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Biomedical subjects

W S Kemper

Publications and source records attributed to W S Kemper.

At least 19 recordsLinked to original sources
PubMed1994

Doppler catheter tip localization using color enhancement.

The objective of this research was to determine if the ultrasound emissions of the Doppler catheter can be used to locate its position in 3 dimensions by conventional echocardiography. A Doppler catheter has previously been shown to permit nonfluoroscopic retrograde catheterization of the aortic root and left ventricular chamber by using velocity waveform polarity for directional guidance. A significant difficulty in providing ultrasound catheter guidance, however, has been the inability to recognize the Doppler catheter tip, because each point at which a flexible catheter crosses the image plane can be misinterpreted as the catheter tip. Initial in vitro water bath trials were performed using the Doppler catheter attached to a standard velocimeter. Using a 5 MHz imaging transducer and color Doppler methods, the presence or absence of a banded color pattern which could demarcate the Doppler catheter tip was recorded at various angles in and out of the scanning plane. Using Doppler retrograde guidance and transesophageal echocardiography, color Doppler banded patterns, which could identify the Doppler catheter tip, were investigated in the dog aorta. In order to understand the physical mechanisms involved, a series of water bath trials were then conducted using the Doppler catheter attached to a velocimeter which was synchronized to the echo machine. Initial nonsynchronized water bath trials revealed distinct banded color patterns demarcating the Doppler catheter tip when it pointed in any direction within the beam width, except for a 40 degrees blind cone directly away from the imaging transducer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Nonuniformity of inner and outer systolic wall thickening in conscious dogs.

Transmural differences in systolic wall thickening were analyzed in 13 conscious dogs by implanting sonomicrometers to continuously measure total wall thickness (WT) and outer WT approximately half the distance through the myocardium at a closely adjacent location. Inner WT was derived by subtraction of outer WT from total WT. Outer wall measurements spanned, on average, the outer 44 +/- 10% (+/- SD) of the wall; derived inner wall measurements spanned the remaining 56 +/- 10%. At rest the fractional contribution (FC) of the outer wall to total systolic wall thickening was 29 +/- 9%, which was significantly less than the FC of the inner wall, 71 +/- 9%. These data are in good agreement with simplified modeling of a cross section of the left ventricle as two concentric rings that predicts that the FC of inner and outer halves of the wall should be approximately 67 and 33%, respectively. During treadmill exercise, the extent of both inner and outer thickening increased significantly (30 and 29%, respectively) but the relative FC of the inner and outer wall remained the same. The data indicate that systolic wall thickening is nonuniform and that this nonuniformity remains constant during the increased inotropic and chronotropic stimulation associated with exercise.

Animals↗
PubMed1985

Coronary blood flow and myocardial segment dimensions during simulated dives in seals.

Three harbor seals Phoca vitulina richardsi and five spotted seals Phoca vitulina largha were used in studies of acute episodes of local myocardial ischemia in open-chest, anesthetized animals and of coronary blood flow and regional function as indicated by left ventricular segment dimensions during experimentally simulated dives of conscious, instrumented animals. We observed that seal myocardium, in which there are few coronary anastomoses, responded to brief local occlusion with prompt local dysfunction and systolic bulging; coronary flow in the nondiving seal oscillated irregularly and declined with spontaneous apnea and related falling heart rate; flow continued to oscillate but was much reduced during dives, frequently ceasing entirely for periods as long as 45 s; ventricular segment dimension shortening was reduced intermittently during dives; and elevated heart rate induced during dives by cardiac pacing or by administration of atropine diminished or eliminated the reductions in coronary blood flow. Responses of seal heart reflect the reduction in cardiac metabolic demand during diving and the seal's myocardial adaptation for enhanced anaerobic glycolysis. The seal heart can maintain mechanical function during dives with minimal coronary perfusion, despite the progressive and ultimately profound hypoxia, hypercapnia, and acidosis. Reduced cardiac metabolism, copious glycolytic reserves, and metabolite washout by intermittent brief bursts of coronary blood flow are apparently sufficient to support continued cardiac function, even though the seal heart has little tolerance for acute localized ischemia.

Animals↗
PubMed1985

Effect of the combination of diltiazem and atenolol on exercise-induced regional myocardial ischemia in conscious dogs.

The effect of combination therapy with diltiazem and atenolol on the regional myocardial blood flow-function relationship was studied in eight conscious dogs with chronic coronary artery stenosis. An ameroid constrictor and hydraulic occluder were placed around the left circumflex coronary artery, sonomicrometers were implanted for measuring wall thickness in control and ischemic regions, and regional myocardial blood flow was measured with the microsphere method. Eighteen days (average) after surgery, resting regional myocardial function and blood flow were normal, but treadmill exercise induced severe regional myocardial dysfunction in the posterior wall (wall thickening during systole reduced from 25.5% to 2.7%, a 90% reduction). Subendocardial blood flow decreased by 68% from the control standing value, while subepicardial flow increased. An identical exercise bout was performed 3 hr after administration of atenolol (1.0 mg/kg orally) and 15 min after administration of diltiazem (0.3 mg/kg iv). Heart rate during running was significantly lower as were left ventricular peak systolic pressure, end-diastolic pressure, and peak dP/dt. Wall thickening in the control region was not augmented during exercise after atenolol and diltiazem. There was less dysfunction in the ischemic region (35% reduction) and the improved performance was accompanied by a substantial increase in subendocardial perfusion (0.31 +/- 0.14 vs 0.61 +/- 0.30 ml/min/g, a 36% reduction from rest). Epicardial flow was unchanged, and the endocardial/epicardial ratio increased (0.27 +/- 0.13 vs 0.62 +/- 0.29). Recovery time for regional wall thickening also improved. The beneficial effects of the combination of atenolol and diltiazem in a preparation of single-vessel chronic coronary stenosis were shown to be significantly greater than those of either drug alone.

Animals↗
PubMed1984

Effects of beta-blockade on regional myocardial flow and function during exercise.

We examined the effects of a cardioselective beta-blocking drug on exercise-induced regional myocardial ischemia in 10 conscious dogs with chronic coronary artery stenosis. An ameroid constrictor, Doppler flowprobe, and hydraulic cuff were placed around the left circumflex coronary artery, and left ventricular pressure (LVP), systolic wall thickening (% delta WT; by sonomicrometry), and myocardial blood flow (MBF; microspheres) were measured during control standing, control treadmill exercise, and identical exercise after atenolol (1 mg/kg po). Prior to study, in every dog % delta WT and MBF in the ischemic area were normal at rest, indicating collateral development. During control exercise, % delta WT in the ischemic region markedly decreased from 27 to 4%, and transmural ischemia was evident in that region. Heart rate, systolic LVP, and LV (+)dP/dt were significantly lower during exercise after atenolol than during control exercise. % delta WT in the normal area was only 81% of that during control exercise, but dysfunction in the ischemic area was improved (77% increase compared with control exercise). Accompanying the improved function was a significant increase of MBF/beat and relative MBF in the ischemic zone; the endocardial-to-epicardial ratio increased from 0.27 to 0.47. Thus atenolol improved regional MBF distribution, thereby diminishing exercise-induced regional myocardial dysfunction and accelerating its recovery.

Adrenergic beta-Antagonists↗
PubMed1984

Regional myocardial perfusion and wall thickening during ischemia in conscious dogs.

We examined in conscious dogs the effects of reductions in myocardial blood flow (MBF) in three different layers across the wall on regional myocardial contractile function in the ischemic zone, measured as systolic wall thickening (%WT). In 16 dogs, %WT was measured with sonomicrometry and MBF was determined with microspheres (10- to 12-microns diam) during coronary stenosis of the left circumflex coronary artery. The stenoses were categorized into six groups by the effect on %WT (each group representing progressive 20% decrements in %WT from control), and individual and pooled regression analyses were performed on data from six of the dogs having multiple data points to evaluate the shape (linear or curvilinear) of the relationships between MBF and changes in %WT. Transmural contractile function was highly sensitive to acute reductions in MBF, especially reductions in the subendocardium. The shape of the normalized subendocardial MBF-%WT relation was mildly curvilinear by regression analysis (quadratic equation, gamma = -0.75x2 + 2.15x -0.39, r2 = 0.92). Likewise, mean transmural and midmyocardial MBF correlated well and closely with changes in %WT. Subepicardial MBF, however, correlated poorly with changes in %WT, there being no change in subepicardial MBF until %WT had been reduced more than 50%.

Animals↗
PubMed1984

Effects of a calcium-entry blocker (diltiazem) on regional myocardial flow and function during exercise in conscious dogs.

We examined the effects of diltiazem, a calcium-entry blocker, on exercise-induced myocardial ischemia in nine conscious dogs with chronic coronary stenoses. An ameroid constrictor, Doppler flow probe, and hydraulic occluder were placed around the left circumflex coronary artery, and left ventricular pressure was measured (Konigsberg micromanometer). Pairs of ultrasonic crystals were implanted for measuring left ventricular systolic wall thickening (% delta WTh) in control (left ventricular anterior wall) and ischemic (left ventricular posterior wall) regions, and regional myocardial blood flow was measured with the microsphere method. Eighteen days (average) after surgery mean coronary blood flow velocity had decreased and reactive hyperemic flow velocity after 10 sec of coronary occlusion was markedly reduced, but % delta WTh at rest remained normal, indicating collateral development. Control treadmill exercise was performed for 3.7 min (average), and 2 hr later administration of 0.3 mg/kg diltiazem was followed by an identical exercise bout. Control exercise increased % delta WTh in the normal region, while in the ischemic region % delta WTh decreased markedly and ischemia was evident (subendocardial flow, 0.29 +/- 0.12[SD] ml/min/g). After diltiazem hemodynamic and % delta WTh values at rest were not changed; during exercise the heart rate was significantly lower (204 +/- 24 vs 227 +/- 33 beats/min, p less than .01), but values for other hemodynamic measures were similar to those during the control run. % delta WTh in the control region was not changed during exercise after diltiazem, but compared with control exercise in the ischemic zone there was less dysfunction and subendocardial flow was greater. Recovery from exercise-induced dysfunction in the ischemic region occurred within 5 min, compared with over 30 min after control exercise. Thus, in a preparation of chronic coronary stenosis, the calcium-entry blocker improved the relationship between regional myocardial flow and function during exercise and led to more rapid recovery of regional myocardial dysfunction.

Animals↗
PubMed1983

End-systolic dimension-wall thickness relations during myocardial ischemia in conscious dogs. A new approach for defining regional function.

Overall and regional left ventricular (LV) function was studied during progressive coronary stenosis in conscious dogs by determining the relations at end-systole between LV pressure, chamber dimensions, and regional LV wall thickness. An index of regional wall stress was also analyzed. Using ultrasonic dimension gauges, measurements were made of LV wall thickness in control and ischemic regions, and the external long- and short-axis LV diameters were determined; an implanted micromanometer measured LV pressure. Internal LV diameters were obtained from the external diameters by subtraction of wall thickness, and the index of regional wall stress employed a thick-walled ellipsoidal model. During regional ischemia, the LV long axis at end-systole did not change, whereas the short-axis diameter progressively increased (from 24 +/- 7 mm [standard deviation] to 30 +/- 9 mm, p less than 0.001, indicating a more spherical LV shape during ischemia). The end-systolic pressure did not change, and therefore the end-systolic pressure-diameter relation shifted progressively, suggesting a global decrease in LV contactility. The end-systolic points relating LV wall thickness in the ischemic region to the end-systolic LV pressure revealed the regional nature of the abnormality, showing a progressive displacement to the left, whereas there was no significant displacement of this relation in the control region. The application of this index over a range of loading conditions during partial vena caval occlusion was illustrated. Thus, the regional end-systolic wall thickness-pressure relation provides a new index for defining the regional contractile state of the LV myocardium which is potentially load-independent and offers the possibility for echocardiographic application.

Animals↗
PubMed1983

Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion.

Prolonged nontransmural ischemia was produced and the early and late effects of reperfusion were studied in 10 conscious dogs instrumented over the long term. Five hours of partial circumflex coronary artery stenosis was produced with a hydraulic occluder, followed by gradual release over 20 min, with measurements of left ventricular pressure, regional myocardial function (systolic wall thickening by sonomicrometry), coronary blood flow velocity (pulsed Doppler), and myocardial blood flow (microspheres). During coronary stenosis the occluder was adjusted frequently to maintain a reduction of systolic wall thickening to 50% to 75% of control (average 62.6% of control). Myocardial blood flow in the ischemic area at 4 hr of partial coronary stenosis was reduced in the inner layers of the myocardium (subendocardium, from 0.81 +/- 0.18 at control to 0.36 +/- 0.08 SD, p less than .01; midwall, from 0.77 +/- 0.20 to 0.46 +/- 0.07 ml/min/g, p less than .01), accompanied by significant ST segment elevation on the subendocardial electrogram (0.83 +/- 0.96 to 4.58 +/- 4.10 mV; p less than .05) and decreased left ventricular dP/dt (3503 +/- 462 to 2991 +/- 339 mm Hg/sec; p less than .01). Within a few minutes after complete release of partial coronary stenosis, ST segments returned to control and myocardial blood flow of the inner layers was increased (subendocardium, 1.37 +/- 0.39, p less than .01; midwall, 0.97 +/- 0.28, p less than .05), but systolic wall thickening and left ventricular dP/dt were significantly depressed and remained reduced at 24, 48, and 72 hr when myocardial blood flow was normal. By seven days, systolic wall thickening and left ventricular dP/dt had returned to control (94.1 +/- 7.0% of control, 3353 +/- 605 mm Hg/sec, respectively; NS). Histologic changes caused by ischemia constituted only 2.7% (average) of the tissue between the crystals in the ischemic wall, but ischemic damage in the posterior papillary muscle, which did not contain crystals, was 31.9%. Thus, regional myocardial dysfunction reduced by nontransmural ischemia for 5 hr persisted for at least 3 days, with only slight damage to the left ventricular free wall but considerable infarction of the posterior papillary muscle. Full recovery of regional and global contractile function of the free wall then occurred within a period of 1 week.

Animals↗
PubMed1983

Effect of exercise on the relationship between myocardial blood flow and systolic wall thickening in dogs with acute coronary stenosis.

Relationships between regional myocardial perfusion and transmural function, both during treadmill exercise and at rest, were examined in conscious dogs with varying degrees of coronary stenosis produced by a hydraulic occluder. In 13 dogs we measured myocardial blood flow with microspheres (10-12 microns in diameter) and regional systolic wall thickening (%). During exercise with coronary stenosis, myocardial blood flow was characterized by nonuniform distribution, and associated with regional dysfunction. The relationships between normalized myocardial blood flow and normalized %wall thickening during exercise with coronary stenosis were linear, with significantly different slopes (mean myocardial blood flow: y = 1.23x - 0.16, r = 0.93; subendocardial myocardial blood flow: y = 1.50x - 0.02, r = 0.86; subepicardial myocardial blood flow: y = 0.83x - 0.18, r = 0.87). To fill the gap between available subendocardial and subepicardial data during exercise with coronary stenosis and control points, however, would require nonlinear components. In 10 of the dogs, coronary stenosis at rest was also produced to compare regional myocardial blood flow - %wall thickening relations at rest with those during steady state exercise. The absolute mean myocardial blood flow - %wall thickening relation during exercise with coronary stenosis (y = 11.6x - 1.9, r = 0.90) was significantly shifted rightward from the resting relation (y = 25.3x -2.1, r = 0.80). However, when changes in %wall thickening were plotted vs. myocardial blood flow per beat, the relationships at rest and exercise were nearly superimposable. Likewise, relations between normalized myocardial blood flow and changes in %wall thickening at rest and exercise were not significantly different. We conclude: %wall thickening during exercise is directly related to changes in mean myocardial blood flow but is related in nonlinear fashion to changes in subepicardial and subendocardial myocardial blood flow; %wall thickening may provide a reliable index of the relative transmural flow distribution during exercise as well as at rest; during brief bouts (5-8 minutes) of exercise with coronary stenosis, the relationship between stabilized regional contractile dysfunction and level of myocardial blood flow per beat is the same as that during coronary stenosis at rest.

Acute Disease↗
PubMed1982

Left ventricular geometry during partial and complete coronary occlusion in the conscious dog.

Seven dogs were instrumented with a left ventricular micromanometer and pairs of ultrasonic crystals to measure left ventricular wall thicknesses (control and ischemic regions) and short and long left ventricular axes; cuff occluders were placed around the left circumflex coronary artery and the inferior vena cava. Measurements were performed at rest, after 2 min of partial and complete coronary occlusion, and 1 and 10 min after release of partial and complete coronary occlusion. Left ventricular wall thickness in the ischemic region showed reduced systolic thickening during partial coronary occlusion and systolic thinning during complete coronary occlusion. During diastole, at zero pressure (inferior vena cava obstruction) the left ventricular short axis was unchanged during partial coronary occlusion but significantly increased (creep) during complete coronary occlusion (P less than 0.05), whereas after release of both partial and complete coronary occlusion the short axis at zero pressure decreased significantly (P less than 0.025). Left ventricular wall thickness at zero diastolic pressure in the ischemic region was significantly thinner during complete coronary occlusion than during control and significantly thicker (reactive hyperemia) 1 min after release of both partial and complete coronary occlusion. The long left ventricular axis remained unchanged during the entire experiment. At end-diastole, the long/short axis ratio was normal during partial (1.72; control 1.68; NS) and complete coronary occlusion (1.69; NS), but it decreased significantly from control of 2.10 to 1.99 with partial coronary occlusion and 1.85 with complete coronary occlusion (P less than 0.01). The changes in the L/S ratio during partial and complete coronary occlusion were proportional to changes in left ventricular chamber volume (correlation coefficient 0.94). Our data show that left ventricular shape remains normal at end-diastole during partial and complete coronary occlusion but becomes significantly more spherical at end-systole, with reduction of the normal tendency for the ventricle to become more elliptical during systole. These elliptical and spherical shape changes of the left ventricle during partial and complete coronary occlusion appear to be closely related to the chamber volume.

Animals↗
PubMed1982

Isoproterenol-induced myocardial dysfunction in dogs with coronary stenosis.

Stress-induced regional myocardial ischemia in the presence of mild coronary stenosis was studied in five dogs 2-4 wk after implantation of pairs of ultrasonic crystals to measure left ventricular wall thickening (% delta WT) and subendocardial segmental shortening (% delta L). Isoproterenol (0.2 micrograms.kg-1.min-1) was infused before and after production of coronary stenosis, which produced no resting dysfunction. During isoproterenol infusion with coronary stenosis % delta WT and subendocardial % delta L were significantly decreased although blood flow was comparable to conditions at rest, indicating that the demand for blood flow exceeded supply. Linear regression analysis of mean transmural blood flow versus % delta WT during isoproterenol demonstrated that wall thickening was significantly related to changes in mean blood flow: y (percentage wall thickening) = 27.5 X (transmural blood flow) -8.2 (r = 0.83); likewise % delta L was significantly related to subendocardial blood flow during isoproterenol infusion: y (percentage shortening) = 17.1 X (subendocardial blood flow) -0.4 (r = 0.85). These results indicate that both regional % delta WT and % delta L sensitively reflect the adequacy of myocardial perfusion even during stress-induced changes in myocardial O2 demands and blood flow.

Animals↗
PubMed1982

Myocardial blood flow and function with critical coronary stenosis in exercising dogs.

Critical stenosis of coronary arteries does not alter myocardial blood flow (MBF) at rest, but eliminates hyperemia and corresponds to a degree of arterial narrowing that expends subendocardial vasodilator reserve. Because subepicardial vasodilator reserve remains with critical stenosis at rest, we tested the significance of this reserve in six exercising dogs chronically instrumented to measure MBF (microspheres), regional function (systolic wall thickening with sonomicrometers), and coronary blood flow velocity (CBFV, pulsed Doppler). Critical stenosis produced with a hydraulic occluder limited CBFV and mean MBF to the resting level during treadmill exercise, but MBF was maldistributed. Subendocardial MBF decreased 50% (P less than 0.05) and subepicardial MBF increased 104% (P less than 0.01) compared with resting control conditions, suggesting that a transmural "steal" phenomenon had occurred, with augmented MBF in the subepicardial region at the expense of subendocardial MBF. Systolic wall thickening decreased markedly from 31.5 +/- 6.8 to 9.4 +/- 2.0% (P less than 0.01) during exercise, indicating that use of subepicardial vasodilator reserve with critical stenosis had little sustaining effect on regional contractile performance. Rather, subepicardial vasodilator reserve is potentially deleterious, inasmuch as a steal effect could contribute to reduced subendocardial perfusion, the primary determinant of systolic wall thickening.

Animals↗
PubMed1982

Comparison of postpacing and exercise-induced myocardial dysfunction during collateral development in conscious dogs.

In 10 conscious dogs, a model was developed for studying regional contractile responses in a coronary collateral-dependent bed. Regional myocardial function was compared after terminating a maximum paced rate of 240 beats/min maintained for 3 minutes (postpacing period) with that during telemetry-monitored exercise at comparable heart rates (average 252 +/- 34 beats/min, duration 2.4 minutes) at different times during collateral development. Ultrasonic dimension gauges were used to measure control and ischemic segment (CS and IS) lengths and ischemic zone regional wall thickness (IW). An ameroid constrictor and a Doppler flow probe were placed around the left circumflex coronary artery, and pacing electrodes were sutured to the right ventricle. An average of 23 days postoperatively, coronary obstruction was complete. Studies at that time showed that percent shortening (% delta L) of IS and percent wall thickening (% delta W) of IW decreased after pacing to 57% and 35% of control, respectively, and during exercise to 37% of control. One week later (average 30 days postoperatively), significant depression of regional function no longer occurred postpacing. However, exercise at a comparable heart rate still provoked regional dysfunction in the collateral-dependent zone: Both IS% delta L and IW% delta W decreased to 51% of control. Regional function at rest did not differ during these studies. Thus, the effectiveness of the postpacing response for detecting limited collateral reserve was eliminated by further collateral development, but regional myocardial dysfunction during exercise stress served to detect ischemia despite increased collateral circulation.

Animals↗
PubMed1981

[Determinants of the diastolic pressure-volume relationship of the left ventricle: significance of myocardial ischemia and vena cava occlusion].

Diastolic pressure-volume relations of the left ventricle were studied in 7 dogs during partial and complete coronary occlusion. The pericardium was widely opened and the dogs were instrumented with a left ventricular micromanometer, cuff occluders around the left circumflex coronary artery and inferior vena cava, and ultrasonic crystals to measure control and ischemic wall thickness as well as both left ventricular long and short axes. Measurements were performed at rest and after 2 minutes of partial and complete coronary occlusion. The first experiment was performed without caval occlusion and a second experiment was carried out a few days later with caval occlusion. During partial coronary occlusion, no shift of the diastolic pressure-volume relationship was observed. However, during complete coronary occlusion the pressure-volume curve was shifted significantly upwards but no shift was observed when occlusion of the inferior vena cava was carried out. These findings suggest that the shift of the diastolic pressure-volume relationship during coronary occlusions (1) depends on the extent of myocardial ischemia and (2) is related to ventricular interaction since the shift was prevented by caval occlusion.

Animals↗