Measurements of Young's modulus of elasticity of the canine aorta with ultrasound.
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Biomedical subjects
Publications and source records attributed to C F Babbs.
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Anesthetized dogs were cooled to a core body temperature of 26 degree C. or maintained at a body temperature of 37 degree C. during periods of 5 and 10 hours of LAD coronary artery occlusion. Subsequent macroscopic dehydrogenase enzyme mapping showed that ischemic injury was 25 per cent less after 5 hours of coronary occlusion and 20 per cent less after 10 hours of occlusion in hypothermic dogs than in normothermic controls. The heart rate and left ventricular minute work in hypothermic dogs decreased to roughly half the levels measured in normothermic animals, while left ventricular contractility was 10 to 40 per cent lower in hypothermic dogs than in normothermic dogs. However, cardiac index and left ventricular end-diastolic pressure were unchanged by whole-body cooling. Thus, hypothermia appeared to diminish the oxygen requirements of the ischemic myocardium without reducing the performance of the heart as a pump. Hypothermia may be useful as a therapeutic adjunct to myocardial revascularization or pharmacologic interventions.
The effect of pentobarbital anesthesia upon the minimal voltage and current required for electrical ventricular defibrillation (the defibrillation threshold) was investigated in dogs. Threshold current, energy, and charge in five dogs averaged 2 per cent, 13 per cent, and 6 per cent less under surgical levels of pentobarbital anesthesia than thresholds in the same animals in the awake, unanesthetized state. In dogs given sufficient pentobarbital to produce apnea and supported by mechanical ventilation, threshold current, energy, and charged averaged 3 per cent, 17 percent, and 2 per cent less than comparable awake values. These differences were far from statistically significant. In a second study, five dogs were kept for 8 to 10 hours at a surgical level of anesthesia with pentobarbital sodium. Defibrillation threshold current, determined at hourly intervals, did not drift outside +/-10 per cent limits. Arterial blood gas measurements revealed a stable, compensated metabolic acidosis in all animals (pH 7.36 +/- 0.06, pCO2 33 +/- 4 mm. Hg, pO2 71 +/- 9 mm. Hg). These data support the validity of defibrillation studies using animals anesthetized with pentobarbital and indicate the stability of the defibrillation threshold under controlled experimental conditions.
Over 200 measurements of the minimum damped sinusoidal current and energy for transchest electrical ventricular defibrillation (ventricular defibrillation threshold) were made to determine the stability and precision of threshold data in 15 pentobarbital-anesthetized dogs. Threshold was determined by repeated trials of fibrillation and defibrillation with successive shocks of diminishing current, each 10% less than that of the preceding shock. The lowest shock intensity that defibrillated was defined as threshold. In three groups of five dogs each, threshold was measured at intervals of 60, 15, and 5 min over periods of 8, 5, and 1 h, respectively. Similar results were obtained for all groups. There was no significant change in mean threshold current with time. Owing to a decrease in transchest impedance, threshold delivered energy decreased by 10% during the first hour of testing. The standard deviations for threshold peak current and delivered energy in a given animal were 11% and 22% of their respective mean values. Arterial blood pH, Pco2, and Po2 averaged change of pH, PCO2 and PO2 were not significantly different from zero. The data demonstrate that ventricular defibrillation threshold is a stable physiological parameter that may be measured with reasonable precision.
In order to minimize interaction of sorbents with food and digestive secretions, an intestinal bypass was created for sorbent administration in normal and uremic rats (N = 18) and goats (N = 5). Two separate limbs of small intestine were fashioned, one for food absorption and one for sorbent function, which joined at a Roux-Y anastomosis before the cecum. Particulate sorbent suspensions were injected into the intestine via a cutaneous stoma, and were excreted with food wastes in the feces. In animals with normal kidneys, sorbent function was calculated from changes in fecal and urinary excretion. Nitrogen clearance by the intestinal bypass was 20 to 40% of normal renal clearance in rats and goats. Potassium clearance was 40% of normal renal clearance in rats, and over 100% in goats. Sorbent treatment in anephric animals caused serum urea nitrogen concentrations to stabilize at 210 mg/dl in rats, and 110 mg/dl in goats. Serum potassium concentrations stabilized at 4.5 mEq/liter in rats, and fell to 2 mEq/liter in goats. Water balance was maintained by producing a mild osmotic diarrhea. At least three substances which accumulate in renal failure--urea, potassium, and water--were removed in therapeutically significant amounts.
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OBJECTIVE: To review the history of external abdominal compression as an adjunct to cardiopulmonary resuscitation (CPR), tracking the development of five major themes over the course of the 20th century: 1) augmentation of peripheral resistance by physical means, 2) risk of hepatic injury with abdominal compression, 3) counterpulsation vs sustained compression, 4) the abdominal pump mechanism, and 5) contact compression techniques. METHODS: Literature retrieved from successive MEDLINE English-language searches was received with a special emphasis on work and concepts highlighted by participants at the First Purdue Conference on Interposed Abdominal Compression-CPR, September 1992. RESULTS: External abdominal compression of one form or another has been studied as a means of resuscitation by many investigators throughout the 20th century. Experimental and clinical studies have shown generally consistent evidence of hemodynamic augmentation by abdominal compression during various forms of CPR. Recent advances include a modified theoretical understanding of hemodynamic mechanisms and demonstration of clinical potential in humans. Inconsistencies in published results may be due to differences in mechanical techniques of abdominal compression. Based on these studies, a modified manual technique for "contact compression" of the abdominal aorta is recommended. CONCLUSIONS: A technique for left-of-center, angled compression of the abdominal aorta against the crest of the spine is recommended. Further well-supervised and controlled clinical trials using this standardized technique are warranted as a prelude to more widespread clinical application of abdominal compression in CPR.
Accurate knowledge of tissue temperature is necessary for effective delivery of clinical hyperthermia in the treatment of malignant tumours. This report compares computer-predicted versus measured intratumoral temperatures in 11 human subjects with intracranial tumours, treated with a conceptually simple 'conductive' interstitial hyperthermia system. Interstitial hyperthermia was achieved by the use of parallel arrays of implanted, electrically heated catheters. The tissue was warmed by thermal conduction and blood convection. Simulation of intratumoral temperatures was achieved by solving a modified bioheat transfer equation on a digital computer using a finite difference method. Comparison of intratumoral temperatures from simulations and measured values differed by about +/- 0.75 degrees C. Further analysis of computed temperature distributions between catheters revealed a rapidly computable relationship between the local minimum tumour temperature and nearby catheter power and temperature that accounts for effects of varying blood flow. These findings suggest that 'on-line' prediction and control of local minimum tumour temperatures are feasible with the conductive interstitial technique.
The goal of heat therapy in the treatment of malignant disease is to raise the temperature of all neoplastic tissue to a cytotoxic temperature for a predetermined period of time. This seemingly simple task has proved difficult in vivo in part because of non-uniform power absorption and in part because of non-homogeneous and time-varying tumour blood flow. We have addressed this difficulty first by utilizing the conceptually simple technique of conductive interstitial hyperthermia, in which the tumour is warmed by multiple, electrically heated catheters, and second by implementing on-line control of minimum tumour temperatures near each catheter, estimated on the basis of the steady-state ratio of catheter power to catheter temperature rise. This report presents an analysis of the accuracy, precision, and stability of the on-line minimum temperature estimation/control technique for 22 patients who received 31 separate courses of conductive interstitial hyperthermia for the treatment of malignant brain tumours, and in whom temperature was monitored independently by 12-16 independent sensors per patient. In all patients the technique was found to accurately and precisely estimate and control the local minimum temperatures. Comparison of measured and estimated temperatures revealed a mean difference of 0.0 +/- 0.4 degrees C for those sensors within 1.0 mm of the expected location for minimum temperatures. This technique therefore offers an attractive method for controlling hyperthermia therapy-even in the presence of time varying local blood flow.
Pulse-wave velocity was measured in isolated canine common carotid arteries using sinusoidal frequency pulses of 1, 2, 5, 10, 15 and 20 Hz at 50, 100 and 150 mmHg. It was found that the pulse-wave velocity was independent of frequency and dependent on pressure. Using the Moens-Korteweg equation, the predicted pulse-wave velocity (y) was compared with measured pulse-wave velocity (x). A good correspondence was found (y = 1.063 x - 0.337, with a correlation coefficient of 0.963). The propagation velocity of the significant harmonic components of the pulsatile pressure waveform is the same for heart rates up to 120 beats/min.
The authors describe a novel system for sensing and displaying the distribution of contact pressure caused by a patient's lying on a hospital bed. The system includes a flexible, pressure-sensitive mat, electronics to activate the mat, a small computer to process data, and a color video display. The present prototypes can sense pressure at 1,536 discrete locations in a rectangular grid of 24 x 64 nodes, each node representing an area of 4 cm2. The computer receives data from each node and displays the results as a false-color map, refreshable every 5 seconds. The pressure-sensitive mat itself includes two orthogonal arrays of ribbon-like conductors, composed of silver-coated nylon fabric, which are separated by insulating open-cell foam rubber. The system monitors the electrical capacitance between selected pairs of horizontal and vertical conductors on opposite sides of the foam. The crossing points form pressure-sensitive nodes. Increased contact pressure compresses the foam, thereby decreasing the distance between the conductors and increasing the capacitance. Node capacitance is determined by measuring the current through it from a voltage source. The outputs of the various nodes are scanned, normalized, and converted to pressures using the known compressive stress-strain relationship for the foam, and the data are then displayed as a false-color image of the pressure distribution.
To efficiently investigate a variety of designs for an accessory skeletal muscle ventricle for circulatory assistance, we developed an electrical model of the human circulatory system. Heart and blood vessels were modeled as resistive-capacitive networks, pressures as voltages, blood flow as electric current, and the cardiac valves as diodes. Pumping of blood was simulated by the application of damped rectangular voltage pulses to the capacitances of the cardiac ventricles and the skeletal muscle ventricle. Three configurations of a skeletal muscle ventricle were studied: the apico-aortic, in which the skeletal muscle ventricle is interposed between the left ventricle and the abdominal aorta; the aorto-aortic, in which the skeletal muscle ventricle is interposed between the thoracic aorta and the abdominal aorta; and the atrial-aortic, in which the skeletal muscle ventricle is interposed between the left atrium and abdominal aorta. The three skeletal muscle ventricle designs were tested as counterpulsatile assist devices in simulations of the normal circulation and congestive heart failure. Performance of the various skeletal muscle ventricle designs was evaluated by comparing total output, mean left ventricular power expenditure, mean skeletal muscle ventricle power expenditure, and mean perfusion pressure of the skeletal muscle comprising the pouch. Under both normal heart and heart failure conditions, the apico-aortic design was superior to the aorto-aortic and to the atrial-aortic designs. With optimal stimulation parameters, the apico-aortic design reduced left ventricular minute work to 16% of normal during simulated heart failure while maintaining a viable resting cardiac output of 3.4 L/min.(ABSTRACT TRUNCATED AT 250 WORDS)
A transient, dose-dependent cardiac depression was produced by defibrillator shocks in an isolated, working canine heart preparation perfused with oxygenated arterial blood from a support dog. Accompanying this depression was an efflux of potassium (K+), forced out of the myocardial cells by the passage of defibrillating current. The transient increase in extracellular K+ concentration was recorded graphically in the venous outflow. It was found that 5-msec rectangular wave shocks, from three to ten times defibrillatory current threshold, released dose-related pulses of K+. It is concluded that because K+ is a myocardial depressant, at least part of the myocardial depression after defibrillation is caused by the release of K+ from the myocardial cells.
Defibrillator shocks ranging in intensity from three to nine times current threshold were delivered to four isolated, metabolically supported, beating canine hearts. The shocks produced an immediate, current-dependent depression of left ventricular isovolumic systolic pressure. This depression was transient, reproducible, and was followed by a transient overshoot in ventricular systolic pressure. Then 1 mg propranolol hydrochloride in 1 ml H2O was injected into the coronary arterial supply of the isolated heart, and the shocks were repeated. The magnitude of the immediate cardiac depression after shock was unchanged; however, the time required for full recovery of left ventricular systolic pressure to a pre-shock control value was prolonged. In addition, the transient overshoot in ventricular systolic pressure seen in the untreated state was absent. These results are consistent with the hypothesis that defibrillatory shocks produce a direct activation of cardiac adrenergic nerves, which aid in recovery of ventricular contractility following defibrillator shocks.
Administration of the vasodilator hydralazine to a single mongrel dog with a transplanted, superficial transmissible venereal tumour in the abdomen permitted tumour-adjacent normal tissue temperature differences produced in local hyperthermia to be enhanced by nearly 2 degrees C. A preliminary study of tumour and normal tissue perfusion rate in the dog, employing the 15O-labelled water-positron emission tomography technique, suggested that administration of the vasodilator led to a significant reduction in the tumour perfusion rate, consistent with the observed tumour temperature enhancement. Computational studies with a multi-layer, one-dimensional cylindrical model of deep-tumour heating suggest that vasodilator-induced reductions of tumour perfusion rates could significantly increase deep tumour-superficial normal tissue temperature differences produced in deep-tumour thermotherapy.
The feasibility of combining local heat treatment with whole-body hypothermia in an effort to improve therapeutic gain was assessed. Superficial, nonperfused phantom tumors were fashioned in eight anesthetized mongrel dogs by transplantation of the spleen from the abdomen to a subcutaneous site on the hindlimb. After pretreatment of the animal with the vasodilator hydralazine (0.5 mg/kg, IV) to enhance normal tissue perfusion, the spleen implant was heated with a 2450-MHz microwave diathermy apparatus, first with the animal's core body temperature in the normal range (39 degrees C) and then after the animal had been packed in ice to reduce core temperature to 30 degrees C. Applied power density and temperatures in both the phantom tumor and underlying muscle tissue were recorded during brief interruptions of diathermy until steady-state temperatures had been achieved. Under normothermic conditions with time-averaged applied power of 0.038 W/ml to phantom tumor and 0.014 W/ml to underlying muscle, tumor temperature rose to 45.9 +/- 1.8 degree C, while muscle temperature remained at 40.5 +/- 0.7 degree C. During whole-body hypothermia applied power could be increased to 0.114 W/ml in phantom tumor and to 0.025 W/ml in muscle. Muscle temperature rose only to 33.8 +/- 1.6 degree C, while that of the nonperfused phantom tumor rose to 53.6 +/- 4.3 degrees C with systemic hypothermia.(ABSTRACT TRUNCATED AT 250 WORDS)
Therapy for severe chronic lung disease currently includes the administration of supplemental oxygen to prevent breathlessness and tissue hypoxia. Although effective, this therapy is unnecessarily costly, because oxygen is administered to the patient during expiration as well as inspiration. To eliminate this inefficiency, a delivery system that senses the inspiratory effort and delivers oxygen to the patient only during inspiration was developed. The 11 X 5 X 8-cm flow control unit attaches easily to a portable oxygen supply. The components of the system have an expected life of five years, and the 9-V battery provides power for about one month of use. Manual controls permit accommodation to the respiratory pattern of the patient. Preliminary evaluation of the system showed that its effectiveness in producing tissue oxygenation is similar to that of continuous oxygen systems. The system has potential applications in ambulatory oxygen therapy and in other clinical settings to improve the cost/benefit ratio of oxygen treatment.