Colorimetric carbon dioxide detection.
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Carbon Dioxide↗
Biomedical subjects
B D Butler
Publications and source records attributed to B D Butler.
Magnetic resonance imaging of hyperbaric oxygen treated rats with spinal cord injury: preliminary studies.
Magnetic resonance imaging (MRI) has been performed to assess the efficacy of hyperbaric oxygen (HBO) treatment on experimental spinal cord injury in a rat animal model. A moderately severe injury, similar to Type III injury seen in humans (Kulkarni et al. Radiology 164:837;1987) has been chosen for these studies. An improvement in the neurologic recovery (based on Tarlov scale) has been observed following HBO treatment over a period of 72 hr. Based on MRI, HBO treatment appears to arrest the spread of hemorrhage and resolve edema.
Animals↗
Doppler detection of decompression bubbles with computer assisted digitization of ultrasonic signals.
Precordial Doppler ultrasonic monitoring is routinely used for detection of venous gas bubbles resulting from decompression in hypobaric or hyperbaric applications. Bubble scoring codes have been devised in an attempt to quantify the number of audible bubble signals heard over the background sounds of the cardiac cycle. The audio interpretation of these ultrasonic backscatter signals remains the most common method for decompression evaluation. We report on the use of an inexpensive, commercially available audio digitizer in conjunction with a personal computer to digitize Doppler bubble signals for visual and electronic evaluation. This device can be operated simultaneously with Doppler audio monitoring. Precordial and arterial Doppler recordings of gas bubbles were obtained from anesthetized dogs after intravascular infusion or following decompression. Additional evaluations were conducted on Doppler bubble recordings obtained from human decompression studies. The device can be used in real-time or for later signal analysis. Accompanying menu-driven software provides for numerous signal modification options and visual displays. This device can provide a simultaneous visual display of Doppler signals normally only available for audio evaluation.
Animals↗
Loss of resistance technique for locating the epidural space: evaluation of glass and plastic syringes.
Location of the epidural space in epidural anaesthesia usually involves the measurement of loss of resistance using glass or plastic syringes. In the present study two varieties of glass syringe and one plastic type were evaluated to determine the resistive forces associated with plunger movement. The mean static (fs) and dynamic (fd) forces for polished glass syringes having a ground plunger only were fs = 0.47 X 10(-3) +/- 0.22 X 10(-3) N and fd = 0.37 X 10(-3) +/- 0.19 X 10(-3) N and for polished glass syringes having a ground barrel and plunger were fs = 0.43 X 10(-3) +/- 0.16 X 10(-3) N and fd = 0.38 X 10(-3) +/- 0.15 X 10(-3) N. Each of these values was significantly lower (P less than 0.5) than those for plastic syringes fs = 2.22 X 10(-3) +/- 0.48 X 10(-3) N and fd = 1.46 X 10(-3) +/- 0.37 X 10(-3) N. It is concluded that glass syringes are favoured over plastic for locating the epidural space because frictional forces developed with glass syringes were significantly lower than with plastic.
Anesthesia, Epidural↗
Changes in microvascular permeability with acceleration of edema in dog lungs.
Elevation of left atrial pressure to 25-40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5-120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.
Animals↗
Effect of lysophosphatidylcholine on the filtration coefficient in intact dog lungs.
Lysophosphatidylcholine (lyso-Pc) is a lysophospholipid normally found in low concentrations in the lung. At high concentrations lyso-Pc, instilled into the airways, causes pulmonary edema. We tested the hypothesis that the edema caused by lyso-Pc was due to an increase in pulmonary microvascular membrane permeability. In 11 anesthetized dogs we continuously weighed the left lower lobes (LLL) while instilling lyso-Pc (20 mM) into the LLL airways. After 30 min we determined the microvascular membrane fluid filtration coefficient (Kf) from the relationship between the rate of LLL weight gain and the pulmonary microvascular pressure. Kf was not significantly different between the lyso-Pc-treated lobes (0.048 +/- 0.018 ml.min-1.mmHg-1) vs. control lobes (0.067 +/- 0.031 ml.min-1.mmHg-1). Our data do not support the hypothesis that lyso-Pc, instilled into the airways, causes an increase in pulmonary microvascular permeability.
Animals↗
Pulmonary hemodynamics, extravascular lung water and residual gas bubbles following low dose venous gas embolism in dogs.
Pulmonary hemodynamic responses, extravascular lung water and bubble longevity times were studied in halothane anesthetized dogs receiving low dose venous gas infusions. Dogs in one group (23.3 +/- 4.3 kg, n = 6) were embolized with air (0.05 ml.kg-1.min -1) for 60 min followed by a recovery period lasting 70 min. During the recovery the ventilatory gases were intermittently switched from nitrogen (68-69%)/oxygen (30%) to nitrous oxide (68-69%)/oxygen (30%) to expand any residual pulmonary vascular bubbles. Subsequent changes in pulmonary artery pressure, pulmonary vascular resistance, end-tidal carbon dioxide and arterial carbon dioxide tensions were used to indicate the presence of remaining bubbles that would have expanded in volume with the nitrous oxide ventilation. This embolization sequence was repeated three times to simulate repetitive exposure of the pulmonary circulation to venous gas emboli. In a second group of dogs (20.2 +/- 2.7 kg, n = 8) the venous gas infusions (0.05 ml.kg-1.min-1) were continuous for 180 min, followed by recovery with intermittent nitrous oxide/oxygen challenges to determine bubble longevity. Pulmonary hemodynamic and carbon dioxide data were significantly changed from baseline following each embolization. These differences as well as the development of extravascular lung water (edema formulation) were not significant when comparisons were made between the Repetitive gas embolism group after 180 min. Residual pulmonary vascular bubbles were indicated (mean +/- S.E.M.) 26.9 +/- 2.3 min following the 180 min Continuous venous gas infusion and 39.5 +/- 5.3, 46.4 +/- 5.0 and 55.5 +/- 4.4 min, respectively, following the three 60 min Repetitive venous gas infusions.
Animals↗
Venous gas embolism: time course of residual pulmonary intravascular bubbles.
The time course of pulmonary intravascular air emboli was studied in anesthetized dogs. In one series of experiments air was infused into the right atrium at 0.10 ml.kg-1.min-1 or 0.25 ml.kg-1.min-1 for 15 min or given as a bolus injection of 2 ml/kg at 2 ml/sec. In a second series of series of experiments venous air was infused into dogs (0.25 ml.kg-1.min-1, 15 min) ventilated with 100% oxygen for 0, 30, or 210 min before the embolization. After the air infusions the animals were allowed to recover, breathing 70% nitrogen:30% oxygen. At 10-min intervals during recovery, the nitrogen was replaced with nitrous oxide (N2O) for 5 min to expand any residual pulmonary vascular bubbles. Subsequent changes in pulmonary artery pressure (Ppa) and end-tidal carbon dioxide (PETCO2) concentrations, pulmonary vascular resistance (PVR) and carbon dioxide tensions (PaCO2) as a result of the N2O challenges indicated the presence of residual gas bubbles in the pulmonary arterial system. Residual times of the pulmonary bubbles were 24.5 +/- 12.3 min (0.10 ml.kg-1.min-1 air dose), 43 +/- 10.8 min (0.25 ml.kg-1.min-1 air dose), and 17.8 +/- 2.5 min (bolus). The latter two were significantly different from each other. With 100% oxygen breathing the residual times were 19 +/- 2.2 (0 min), 22 +/- 6.7 min (30 min), and 17 +/- 4.0 (210 min). These values were reduced significantly when compared to the dogs ventilated with 30% oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of the Trendelenburg position on the distribution of arterial air emboli in dogs.
We examined the effects of buoyancy on the distribution of arterial gas bubbles using in vitro and in vivo techniques in dogs. A simulated carotid artery preparation was used to determine the effects of bubble size and vessel angle on the velocity and direction of bubble movement in flowing blood. Because buoyancy tends to float bubbles away from dependent areas, bubble velocity would be expected to decrease as the vessel angle increased. We found that larger bubbles increased in velocity in the same direction as the blood flow at 0-, 10-, and 30-degree vessel angles and decreased when the vessel was positioned at 90 degrees. Smaller bubbles did not change velocity from 0 to 30 degrees and increased in velocity in the same direction as blood flow at 90 degrees. In 10 anesthetized dogs, we studied the effects of 0-, 10-, 15-, and 30-degree Trendelenburg's position on carotid artery distribution of gas bubbles injected into the left ventricle or ascending aorta. Regardless of the degree of the Trendelenburg position, the bubbles passed into the carotid artery simultaneously with passage into the abdominal aorta. We conclude that the forces of buoyancy do not overcome the force of arterial blood flow and that the Trendelenburg position does not prevent arterial bubbles from reaching the brain.
Animals↗
Effects of inhalation anaesthetics on filtration of venous gas emboli by the pulmonary vasculature.
Venous gas emboli are prevented from reaching the systemic circulation by filtration in the pulmonary vasculature. This filtration can be overwhelmed by exceeding certain critical rates of venous air infusion. To characterize further these filtration phenomena, the effects of pentobarbitone, isoflurane and halothane anaesthesia on the incidence of spillover of venous bubbles into the arteries were studied in groups of nine dogs. Venous air was infused at rates of 0.25, 0.30, and 0.35 ml kg-1 min-1. Spillover of venous bubbles into the arteries was detected with a Doppler ultrasonic probe located over the suprarenal aorta. At the lowest venous air dose (0.25 ml kg-1 min-1), no bubbles were detected in the systemic circulation in the pentobarbitone- or halothane-anaesthetized dogs, while arterial bubbles were detected in two with isoflurane anaesthesia. At 0.30 ml kg-1 min-1 air, one, four and two dogs had arterial bubbles detected with pentobarbitone, halothane or isoflurane anaesthesia, respectively, while at 0.35 ml kg-1 min-1 spillover of bubbles occurred in four, five and three, respectively. The spillover of venous bubbles into the arteries was dose-related for the pentobarbitone- and halothane-anaesthetized dogs.
Anesthesia, Inhalation↗
Balloon aspiration of tracheal secretions.
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Airway Obstruction↗
A comparison of different methods of lubrication of glass syringes used to identify the epidural space.
Measurement of loss of resistance in glass syringes is a method widely used to locate the epidural space in epidural anaesthesia. Static and dynamic forces were measured under four experimental conditions in new glass syringes: unpolished, dry; polished, dry; unpolished, saline lubricated; and polished, saline lubricated. The unpolished saline lubricated syringes had a mean (SD) static force of 53.18 (15.0) g and dynamic force of 40.88 (15.2) g. These values were significantly greater than for polished dry syringes where the values were 5.27 (2.1) g and 4.38 (0.94) g, respectively. The results show that the least amount of resistance to plunger movement is obtained by dry polishing glass syringes.
Anesthesia, Epidural↗
Vascular pressures and passage of gas emboli through the pulmonary circulation.
Anesthetized dogs received venous air infusions at 0.35 ml.kg-1.min-1. In 60% of a group of 15 dogs, venous bubbles spilled over into the arterial circulation and were detected with the ultrasound Doppler technique. The pulmonary vascular pressure gradient (pulmonary artery pressure-pulmonary venous pressure or left atrial pressure) measured at the instant that spillover occurred was 34.7 +/- 4.7 mmHg. In a 2nd group of dogs we raised the pulmonary vascular pressure gradient before the venous air infusions to achieve spillover of bubbles 100% of the time. The resultant pressure gradient at the time of spillover of venous bubbles was 52.0 +/- 2.0 mmHg (P less than 0.05). It is concluded that venous bubbles can cross the lungs of anesthetized dogs when the driving pressures are sufficient to overcome the normal filtering function.
Animals↗
Arterial air embolism of venous origin in dogs: effect of nitrous oxide in combination with halothane and pentobarbitone.
The effects of using nitrous oxide (N2O) with halothane or pentobarbitone anaesthesia on the filtration of venous air emboli (VAE) by the pulmonary circulation were studied in dogs. Dogs anaesthetized with either pentobarbitone, pentobarbitone/N2O, halothane, or halothane/N2O were embolized with venous air into the right atrium at 0.25 to 0.35 ml.kg-1.min-1 for 30 min. The animals were in a supine, head down position. A Doppler ultrasonic probe located over the suprarenal aorta detected arterial bubbles that escaped filtration by the lungs. No bubbles were detected at 0.25 ml.kg-1.min-1, but at 0.30 ml.kg-1.min-1 the incidence was 11 per cent (pentobarbitone), 0 per cent (pentobarbitone/N2O), 33 per cent (halothane), and 63 per cent (halothane/N2O) and at 0.35 ml.kg-1.min-1, 44 per cent (pentobarbitone), 14 per cent (pentobarbitone/N2O), and 56 per cent (halothane). Half of the dogs receiving VAE with halothane/N2O at 0.30 ml.kg-1.min-1 died within the first 10 min of the air infusion. Thus, no animals were studied at the next higher dose (0.35 ml.kg-1.min-1). The results suggest that the occurrence of VAE with nitrous oxide anaesthesia may result in greater haemodynamic consequence and increased likelihood for spillover of the venous bubbles into the arteries if used with halothane as compared to pentobarbitone.
Anesthesia, Inhalation↗
Removal of tracheal secretions in anesthetized dogs: balloon catheters versus suction.
Artificial secretions were removed by suction (using 12- or 18-French suction catheters) or by means of a balloon-tipped catheter (6-French Fogarty arterial embolectomy catheter) in 20 experiments performed on five dogs anesthetized with halothane. Each dog had 5 ml of mucin injected 10 cm down the endotracheal tube prior to a 30-sec period of intermittent positive pressure ventilation. After this procedure, the ventilator was disconnected and the secretions were removed by suction with the 12- or 18-French catheters or by the Fogarty catheter. Each dog had balloon removal performed twice and suction performed once with the 12-French and once with the 18-French catheter. The endotracheal tube was cleaned and a 15-min stabilization period was allowed between each experiment. Arterial blood pressure (MAP) and pulmonary artery pressure (PAP) did not change after either technique. There were no ECG changes, arrhythmias, or alterations in PaCO2. The PaO2 was significantly lower in the two suction catheter groups [520 +/- 33 mm Hg (12 French) and 451 +/- 31 mm Hg (18 French)] than in the balloon removal group (564 +/- 10 mm Hg) (P less than 0.05). The balloon technique removed more secretions (4.52 +/- 0.06 ml) than did suction (12 French, 1.32 +/- 0.17 ml; 18 French, 2.11 +/- 0.44 ml). Balloon removal of tracheal secretions has two advantages over conventional suction techniques: it removes more secretions, and it has less detrimental effect on arterial oxygenation.
Anesthesia, Endotracheal↗
Mechanisms of succinylcholine-induced arrhythmias in hypoxic or hypoxic:hypercarbic dogs.
To evaluate the effects of succinylcholine on cardiac arrhythmias and serum levels of potassium and catecholamines, dogs with hypoxia alone and with hypoxia and hypercarbia were studied during anesthesia with halothane or enflurane. After the injection of succinylcholine (0.3 mg/kg), cardiac arrhythmias occurred in all halothane:hypoxia dogs and in 70% of dogs given halothane during hypoxia:hypercarbia. No dogs given enflurane anesthesia developed arrhythmias. Serum potassium levels increased significantly 3 and 5 min after succinylcholine in all groups. Serum epinephrine levels increased in the halothane-hypoxia:hypercarbia and enflurane:hypoxia groups and, after the injection of succinylcholine, epinephrine levels increased further in dogs in the halothane:control, halothane:hypoxia, halothane-hypoxia:hypercarbia, enflurane:hypoxia, and enflurane-hypoxia:hypercarbia groups. Norepinephrine levels increased with enflurane-hypoxia:hypercarbia and after the succinylcholine in the halothane:hypoxia, halothane-hypoxia:hypercarbia, and enflurane-hypoxia:hypercarbia groups. The results suggest that succinylcholine induces arrhythmias by sympathetic stimulation and that halothane sensitizes the myocardium to arrhythmias at the same levels of serum catecholamines and potassium in the presence of hypoxia or hypoxia:hypercarbia more than does enflurane.
Anesthesia, Inhalation↗
Production of microbubbles for use as echo contrast agents.
A variety of agents have been proposed for use as contrast for ultrasound studies. Several reports suggest the use of microbubbles because of their superior sonographic resolution. We describe a method of producing calibrated microbubbles utilizing differential absorption and gas injection techniques. Gas injection methods are described using a Plexiglas microbubbler apparatus with a fine needle orifice. The bubbles originally produced by this device are in a size range of 40-100 microns and consist of nitrogen (10%) and carbon dioxide (90%). The differential absorption technique uses THAM [tris(hydroxymethyl)aminomethane hydrochloride] to absorb the carbon dioxide (diluent gas) from the bubbles selectively, leaving smaller microbubbles. The microbubbles can be calibrated using the electric gating principle of the Coulter Counter.
Bicarbonates↗
Fluorocarbon treatment for cerebral air embolism.
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Animals↗