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Biomedical subjects

W A Tacker

Publications and source records attributed to W A Tacker.

At least 19 recordsLinked to original sources
PubMed1992

Output power and metabolic input power of skeletal muscle contracting linearly to compress a pouch in a mock circulatory system.

Output power and metabolic input power values were determined for unconditioned canine latissimus dorsi (two), gastrocnemius (seven), and triceps (three) muscles contracting linearly to cause compression of a doubly valved pouch in a hydraulic model of the circulation. The motor nerves to the muscles were stimulated tetanically with 450 msec trains of 0.1 msec pulses having a frequency of 50/sec. The muscles were contracted 10, 20, 30, and 40 times per minute and pouch output in milliliters per minute was measured directly for each muscle at each contraction (train) rate. The output power in milliwatts was determined by two methods: (1) by using the pouch output and the pressure rise imparted to the stroke volume (average power) and (2) by using the pressure-volume loop. Metabolic input power in milliwatts was determined from the oxygen consumption in milliliters per minute of the working muscle. It was found that as the pouch output was increased, the pouch output power and the metabolic input power both increased. The average power output was slightly less than that computed from the pressure-volume loop. The mean output power values, when pumping at L liters per minute, were 0.62 L (average) and 0.75 L mW/gm (pressure-volume loop) for the latissimus dorsi muscles; 0.83 L (average) and 1.16 L mW/gm (pressure-volume loop) for the gastrocnemius muscles; and 0.55 L (average) and 0.66 L mW/gm (pressure-volume loop) for the triceps muscles. The percent efficiency of energy conversion ranged from 9.2% to 17.8% for the latissimus dorsi muscles, from 5.1% to 19.5% for the gastrocnemius muscles, and from 10.5% to 27.3% for the triceps muscles. However, it should not be concluded that one muscle type is better than another on the basis of percent efficiency because efficiency does not take endurance into account. An important observation in this study relates to the large output obtained with the three linearly contracting muscle types. All were capable of pumping in excess of 1.5 L/min. A second observation relates to the absence of fatigue, although determination of endurance was not an objective in these studies.

Animals↗
PubMed1992

Correlation of motor-evoked potential response to ischemic spinal cord damage.

The prevalence of morbidity is a major deterrent to the success of aortic aneurysm replacement operations. We have developed a model of spinal cord ischemia, based on the amplitude reduction of the motor-evoked potential, which produces approximately a 90% prevalence of paraplegia. Regional blood flow was studied with the use of radioactive microspheres, and results showed that there was a significant decrease in flow to the lumbar cord (85% reduction) during aortic occlusion, followed by a twofold to threefold hyperemia that persisted for 24 hours. Histopathologic examination of the cord revealed that the greater portion of microgliosis, spongiosis, and neuronal damage was confined to the gray matter of the cord, and its severity increased as one progressed caudally. The somatosensory-evoked potential disappeared before the motor-evoked potential L-2 signal in all dogs, with a mean disappearance time of 10.9 +/- 5.6 minutes, compared with 21 +/- 6.6 minutes for the motor-evoked potential. Both the sensory-evoked potential and the motor-evoked potential cord signal were present 24 hours later in all dogs tested. The peripheral nerve motor-evoked potential disappeared within 1 minute of cord ischemia, was not present 24 hours later, and hence appears to be too sensitive to use as an indicator of spinal cord damage. Plotting spinal cord motor-evoked potential amplitude reduction versus both histopathologic damage and regional blood flow revealed a positive correlation between motor-evoked potential amplitude reduction, decreased cord perfusion, and increased histopathologic damage. In addition, it may be possible to make inferences about the neurologic status of a subject based on the magnitude and time-course of the motor-evoked potential's amplitude reduction and wave morphology.

Animals↗
PubMed1991

Limitations of open-chest cardiac massage after prolonged, untreated cardiac arrest in dogs.

STUDY OBJECTIVES: Open-chest cardiac massage is an effective method of resuscitation if instituted within 15 minutes of normothermic cardiac arrest that has failed to respond to ongoing closed-chest CPR efforts. The usefulness of invasive forms of CPR after various periods of untreated cardiac arrest is less certain. This study was performed to determine the effectiveness of open-chest resuscitation after prolonged periods of untreated cardiac arrest. SETTING AND DESIGN: Prospective, controlled laboratory investigation using an animal model of cardiac arrest. Open-chest cardiac massage initially was compared to standard closed-chest compression CPR. The efficacy of open-chest CPR then was evaluated after ten and 40 minutes of untreated ventricular fibrillation. TYPE OF PARTICIPANTS: Twenty mongrel dogs (24 +/- 1 kg). MEASUREMENTS AND MAIN RESULTS: After 20 minutes of untreated ventricular fibrillation, open-chest resuscitation was significantly better than closed-chest efforts for the production of coronary perfusion pressure (58 +/- 14 vs 2 +/- 1 mm Hg; P less than .05) and initial resuscitation success (five of five vs one of five; P less than .03). Open-chest cardiac massage was equally effective for initial resuscitation if begun after ten or 20 minutes of untreated ventricular fibrillation (five of five vs five of five), but if untreated ventricular fibrillation continued for 40 minutes prior to instituting open-chest massage, no resuscitation benefit was found (none of five; P less than .005). There were marked differences in 24-hour survival depending on the length of time untreated cardiac arrest continued prior to instituting open-chest resuscitation efforts. After 20 minutes of ventricular fibrillation, initial resuscitation was successful with open-chest massage, but long-term survival was poor. CONCLUSION: Open-chest cardiac massage did not produce long-term survival if untreated cardiac arrest persisted for 20 or more minutes prior to invasive resuscitation efforts.

Animals↗
PubMed1991

Comparison of canine skeletal muscle power from twitches and tetanic contractions in untrained muscle: a preliminary report.

Power output and blood flow were determined in dogs for four muscles (gastrocnemius, latissimus dorsi, rectus abdominis, and triceps) to determine effects of choice of muscle, tetany or twitch rates, force loading of the muscle, and blood flow on muscle power output. Total power for a 20-Kg dog was greatest for triceps at 0.77 watts (W) and least for rectus at 0.22 W; power per gram was greatest for gastrocnemius at 5.77 mW/g. Muscle perfusion of latissimus and rectus is greatly decreased by overstretching of the muscle. Overstretching also produces severe, persistent, power loss in latissimus and rectus muscles. Gastrocnemius and triceps tolerate stretching much better. We conclude that power can be improved without causing muscle fatigue by choice of muscle, choice of electrical stimulation parameters, linear geometry for contraction of the muscle, and matching the force load to each individual muscle.

Abdominal Muscles↗
PubMed1990

Suprathreshold brain stimulation activates non-corticospinal motor evoked potentials in cats.

In the feline model of the motor evoked potential (MEP) test, a multiphasic spinal cord signal can be elicited in response to bipolar or transcranial brain stimulation. Previous studies have shown that signals produced by threshold stimulation travel mostly in the corticospinal tract. However, from this study we show that suprathreshold stimulation produces very large amplitude MEPs which travel in the ventral funiculus and therefore are most likely associated with extrapyramidal tract activation. The data supporting this conclusion are: (1) apparent conduction velocities of the first two large amplitude peaks are at least 80 m/s with transcranial stimulation; (2) latency of the transcranial MEP at L2 in the cord is less than or equal to 3.50 ms; (3) large amplitude, positive monophasic potentials are recorded in the ventral but not dorsal-lateral funiculus for either bipolar or transcranial MEPs; (4) both bipolar and transcranial MEPs are significantly reduced or abolished by selective lesion of the ventral funiculus. The two tracts which we believe are responsible for mediating the suprathreshold MEP in the cat are the reticulospinal and vestibulospinal tracts. This is significant because suprathreshold MEPs can be used to monitor feline ventral cord function. Furthermore, combining the use of threshold and suprathreshold MEPs may provide a differential diagnostic test for pyramidal vs. extrapyramidal motor function.

Animals↗
PubMed1990

Depletion of myocardial adenosine triphosphate during prolonged untreated ventricular fibrillation: effect on defibrillation success.

We studied left ventricular endomyocardial adenosine triphosphate levels in 13 large mongrel dogs before and during ventricular fibrillation induced cardiac arrest to assess whether myocardial adenosine triphosphate content could predict successful cardiopulmonary resuscitation. Endomyocardial biopsies were performed during sinus rhythm (control), after 15 min of ventricular fibrillation or 10 min of ventricular fibrillation and 5 min of open chest cardiopulmonary resuscitation, after 20 min of ventricular fibrillation and 10 min of open chest cardiopulmonary resuscitation and after 40 min ventricular fibrillation and 15-20 min open chest cardiopulmonary resuscitation. Myocardial adenosine triphosphate was measured utilizing a bioluminescence method adapted for use with endomyocardial biopsies and normalized to protein content. Left ventricular endomyocardial adenosine triphosphate content fell significantly over time from a control level of 8.88 +/- 0.9 micrograms/mg protein to 5.73 +/- 0.5 micrograms/mg protein at 15 min of cardiac arrest, to 3.4 +/- 0.4 micrograms/mg protein after 30 min of cardiac arrest and to 1.98 +/- 0.3 micrograms/mg protein after 60 min of cardiac arrest (P less than 0.001). Adenosine triphosphate levels were significantly different between animals that received 10 min of ventricular fibrillation and successful open chest cardiopulmonary resuscitation and those that received 40 min of ventricular fibrillation and unsuccessful open chest cardiopulmonary resuscitation (4.35 +/- 0.48 vs. 2.11 +/- 0.43 micrograms/mg protein; P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

The use of electrically stimulated skeletal muscle to pump blood.

Electrically stimulated skeletal muscle can be used in many ways to pump blood. The important physiological characteristics of skeletal muscle for use in a cardiac assist role are presented. The force developed by a twitch and tetanic contraction are quantitated and the considerations in the choice of the stimulus applied to the innervating motor nerve are discussed. The importance of stimulus frequency and duration of the stimulus train are presented in terms of the stroke volume produced by skeletal muscle contracting around a pouch. The effect that preload has on pouch stroke volume and muscle blood flow are demonstrated. Finally an example is given in which cardiac output is augmented by an untrained, electrically stimulated, canine rectus abdominis muscle wrapped around a pouch connected between the apex of the left ventricle and the aorta. In this study, the augmentation in cardiac output was measured when the skeletal muscle was contracted after each second, third, and fourth ventricular contraction. The augmentation was 46% +/- 4, 31% +/- 7, and 25% +/- 4, respectively, for the three contraction regimens. Although electrically stimulated skeletal muscle can be used as a power source to assist the failing heart, the optimum application is yet to be discovered. Important considerations in selecting the optimal application are preload, stimulus train duration, train rate, and muscle blood flow.

Abdominal Muscles↗
PubMed1990

The use of an electrically activated valve to control preload and provide maximal muscle blood flow with a skeletal-muscle ventricle.

A new method for optimally loading a skeletal muscle-wrapped pouch to act as a blood pump is described. The method takes advantage of the fact that the high preload pressure required for a forceful contraction needs to be present for only a short time. By using an electrically controlled valve to delay pouch filling until just before muscle contraction, pouch diastolic pressure can be kept low, which in turn maintains a high muscle capillary blood flow. The intrapouch precontraction pressure can be controlled by selecting the appropriate valve-open time (VOT). The pumping capabilities of untrained rectus abdominis and latissimus dorsi muscles were evaluated using a hydraulic circulatory system in a ten dog study (weight range 20-32.7 kg). The afterload was constant at 100 mmHg, and the pouch precontraction pressure, selected by choice of the VOT, was the test variable. It was found that for maximum pouch output, a precontraction pressure of 60-100 mmHg was required, being attained in this hydraulic model with a VOT of 400-500 msec. Typical pouch outputs were 400-600 mL/min with a muscle contraction rate of 40/min. Muscle capillary blood flow, measured with a periarterial electromagnetic flowmeter, varied inversely with pouch diastolic pressure and was near zero during tetanic muscle contraction. In one animal, a pouch output of 200 mL/min or more was maintained for more than 20 hours of continuous pumping without fatigue. In a related experiment, the method was applied to pump blood in a 32.7 kg dog, in which the muscle-wrapped pouch was connected between the descending thoracic aorta and the abdominal aorta. A pouch output of about 400 mL/min was obtained when the muscle was contracted 30 times/min and the VOT was 400 msec. This flow represented about 20% of the animal's cardiac output. This study demonstrates that by delaying pouch filling until just before the muscle is to be contracted, a low pouch diastolic pressure can be maintained, thereby maximizing muscle capillary blood flow and, in turn, providing the best opportunity for prolonged pumping.

Animals↗
PubMed1979

Elevation of ventricular defibrillation threshold in dogs by antiarrhythmic drugs.

Effects of antiarrhythmic drugs upon the threshold delivered energy (TDE) and threshold peak current (TPC) for electrical ventricular defibrillation by damped sinusoidal shocks were investigated in 25 pentobarbital-anesthetized dogs. TDE and TPC were increased by the three antiarrhytmic drugs tested. Bolus injections produced a transient rise and continuous infusions produced a steady rise in difibrillation threshold. The maximal percent elevations in mean defibrillation threshold during the 60 minutes after intravenous drug treatment in groups of n = 5 dogs were: (formula: see text). Accordingly, individuals receiving antiarrhythmic drugs who nonetheless fibrillate may require greater electric shock strength for defibrillation.

Animals↗
PubMed1979

Electrocardiographic and serum enzymic alterations associated with cardiac alterations induced in dogs by single transthoracic damped sinusoidal defibrillator shocks of various strengths.

The safety margin between the strength of shock needed to defibrillate the ventricle and shocks which produce cardiac damage has not previously been reported. This study quantitates the shock intensity required to produce ECG alterations, serum alpha-1LDH and MB CPK isoenzyme elevation and myocardial damage using single transchest damped sinusoidal defibrillator shocks. Shocks of 1 to 20 amperes per Kg. of body weight were applied. Fifty-six dog weighing 2.4 to 15 kilograms were shocked with defibrillator pulses via 10 centimeter diameter electrodes applied to the thorax. Electrocardiograms were taken to be analyzed for arrhythmias, S-T segment changes, and T wave changes. Serum enzyme levels were determined in 25 dogs. Macroscopic and histopathologic studies were conducted on the hearts. Transchest single damped sine wave shocks did not produce microscopically detectable cardiac damage until at least a threefold current overdose was applied. No macroscopic morphologic alterations were observed until at least a sixfold current overdose was applied and no deaths occurred until a twelvefold or greater current overdose was delivered. Incidence and severity of ECG changes, increase in serum enzyme activity, incidence and severity of cardiac damage, and incidence of mortality all correlated positively with shock strength. However, these four adverse effects did not correlate well with each other. Transient ECG changes were very frequent following shock application regardless of the morphologic damage produced, and hence the transient changes have little value as indicators or predictors of damage. Persistent ECG changes were predictive of morphologic changes but were not sensitive enough to detect damage in mildly injured hearts. Likewise, elevated serum cardiac isoenzyme activity was a reliable but insensitive indicator of damage.

Animals↗
PubMed1978

Protection of ischemic myocardium by whole-body hypothermia after coronary artery occlusion in dogs.

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.

Animals↗
PubMed1978

The electrical dose for direct ventricular defibrillation in man.

The threshold electrical energy for direct ventricular defibrillation was measured in 100 patients whose hypothermic hearts were fibrillated for cardiac operations. In 93 cases 10 joules or less was sufficient, and in 48 of these cases 5 joules or less defibrillated the ventricles. Because a shock of 10 joules defibrillated the heart of most of our patients, we recommend an initial shock of 5 to 10 joules rather than the 20 joules used more commonly. Until the safety margin between defibrillation threshold and damage threshold is established for direct defibrillation, use of shocks with adequate but not excessive strength may avoid unnecessary damage to the myocardium. When hearts refibrillate after defibrillation, it is unnecessary to use higher energy settings for subsequent defibrillation attempts. Instead, an antiarrhythmic drug should be administered and another shock of the same intensity that defibrillated the first time should be applied.

Adult↗
PubMed1978

Effect of shock strength on survival and acute cardiac damage induced by open-thorax defibrillation of dogs.

The safety of open thorax defibrillation with single damped sine-wave shocks and 6-cm-diameter electrodes was evaluated in healthy anesthetized dogs. Twenty-one dogs were allotted to 6 groups: Group A were nonshocked controls and groups B through F were given single shocks of 4-, 7-, 12-, 19-, or 32-fold, respectively, greater than a defibrillation threshold dose (30 mA/g of heart). Immediate postshock death resulted in group F dogs; group A through E dogs survived and were killed after 2 days. The incidence and severity of cardiac morphologic damage increased with shock strength (mild damage occurred in 1 of 3 dogs in group C and in 3 of 4 dogs in group D and severe damage occurred in 2 of 3 dogs in group E). The cardiac lesions were characterized grossly and microscopically. In dogs that died immediately after shocking, damage was apparent as pale circular zones of edema and myofibrillar degeneration in the ventricular free walls beneath the electrode placement sites on the cardiac surface. In the dogs that survived 2 days, the defibrillator-induced areas of myocardial necrosis and calcification were concentrated in arc or ringlike patterns beneath the periphery of the electrode placement sites. All dogs that were studied 2 days after shocking had mild fibrinous pericarditis. Postshock electrocardiographic changes were not good indicators of cardiac damage because the mild epicardial inflammatory reaction associated with the surgical procedure produced large ST and T wave changes which masked any changes associated with myocardial necrosis induced by the electric shocks. It was concluded that a substantial safety margin exists between the required defibrillation threshold shock dose and the large shocks required to produce marked cardiac damage or death in healthy dogs.

Animals↗