Biomedical subjects
Publications and source records attributed to J D Laird.
A case of metastatic phaeochromocytoma is presented. Meta-iodobenzylguanidine was used to locate the tumour but failed to show two functioning abdominal metastatic deposits. Although meta-iodobenzylguanidine appears to be highly specific for phaeochromocytoma, a negative scan does not exclude a functioning tumour with confidence.
The hypothesis that tissue oxygen tension controls coronary vascular resistance during changes in perfusion pressure and oxygen consumption was expressed in a simplified mathematical form capable of making quantitative predictions. The predictive value of this formulation of the hypothesis was tested in experiments on anaesthetized mongrel dogs subjected to constant-pressure perfusion of the left main coronary artery, with measurements of coronary blood flow and arterio-venous oxygen content differences. Coronary venous oxygen content was used as an index of tissue oxygenation. The responses of coronary blood flow and arterio-venous oxygen content difference, made over a range of perfusion pressures (which caused autoregulation) and heart rates (which caused metabolic regulation) were predicted qualitatively by the model. Coronary vascular conductance was positively related to metabolic rate only during metabolic regulation (heart rate changes); during autoregulation the relationship between these two variables was inverse. Coronary vascular conductance and resistance values taken from both interventions (both perfusion pressure and heart rate variations) were closely related to coronary venous oxygen content and calculated PO2. These findings suggest that further examination of oxygen tension, as the controller of the coronary vascular bed under physiological conditions should be considered.
The viscoelastic behavior of single resting vascular smooth muscle cells from bovine coronary artery was studied. No maintained passive force could be recorded, even when the cells were stretched to two to four times their initial length; this finding suggests that the smooth muscle cells do not contribute to the parallel elastic component in arterial smooth muscle tissue. The force during stretch of resting arterial cells was proportional to the rate of stretch (which varied between 20 and 60% of the initial length per second). This linear viscous resistance was also found for toad stomach cells when similar stretches were applied. The stress-relaxation curves of the arterial cells could be fitted to the sum of two exponential components (with half-lives of 13.1 and 0.5 s, respectively). As a result of the above findings, a model consisting of two viscoelastic elements in parallel was proposed for a single resting arterial smooth muscle cell. The viscous resistance to stretch of resting cells in a Ca2+-containing solution was not significantly (P greater than 0.01) different from that in a Ca2+-free solution. The same result was obtained for bovine coronary arterial rings. It is concluded that an adequate model for resting arterial smooth muscle should include an intracellular viscous element.
Single smooth muscle cells from bovine coronary artery were obtained by enzymatic digestion. 20.1 +/- 3.2% (mean value of seven experiments) of the dispersed cells were in a relaxed, noncontracted state. These cells responded to electrically induced depolarization with a graded contraction to a maximum shortening of 47.8% of initial length; the corresponding maximum for K+-induced depolarization was 61.7% of initial length. Cells relaxed only a small percentage (approximately equal to 20%) of the amount of shortening, but could be restimulated several times to contract to even shorter lengths. The decrease in mean cell length of dispersed cells exposed to serotonin, acetylcholine, and ergonovine maleate was 21.0, 23.0 and 25.5%, respectively (p less than 0.05). No significant decrease in cell length was obtained with norepinephrine. The ultrastructure of the relaxed cells seemed to be unaltered, suggesting that the accuracy of the physiological results is not impaired by induced structural damage.
The value of gallium ((67)Ga) scanning in the diagnosis of septic disease of bone or joint was assessed in 34 patients. The results show a sensitivity of 60 per cent and specificity of 64 per cent. The low accuracy of this method for the detection of bone and joint sepsis (62 per cent) means that gallium scanning can be used only as an adjunct to other investigative techniques.
Indium-111 labelled autologous leucocyte imaging was used to assess severity in 13 patients with acute pancreatitis. All three patients with severe disease as judged by a prognostic factor grading system had a positive result on imaging. A fourth patient with mild disease as judged by prognostic factors had a positive imaging result and 14 days later developed a pseudocyst. There were no false positive or false negative scans. Evidence from three patients suggested that a positive 111In-leucocyte imaging result implies substantial fat necrosis. In this study imaging was as accurate as prognostic factor grading. The technique may be a useful method of separating mild from severe acute pancreatitis.
A technique is described for investigating tumors of the carotid body and glomus jugulare. The examination comprises an easily performed radionuclide angiogram, and has been used to investigate 30 patients. This technique demonstrated seven carotid-body tumours, including two unsuspected clinically, and one tumor of the glomus jugulare. There was also one patient with a false-positive test for bilateral carotid-body tumors. Angiographic and/or surgical confirmation was obtained in all cases but one. A significant incidence of complication during contrast angiography was noted (two cases of transient hemiparesis). The radionuclide angiogram proved safer than contrast angiography and more reliable than clinical examination; it therefore appears to be the method of choice as the primary screening test in patients with suspected carotid-body and glomus-jugulare tumors.
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Coronary vasodilation after brief (less than 15 s) occlusions was studied in closed-chest, anesthetized dogs, using constant-flow perfusion of a large coronary artery. We assumed occlusion duration to be a measure of the concentration of endogeneous adenosine and determined adenosine dose-response curves by varying occlusion duration and measuring the resulting drop in vascular resistance. The curves were compared to dose-response curves measured by continuously infusing adenosine. Both dose-response relations were found to follow the Hill equation for ligand receptor interaction; the slopes of the two curves were not significantly different, and the estimated adenosine accumulation rate in the myocardium was found to be in close agreement with data in the literature, measured by direct tissue assay. The time course of recovery of vascular tone after short occlusions was not very sensitive to flow, at least not for normal flow levels or higher. The results confirm that adenosine accumulation plays an important role in causing postocclusion vasodilation. However, autoregulation of coronary flow based on an adenosine washout mechanism additionally requires tissue clearance to be highly flow dependent for flow levels below normal, but approaches a constant value when flow increases above normal.
Isolated externally paced (300 beats/min) rat hearts were perfused at constant pressure (70 mmHg) using a modified Krebs-Henseleit solution with (n = 52) and without (n = 15) washed bovine red cells. Albumin concentration varied from 1 to 10 g/dl. With increasing albumin concentration in blood-perfused hearts, wet-to-dry weight ratio, peak reactive hyperemic flow, and control geometric resistance were decreased, whereas oxygen consumption, control flow, and minimal geometric resistance remained constant. For plasma-perfused hearts, there was a decrease in both control and peak flow, and the other results were similar to the blood-perfused hearts. These results indicate the following. 1) Increase in interstitial fluid volume is not sufficient to cause a significant increase in minimal vascular resistance. 2) Increase in blood viscosity is compensated by vasodilation maintaining steady flow constant. 3) Minimal vascular resistance is determined by physical geometry of the vascular bed. 4) Regulation of coronary flow is postulated to be achieved by smooth muscle response to interstitial osmolarity, with a negative feedback signal coming from variation of capillary arterial pressure to variations in flow.
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Oxygen uptake during myocardial hyperemia (MRH) following occlusions of 2.5-30 s was studied in nine anesthetized open-chest dogs by continuous measurement of left anterior coronary blood flow and anterior coronary vein oxygen saturation with electromagnetic flowmeter and fiber-optic catheters, respectively. The ratio of excess oxygen uptake to debt multiplied by 100% was defined as the oxygen repayment ratio (RR) and varied between -50% and +150% (mean 78%). Application of a steady-state Fick formula, as used by previous investigators, results in a profound overestimate of the RR (70-400%, mean 295%). RR is severely distorted by the venous catheter system, and after consideration of these effects we would conclude that the "true" RR in MRH is even lower than we found. Comparing our results with steady-state exercise autoregulation leads us to the following conclusions: 1) chemical kinetic limitations in oxygen release by red blood cells are excluded, 2) a simple direct PO2 regulation of flow is unlikely, but 3) our results are not inconsistent with a more complex integral oxygen regulation or with the metabolic hypothesis.
Twenty-five patients with class III or class IV left ventricular failure (Myocardial Infarction Research Unit criteria) after a recent myocardial infarction were treated with intraaortic balloon pumping between December 1, 1972 and December 1, 1976. Three patients had no improvement and died during pumping. Two patients with improvement died during at attempt at weaning from circulatory assistance. Of 20 patients successfully weaned, 6 died within 3 months, 5 of these within 10 days after the weaning procedure. Of 14 patients who survived for more than 3 months, 13 were alive on February 15, 1977. Twelve of these 13 were in functional class II and 6 had resumed professional activities. Intraaortic balloon pumping proved an effective method for treating severe left ventricular failure after an acute myocardial infarction. Even withour surgery, 14 of 25 patients survived 3 or more months after an acute infarction complicated by serious pump failure.
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Given the substantial reserve of normal myocardium, its inability to sustain life in the presence of 30-50% necrosis of the left ventricle (LV) seems a paradox. It is known that dyskinesia of the infarcted area probably plays a dominant role in initiating failure after an infarction. To study this problem, a well defined experimental infarction was produced by cryogenic means in 58 rabbits, and the animals were allowed to recover. Groups of rabbits were killed 4 hours and 1,2,5, or 10 days following infarction. As quickly as possible (within 4 minutes) a sample specimen from the infarcted area was removed from the LV and subjected to a force-elongation test while being bathed in Ringer solution at 37 degrees C equilibrated with 95% O2-5% CO2. The data were interpreted assuming an exponential stress-strain law with constants K and C. Mean values of K of 10.6 +/- 0.94 (SEM) were found for the noninfarcted control group, whereas, rather surprisingly, no significant trend in K over 10 days was found in the infarcted group. Mean values of K +/- SEM for the postinfarction groups were as follows: 4 hours, 9.51 +/- 0.63; 1 day 10.54 +/- 1.13; 2 days, 13.15 +/- 2.28; 5 days, 11.59 +/- 1.36; and over 10 days, 12.93 +/-1.02. The functional implications were estimated with a simple model of the shortening required of the viable muscle during the isovolumic phase. It was found that contractile reserve fell rapidly with increasing infarct size, reaching zero for a 60% infarct when K = 10. With K greater than 100, there was no appreciable reduction in reserve. With a constant infarct size, variation in reserve with the afterload-preload ration was found to be logarithmic.
Resolution is the ability of the echocardiographic system to distinguish closely lying structures. This is usually defined in two directions: laterally (lateral resolution) and in depth (axial resolution). With use of short ultrasonic pulses, axial resolution is not a major problem. By far the more important problem is the limited lateral resolution that results from the finite beam width of current ultrasonic devices. This results in the display of echoes that originate from off-axis structures. How these off-axis or "spurious echoes" affect the display is a function of the way the echographic information is handled. In conventional M-mode tracings, spurious echoes are displayed at a site where there is no directly corresponding anatomic structure, whereas with two-dimensional imaging, these echoes may result in important distortions of structures. The underlying principles are illustrated by a clinical experiment wherein the ball of a Starr-Edwards mitral valve prosthesis serves as a target of known shape and dimensions. These data are used to elucidate some of the problems and potential errors encountered in the interpretation of clinical M-mode recordings of the aorta, mitral valve and the left ventricular endocardium as well as their cross-sectional analysis. They also explain the present limitations of quantification of left ventricular performance from cross-sectional images.
The goal of this study was to develop, on a rational basis, an index of the intrinsic diastolic elastic properties of the left ventricle. A relatively simple analytic model employing a thin-walled spherical geometry coupled with an approximate formulation of a two-dimensional constitutive relation, was used to examine the primary determinants of the pressure-volume relationship of the intact heart. The results permit comparison with other indices of compliance or wall stiffness. The slope of the dP/dV vs P curve was found to be sensitive to the non-linear elastic constant K, but is also sensitive to variations in cardiac muscle volume. VdP/dV was found to be sensitive to pressure. m = d(log P)/d(log V) = (V/P)(dP/dV) is proposed as an index sensitive to K and relatively insensitive to both pressure and initial cardiac geometry. The index is compared with published studies. Using the data of Fester and Samet, mean values of the asymptotic log-log P-V slope, m, evaluated at end-diastole for normal, idiopathic hypertrophy, mild, moderate and severe coronary artery disease were 3.95 +/- 0.60 (SEM), 5.05 +/- 1.60, 5.24 +/- 0.96, 8.35 +/- 2.06, and 15.13 +/- 3.0, respectively. At values of LVEDP less than 7 mm Hg the concept of simple distension is questioned. The advantages and limitations of this approximate index are discussed. This index seems to afford a practical measure of the elastic properties of the wall over a rather wide range of pressure, volume, wall mass and wall thickness.