial infarction. Left ventricular short-axis images were digitized from end-diastole to end-systole and endocardial fractional radial change along 36 evenly spaced rays was calculated. The circumferential extent of dyskinesia and the number of rays that exhibited maximal dyskinesia were determined for each decile of the normalized contraction sequence. Between 10 min and 1 week after infarction, the greatest circumferential extent of dyskinesia occurred between the 3rd and 4th deciles of the normalized contraction sequence. However, as the infarct matured, the greatest spatial expanse of dyskinesia was noted to occur progressively earlier in the contraction sequence (second decile at 6 weeks), and the extent of mid- to late-systolic dyskinesia decreased markedly. Whereas end-systolic dyskinesia was present in 30% to 50% of ischemic/infarct zone rays from 10 min to 48 h, end-systolic dyskinesia was no longer observed at 6 weeks. Similarly, the maximal amplitude of dyskinesia was most commonly observed during midsystole from 10 min to 48 h, but occurred progressively earlier as the infarct matured, falling during the first decile at 6 weeks after infarction. These data suggest that maximal circumferential extent and amplitude of dyskinesia occur progressively earlier in the systolic contraction sequence as the infarct matures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Relationship of functional recovery to scar contraction after myocardial infarction in the canine left ventricle.

We have previously reported that regional wall motion abnormalities in a canine model of acute myocardial infarction may show substantial improvement in the first 6 weeks after infarction. To determine whether the mechanism of this improvement in function is the result of scar contraction within the infarct, we studied the relationship between changes in regional wall motion defined by cross-sectional echocardiography and the regional concentration of radioactive microspheres injected immediately before coronary occlusion and sampled 6 weeks after occlusion. Eight dogs underwent serial echocardiographic and microsphere blood flow measurements immediately before and 30 minutes, 48 hours, 1 week, 3 weeks, and 6 weeks after ligation of the left anterior descending or the left circumflex coronary artery. Wall motion and blood flow were measured in the short-axis section of the left ventricle at the level of the midpapillary muscle in each 10-degree radial segment around the circumference of the ventricle. Infarct histology was assessed at 6 weeks by means of the same radial coordinate system. Control data were collected in a similar manner from four dogs that underwent sham operations and had no histologic evidence of infarction. In all of the animals with infarcts, but not in the sham animals, the calculated preocclusion endocardial and epicardial blood flow values in the histologic infarct zone (252 +/- 44 and 168 +/- 17 ml/min/100 gm, respectively, mean +/- SEM) were significantly higher than those in the normal opposite wall (endocardial: 106 +/- 3 ml/min/100 gm, p less than 0.01); epicardial: 108 +/- 3 ml/min/100 gm, p less than 0.01. The location and circumferential extent of myocardium showing this elevation of preocclusion blood flow correlated well (r = 0.93, p less than 0.001) with the location and circumferential extent of the histologic infarct. The amount of wall motion abnormality, measured from the "correlation plot area," decreased significantly from its maximum value of 39 +/- 3 degrees at 48 hours after coronary occlusion to 3 +/- 1 degrees (p less than 0.001) at 6 weeks after occlusion. The ratio of the preocclusion transmural blood flow in the infarct zone to that in the noninfarct zone, a measure of the condensation of the microspheres injected before coronary occlusion, and therefore of the degree of scar contraction at 6 weeks, correlated well (r = 0.83, p less than 0.01) with the recovery of wall motion 6 weeks after infarction.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Modulation of the spontaneous contractions of the initial lymphatics of the bat's wing by arterial and venous occlusion.

The spontaneous contractions of the initial lymphatics of the bat's wing were observed to be modulated by changes in local blood flow. Lymphatic pressure and frequency of contraction were measured with the servo-null technique during the occlusion of the ulnar artery or vein. Lymphatic contractile activity was decreased during arterial occlusion but was increased during venous occlusion and postocclusion hyperemia. These changes in lymphatic activity are not consistent with the hypothesis that flow-associated changes in lymphatic contractile activity is mediated primarily by metabolic factors.

Animals↗
PubMed1987

The effect of vasoactive agents on the contractions of the initial lymphatics of the bat's wing.

The effect of vasoactive agents on the spontaneous contractions of the initial lymphatics of the bat's wing was investigated. Initial lymphatic contractile frequency and pulsatile pressure were measured with the servo-null micropressure system. Norepinephrine, phenylepinephrine, isoproterenol, acetylcholine, histamine, serotonin, bradykinin, prostaglandin F2a, prostaglandin E2, indomethacin and ibuprofen were delivered to the immediate vicinity of the initial lymphatic by microinjection or iontophoresis. Only bradykinin produced changes in initial lymphatic contractions which were significantly different from control. The response to bradykinin was characterized by an increase in the frequency, strength or duration of the contraction.

Animals↗
PubMed1987

Vasomotor control: functional hyperemia and beyond.

Historically, functional hyperemia has been viewed largely as an interaction between a parenchymal cell and its associated microvasculature. Locally released metabolites have been thought to produce relaxation of the smooth muscle and a vasodilation that increases blood flow in proportion to metabolic need. This symposium report presents evidence from a variety of disciplines and a number of different types of biological preparations that demonstrates that functional hyperemia is a complex process involving several classes of microvessels including capillaries, arterioles, and small arteries. These vessels do not function independently but are coordinated by a complex set of interrelations involving at least three different modes of interaction between parenchymal cells and the various segments of the vascular bed. These are local metabolic effects, propagated effects extending over long segments of the vasculature, and flow-dependent vasodilation induced by local changes in blood flow. In addition to these acute responses to metabolic demand it appears that tissues may be capable of more long-term structural alterations of the arterial and arteriolar network in response to sustained changes in the relationship between supply and demand. The vascular bed appears to be able to adapt either by increasing the maximal anatomic diameter of the large arteries or by inserting new arterioles into the parenchyma. Thus, classical functional hyperemia appears to be but one manifestation of a multifaceted process leading to highly coordinated responses of many vascular elements, resulting finally in vascular patterns that are optimized to meet parenchymal cell demands.

Animals↗
PubMed1986

The initial lymphatics as sensors of interstitial fluid volume.

Lymphatic luminal pressure and interstitial fluid pressure (IFP) were measured simultaneously in the bat's wing with two servo-null micropressure systems during interstitial fluid volume expansion induced by direct interstitial infusion. Lymphatic baseline pressure, pulsatile pressure, and IFP were elevated by the interstitial infusion. Transmural pressure gradients occurred only transiently. The increased lymphatic pulsatile pressure was not dependent upon the transmural pressure gradient but remained elevated as long as the increased interstitial fluid volume (IFV) was maintained. The results suggest that lymphatic pumping capacity during edema is modulated by IFV rather than IFP and that this mechanism may play an important role in the regulation of interstitial hydration. A mechanism whereby the initial lymphatics may directly sense and control IFV is proposed based upon physiological and anatomical data.

Animals↗
PubMed1986

The natural history of regional wall motion in the acutely infarcted canine ventricle.

Two-dimensional echocardiography was employed to define the natural history of regional wall motion abnormalities in a canine model of acute experimental myocardial infarction. Serial short-axis two-dimensional echocardiograms were recorded in 11 closed chest dogs before coronary occlusion and 10, 30, 60, 180 and 360 minutes after permanent coronary ligation. Radiolabeled microsphere-derived blood flows were obtained in each study period and the histochemical (triphenyltetrazolium chloride) extent of infarction was determined at 6 hours. Previously published methods were used to quantitate field by field (every 16.7 ms) excursion of 36 evenly spaced endocardial targets. The circumferential extent of abnormal wall motion was followed sequentially using previously published definitions of abnormality: 1) systolic fractional radial change of less than 20%; 2) dyskinesia (systolic bulging) at the point in time (echocardiographic field) in which there is maximal dyskinesia; and 3) correlation with composite normal ray motion falling outside the 95% confidence limits defined in the control period. On the basis of the triphenyltetrazolium chloride staining pattern, the ventricle was divided into five zones: central infarct zone, zone with greater than 25% transmural infarction, total infarct zone, border zones and normal zone. Mean systolic fractional radial change was calculated for each zone and used as an index of the magnitude of abnormal wall motion. Regardless of the definition of abnormality employed, the circumferential extent of abnormal wall motion manifested at 10 minutes after occlusion did not significantly change, even up to 6 hours later. Similarly, 10 minutes after coronary occlusion the three infarct zones and border zones demonstrated significantly reduced systolic fractional radial change. This remained stable over the remainder of the 6 hour study period. It is concluded that once established at 10 minutes after coronary occlusion, the circumferential extent and magnitude of abnormal wall motion do not significantly change in the immediate postinfarct (6 hour) period.

Animals↗
PubMed1986

Mechanical control of initial lymphatic contractile behavior in bat's wing.

The initial lymphatics of the bat's wing demonstrate spontaneous rhythmical contractions that contribute to the active formation of lymph. In the present study, modulation of lymphatic activity by mechanical factors was examined. Oil was injected to block the outflow tract of individual initial lymphatic bulbs to create a state of near isovolumetric contraction. Pulse pressure, base-line pressure, and contractile frequency were measured with the servo-null technique, while base-line pressure within the bulb was controlled by the infusion or withdrawal of fluid. Increasing the base-line luminal pressure from its resting level (near atmospheric pressure) produced an increase in pulse pressure up to an optimal level and then a subsequent decline in pulsatile strength. The magnitude of the pulsations changed by three to four times over the range of distending pressures. Contractile frequency increased 14% over the same range.

Animals↗
PubMed1985

Interspecific comparison of subcutaneous tissue fluid pressure in the bat wing.

Tissue fluid pressures were recorded from subcutaneous tissues of three bat species by means of an improved servo-micropipet pressure recording system. Experimental animals were restrained but unanesthetized during the procedure by methods which avoided vascular occlusion. Tissue fluid pressures averaged +0.46 +/- 2.08 mm Hg (n = 12) in the Mexican free-tailed bat, +0.21 +/- 0.63 mm Hg (n = 14) in the pallid bat, and -0.31 +/- 1.01 mm Hg (n = 12) in the little brown bat. None of the average values differed significantly (P greater than 0.25) from the others or from atmospheric pressure (P greater than 0.20). Tissue fluid pressures in the subcutis of the bat were near atmospheric in agreement with the results obtained in the bat and other species by earlier investigators using both hypodermic needles and micropipets.

Animals↗
PubMed1985

The natural history of regional dysfunction in a canine preparation of chronic infarction.

We used a canine preparation of experimental infarction to study the natural course of echocardiographically defined regional wall motion abnormalities in the 6 weeks after acute coronary ligation. Eight dogs underwent serial short-axis echocardiographic evaluation and microsphere blood flow determinations at control, and 30 min, 48 hr, 1 week, 3 weeks, and 6 weeks after acute coronary artery ligation. Wall motion analysis and blood flow calculations were applied to 10 degree radial segments of the left ventricle (short axis) and correlated to the size and extent of infarction as defined histologically at 6 weeks. All animals had at least 50% transmural histologic infarction. The ratio of flow in infarcted tissue vs noninfarcted myocardium fell to 0.40 +/- 0.13 for endocardium and 0.56 +/- 0.13 for epicardium at 30 min after ligation, but recovered to 0.83 +/- 0.15 for endocardium and 1.12 +/- 0.11 for epicardium by 6 weeks. The maximum circumferential extent of abnormal regional wall motion was observed at 48 hr after infarction (mean circumferential extent = 51%), but was resolved to a significant extent by 6 weeks (circumferential extent = 21%, p less than .001). Four animals had virtually normal wall motion by 6 weeks after infarction. Segment-by-segment regional dysfunction correlated highly with the regional transmural reduction in blood flow of 20% )r = .89, p = .0001) for the experiment as a whole, but the echocardiogram tended to underestimate the size of the histologic infarct at 6 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

A digital video image splitting device for microvascular measurements.

An improved video image splitting device for the measurement of vessel lumen diameter and wall thickness has been developed. The use of digital electronics allows a split image to be displayed on a standard CCTV monitor with image shifting allowed to both the right and left. Testing of the device shows it to be linear to within 1% and accurate to 0.5% of full screen.

Electronics, Medical↗
PubMed1984

Arteriolar proliferation in the rat cremaster muscle as a long-term autoregulatory response to reduced perfusion.

Long-term autoregulation of arterial blood flow to sustained increases or decreases in arterial pressure has been previously reported. It is not clear whether the adaptive process at the microscopic level is a modification of vessel caliber or density. The present study was undertaken to assess morphological and hemodynamic changes resulting from a sustained decrease in perfusion to the cremaster muscle in normal rats. The main feeding arteriole to the cremaster muscle was ligated at age 3 weeks in 11 male Wistar rats. At 6 weeks, the cremaster muscles on the ligated and control sides were evaluated microscopically for hemodynamic status and vascular architecture differences. Pressure was reduced 30% on the ligated side without a decrease in volume flow. This was possible because the number of second-order arterioles increased by 48% and the number of third-order arterioles increased by 98% on the ligated side. Although twice as many third-order arterioles were present in the ligated muscle, the same percentage was closed to flow in the resting state as in the control muscle (31 vs 29%). These findings are consistent with a long-term autoregulatory process which modulates arteriolar density in response to altered perfusion or distending pressure. The same process may be responsible for arteriolar rarefaction in response to sustained elevation in arterial pressure in the cremaster muscle of the spontaneously hypertensive rat (SHR).

Animals↗
PubMed1984

Importance of temporal heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia.

A number of recent two-dimensional echocardiographic studies have attempted to relate quantitative changes in short-axis left ventricular radial wall motion to underlying myocardial ischemia/infarction. The significance of temporal variation in the contraction sequence within these ischemic regions in the overall evaluation of segmental left ventricular dysfunction, however, remains undefined. To assess this, we examined the motion of 192 individual radii that intersected known ischemic segments at 16.7 msec intervals from end-diastole to end-systole. The studies were performed in 13 dogs 1 hr after acute coronary ligation (six of the left anterior descending and seven of the circumflex coronary artery). Zones of infarction were confirmed by triphenyltetrazolium chloride staining at the termination of the experiment and by a corresponding decrease of more than 75% in myocardial perfusion at the 1 hr sampling period. Dyskinesis (defined for each radius as negative or outward excursion relative to the end-diastolic reference on two consecutive fields) was noted along 168 of 192 radii (88%) at some point in the contraction sequence. The maximal outward or dyskinetic motion occurred most commonly in the fourth decile of the normalized contraction sequence. In 147 of the 168 dyskinetic radii (88%) the maximal outward motion occurred during the first half of systole while in only two radii in one animal was the maximal outward motion noted at end-systole. The total number of radii showing dyskinetic motion at any given point in the contraction sequence likewise varied with time. Although again the greatest number of radii showed abnormal motion during the fourth decile of the normalized contraction sequence, only 66 of 168 or 39% remained dyskinetic to end-systole. No relationship was observed between the point of maximal dyskinesis (time-weighted average of all dyskinetic radii for a given animal) and (1) the total number of radii showing dyskinesis, (2) the total number of radii within the infarct zone, or (3) the infarct area expressed as a percent of the slice area. The major factor determining persistence of dyskinesis to end-systole for any radius was the maximal outward motion of the endocardial segment at the point of maximal dyskinesis. Therefore, simple measurement of endocardial excursion from end-diastole to end-systole may fail to detect important wall motion abnormalities and, in some cases, may miss dyskinetic segments completely.

Acute Disease↗
PubMed1984

A comparison of quantitative echocardiographic methods for delineating infarct-induced abnormal wall motion.

Current echocardiographic methods for quantitating abnormal regional left ventricular wall motion rely primarily on changes in endocardial excusion from end-diastole to end-systole. Recent studies demonstrating important spatial and temporal heterogeneity in wall motion within ischemic regions, however, raise questions about the validity of this approach. To determine the optimal method for defining abnormal left ventricular wall motion, we used a canine preparation of acute experimental infarction to examine four quantitative methods of wall motion analysis. The circumferential extent of abnormal wall motion assessed by each method was compared with the circumferential extent of infarction (defined by triphenyltetrazolium chloride staining) and the circumferential extent of reduced transmural blood flow (determined by radiolabeled microsphere techniques) 6 hr after acute coronary occlusion. The following methods of quantitating abnormal wall motion were examined: (1) determination of end-diastolic to end-systolic endocardial excursion (less than 0.20 end-diastolic radius), (2) determination of the extent of maximal dyskinesis (systolic bulging), and (3) and (4) two derived correlation methods that consider the entire course of systolic radial motion by correlating the observed echocardiographic field-by-field (every 16.7 msec) motion of each of 36 evenly spaced endocardial targets with the course of normal motion established from pooled normal data. Results obtained with the correlation methods showed a better correlation with the triphenyltetrazolium chloride-defined circumferential extent of infarction (r = .87 and r = .78) than did determinations of reduced end-diastolic to end-systolic endocardial excursion (r = .35) or the extent of maximal dyskinesis (r = .37). Similarly, the best correlation with the extent of reduced flow was obtained with one of the correlation methods (r = .80). We conclude that correlation methods that "integrate" endocardial motion over the entire systolic contraction sequence provide better definition of ischemic left ventricular dysfunction than do methods that consider motion at only single points in time.

Acute Disease↗
PubMed1983

Thrombolytic agents: effects of local infusion on microvascular physiology and macrovascular ultrastructure.

Microvascular responses in live preparations of rat cremaster muscle were studied with intravital light microscopy following infusions of streptokinase, streptokinase-plasminogen complex, or urokinase into the iliac artery. Structural changes occurring in the endothelium of the iliac arteries were documented by electron microscopy. Though no functional microvascular changes were documented, endothelial cell injury and luminal surface fibrin deposits were identified in the iliac arteries locally infused with the thrombolytic agents. In addition, platelets in various stages of activation were identified. It is concluded that the commonly employed thrombolytic agents, urokinase and streptokinase, caused injury to the endothelial cells of our animal model. It is further concluded that platelet activation, due to local endothelial injury or some other mechanism, occurred following local infusion in our animal model. The long-term effects and potential clinical implications of the findings are not known.

Animals↗