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Biomedical subjects

W J Powell

Publications and source records attributed to W J Powell.

At least 37 records · Page 2Linked to original sources
PubMed1983

Life outcomes and satisfaction ratings of multihandicapped adults.

Ten and 20 year longitudinal data were collected on 180 multihandicapped adults. Subjects completed a 50-item questionnaire which was divided into five sections: (a) living circumstances, (b) physical status, (c) social situation, (d) education, and (e) vocational training and employment. Respondents provided both outcome data and their satisfaction with those outcomes. The results indicated that most lived at home, were financially dependent and were not married. However, they reported that they were satisfied with these life outcomes and that they were very satisfied with their social activities. Few significant differences separated the age groups, suggesting that societal and legal changes over the last 20 years have had a limited impact. The variable most strongly related to life outcome and satisfaction with life outcome was functional status. In addition, perceived (self-reported) functional skills were highly correlated with more objective clinical ratings of functional status.

Activities of Daily Living↗
PubMed1983

Early membrane damage during coronary reperfusion in dogs. Detection by radiolabeled anticardiac myosin (Fab')2.

There is currently great interest in acute coronary reperfusion as a therapeutic modality for severe myocardial ischemia. While some studies have demonstrated a reduction in the overall extent of necrosis by early reperfusion, other studies have identified potentially deleterious effects produced by reflow. Because membrane disruption may be an important mechanism of irreversible cell injury, we measured changes in cell membrane integrity early during reperfusion using radiolabeled anticardiac myosin (Fab')2 antibody fragments in dogs. Our method involved brief periods of exposure to the (Fab')2 so that the levels of (Fab')2 binding indicated the degree of membrane disruption at discrete times during the progression of cell injury. In the first protocol (Fab')2 fragments labeled with either 125I and 131I were injected into the left circumflex coronary artery at the onset of reflow and at 45 min of reflow after a 1-h circumflex artery occlusion. Coronary sinus flow was diverted for 5 min following each injection to prevent recirculation. The (Fab')2 binding ratio (ischemic/control) increased during the first 45 min of reflow in each of eight experiments (mean increase 170%, P less than 0.01). No significant increase in (Fab')2 binding was observed in five additional experiments in which nonspecific (Fab')2 was injected. This indicates that the increase in binding seen with antimyosin-specific (Fab')2 was due to changes in specific binding rather than to alterations in (Fab')2 delivery produced by changes in blood flow distribution. The increase in membrane damage during reflow was confirmed by a second protocol in which each animal received only a single left atrial injection of (Fab')2 followed by rapid excision of the heart. The (Fab')2 binding ratio was 1.7 +/- 0.3 (SEM) in the group that received (Fab')2 at the onset of reflow and 3.7 +/- 0.6 (SEM) (P less than 0.05) in the group that received (Fab')2 after 45 min of reflow. In a third set of experiments in which hyperosmotic mannitol was infused during reflow the mean increase in (Fab')2 binding using the first protocol was only 80 +/- 40 vs. 170 +/- 30% without mannitol (P less than 0.05). Thus, membrane damage develops early during coronary reperfusion following 1 h of circumflex coronary artery occlusion, and part of this membrane damage can be prevented by altering the conditions of reflow. A method involving brief exposure of the myocardium to antimyosin (Fab')2 is promising for detecting changes in membrane integrity during evolving ischemic injury.

Animals↗
PubMed1982

Effect of ouabain on total vascular capacity in the dog.

Whereas the cardiac effects of digitalis glycosides have been extensively studied, less is known of the extracardiac effects of the drug, in particular the effects on vascular capacity. We investigated the effects of parenteral ouabain on vascular capacity in the dog with particular emphasis on transhepatic resistance and its interaction with splanchnic and total intravascular capacity. We studied 49 dogs on total cardiopulmonary bypass in which the splanchnic and extrasplanchnic circulations could be separately perfused and drained, and the portal vein could be vented to systemic venous pressure. The results indicate: (a) ouabain produces a net central displacement of blood at 30 min after administration of 150 +/- 70 ml (SEM), (b) this displacement occurs despite a substantial increase in transhepatic resistance, although the early rise in transhepatic resistance may delay the net displacement of blood, and (c) the decrease of overall vascular capacity is due to an effect of ouabain on the capacitance vessels of both the splanchnic and extrasplanchnic circulations. The peripheral vascular capacity effects of ouabain may therefore contribute to overall cardiac performance.

Animals↗
PubMed1981

Centrally mediated effect of phenytoin on digoxin-induced ventricular arrhythmias.

Studies on the efficacy of phenytoin administered directly into the cerebrospinal fluid in protecting against digoxin-induced arrhythmias were carried out in 20 anesthetized dogs. Phenytoin was administered in an average dose of 10 mg directly into the cisterna magna of 10 dogs. The other control dogs received only the vehicle for phenytoin intrathecally. Both groups of dogs subsequently received a toxic dose of digoxin (0.2 mg/kg) intravenously. The time after intravenous digoxin to the onset of ventricular premature beats, ventricular tachycardia and ventricular fibrillation (VF) was significantly shorter in control animals compared to the phenytoin-treated dogs. In the control group, one dog survived the 3-h observation period without developing ventricular fibrillation, whereas 5 of the 10 phenytoin-treated dogs survived this period without VF (P less than 0.05). Phenytoin had a similar protective effect against digoxin-induced arrhythmias in 10 other dogs that received phenytoin intravenously. In the animals that received phenytoin intrathecally, plasma concentrations of phenytoin were undetectable. Thus, in this experimental model, phenytoin exerts a protective effect against digoxin-induced ventricular arrhythmias which is mediated via the central nervous system.

Animals↗
PubMed1981

Effect of acetylcholine on vascular capacity in the dog.

Acetylcholine produces venoconstriction of isolated vein strip preparations. However, the effect of acetylcholine on overall vascular capacity is not known. To investigate this effect and to elucidate the mechanisms involved, 38 anesthetized dogs were placed on total cardiopulmonary bypass, splenectomized, and given intraarterial infusions of acetylcholine. Almost all of the effect on vascular volume was found to be in the splanchnic circulation, because in four eviscerated animals there was no significant change in capacity. In the animals in which the mesenteric arteries were cannulated to provide constant inflow, and the hepatic vein was cannulated to measure splanchnic venus outflow, acetylcholine infusion for 5 and 21 min increased splanchnic vascular capacity in all animals by 107 +/- 28 (SEM)ml (p less than 0.01) and 291 +/- 132 ml (p less than 0.05), respectively. This increase in splanchnic vascular volume was associated with a rapid and sustained increase in transhepatic resistance to portal blood flow for the duration of the infusions (p less than 0.01). In the animals in which the portal vein was vented proximal to the liver, no significant volume change occurred in the splanchnic vasculature with acetylcholine infusion. Increasing hepatic venous pressure to elevate portal venous pressure to the same level as that achieved with acetylcholine resulted in a similar increase in splanchnic vascular volume. Atropine, but not adrenergic blockade, blocked the acetylcholine-induced volume retention, indicating that the effect of acetylcholine was direct. Substantial volume retention was also achieved by stimulation of the distal ends of the sectioned cervical vagi. Thus, acetylcholine administration directly increases transhepatic resistance and is associated with a pooling of volume in the splanchnic vasculature that would, in the intact animal, result in a decrease in venous return to the heart.

Acetylcholine↗
PubMed1980

Neural effect of digitalis glycosides on gracilis vascular resistance in hypotension.

This study was undertaken to investigate the effect of intravenous acetylstrophanthidine and digoxin on the gracilis vascular resistance of hypotensive dogs. The gracilis muscle was isolated and separately perfused, but the nerve to the muscle was left intact. Acetylstrophanthidin, 0.5 mg iv, and digoxin, 1.0 mg iv, both produced a sustained vasodilator response in the gracilis vascular bed of all the hypotensive animals (mean arterial pressure 50 mmHg). A short-lasting vasoconstriction preceded the vasodilation in response to acetylstrophanthidin in 6 of the 8 animals. Prior local alpha-adrenergic blockade with phenoxybenzamine did not have any significant effect on vasodilation. Prior local cholinergic receptor blockade with atropine, however, abolished the sustained vasodilator response, thus indicating that the mechanism responsible for this neurogenic effect is cholinergic. In contrast, in the normotensive dogs, the response to intravenously administered digoxin was sustained vasoconstriction, which was abolished by prior local alpha-adrenergic receptor blockade. Thus, the effect of digitalis glycosides on peripheral vascular resistance is importantly affected by the background level of sympathetic activity.

Animals↗
PubMed1979

Assessment of drug intervention on the ischemic myocardium: serial imaging and measurement with computerized tomography.

Computerized tomography was evaluated as a technique for imaging and measuring the effect of an intervention on acutely ischemic myocardium. Because cell edema occurs with acute myocardial ischemia and decreases the X-ray attenuation coefficients (tissue density) of myocardium, computerized tomographic images were used to quantitate the effect of hyperosmotic mannitol on ischemia-induced edema. Canine hearts were arrested and scanned after (1) temporary occlusion of the proximal circumflex artery followed by reflow of blood, or (2) continued occlusion of the distal left anterior descending coronary artery. X-ray attenuation values (Hounsfield units) were linearly related to tissue wet/dry weight ratios (r = 0.87, P less than 0.001). After 2 hours of occlusion of the left anterior descending coronary artery the hearts that received mannitol manifested a significant reduction (P less than 0.05) in the volume of left ventricular wall involved with edema. Although the area of edema measured with computerized tomography tended to be smaller in the hearts treated with mannitol than in untreated hearts subjected to a 6 hour occlusion of the left anterior descending coronary artery, the size of the lesion was variable and did not differ significantly from that in untreated hearts. With either short periods of circumflex arterial occlusion followed by blood reflow or with 2 or 6 hours of prolonged occlusion of the left anterior descending coronary artery, the difference in mean attenuation coefficients between the ischemic and nonischemic areas of myocardium in mannitol-treated and untreated hearts was significantly less. These results indicate that computerized tomography in the arrested heart can detect and quantitate the lesion of early acute myocardial ischemia and can quantitate the effect of drug intervention.

Animals↗
PubMed1979

Effect of hypoxia on mechanical properties of hyperthyroid cat papillary muscle.

It has been previously established that hyperthyroid myocardium exhibits increased performance under well-oxygenated conditions. To date, it is not known whether hyperthyroid cardiac muscle can maintain this increased performance during hypoxia. The responses of isolated right ventricular papillary muscles from hyperthyroid and euthyroid kittens to hypoxia were compared under isometric conditions at 31 degrees C. Under well-oxygenated conditions, the hyperthyroid cardiac muscle exhibited both an increased contractility and an accelerated rate of relaxation. A similar degree of acute hypoxic stress for 15 min resulted in a greater decrease in contractility in the hyperthyroid compared with the euthyroid papillary muscle as indicated by a greater fall in both peak tension development (2.2 +/- 0.25 from 4.2 +/- 0.2 vs. 0.9 +/- 0.15 from 3.2 +/- 0.4 g/mm2, P less than 0.01) and +dT/dt (12.9 +/- 2.3 from 25 +/- 3 vs. 4.0 +/- 0.6 from 14 +/- 1 g-s-1-mm-2, P less than 0.01). In addition, compared with the euthyroid data, hypoxia resulted in impaired myocardial relaxation in the hyperthyroid cardiac muscle. Thus, the hyperthyroid compared with the euthyroid papillary muscle exhibits both a greater decrease in contractility and an impairment of myocardial relaxation during hypoxia, indicating a greater susceptibility to a given hypoxic stress.

Animals↗
PubMed1978

Effects of acute global ischemia on diastolic relaxation in canine hearts.

It is not known whether ventricular relaxation can be altered by ischemia independent of associated hemodynamic changes. The effect of acute myocardial ischemia on diastolic relaxation was studied under controlled hemodynamic conditions in 16 anesthetized dogs on right-heart bypass. In nine dogs, left ventricular end-diastolic pressure was maintained constant throughout the experiments. Ischemia produced a significant prolongation of the isovolumetric relaxation period (IVRP) from 29 +/- 3 (SE) to 88 +/- 7 ms (P less than 0.01). Ischemia, per se, the associated decrease in contractility, or the fall in peak left ventricular pressure (LVP) may have contributed to the increase in IVRP. The latter was not the only mechanism involved, because in seven dogs studied with constant peak LVP, IVRP again was prolonged from 64 +/- 8 to 95 +/- 8 ms (P less than 0.01). Moreover, in five nonischemic hearts in which peak LVP was maintained constant, contractility was decreased by sodium pentobarbital to the same extent as with ischemia; IVRP did not change. Thus, the additional prolongation of the IVRP in the ischemia experiments is secondary to a direct effect of ischemia on the relaxation process of the myocardium.

Animals↗
PubMed1978

Ventricular performance and myocardial water content during hemodilution in dogs.

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.

Anemia↗
PubMed1978

Effect of hypoxia on myocardial relaxation in isometric cat papillary muscle.

Myocardial relaxation is an important energy-dependent process. Hypoxia, unlike ischemia, has not been shown to impair myocardial relaxation. This difference may be because (a) the traditional index to assess isometric muscle relaxation (half time to relaxation or RT((1/2))) reflects both changes in developed tension as well as relaxation and (b) the relaxation process is highly sensitive to temperature and previous papillary muscle studies have been conducted under hypothermic conditions. The present study examines the effect of hypoxia on the relaxation process of 31 isometrically contracting kitten papillary muscles at hypothermic (29 degrees C) and euthermic (38 degrees C) conditions using RT((1/2)), the peak rate of tension fall (-dT/dt) and -dT/dt normalized for tension ([peak -dT/dt]/T and max [-dT/dt per T]). Hypoxia at 29 degrees C resulted in a fall in RT((1/2)) from 278+/-11 (SEM) to 230+/-17 ms (P < 0.01) and no change in (peak -dT/dt)/T and max (-dT/dt per T). However, at 38 degrees C, hypoxia impaired relaxation as reflected in a prolongation of RT((1/2)) from 101+/-6 to 126+/-8 ms (P < 0.01) in spite of a substantial fall in peak tension. Moreover, (peak -dT/dt)/T decreased from -15.4+/-0.7 to -11.0+/-0.8/s (P < 0.01) and max (-dT/dt per T) decreased from -25.1+/-1.8 to -13.8+/-0.9/s (P < 0.01). In conclusion, the present study demonstrates that hypoxia impairs the relaxation process of cardiac muscle.

Animals↗
PubMed1977

Definition of cardiac structures using computerized tomography in isolated arrested and beating canine hearts.

Computerized axial tomography of the brain is a revolutionary noninvasive technique that has provided remarkable resolution of intracerebral structures. This study was undertaken to determine the potential of computerized tomography for defining the anatomy of 40 arrested and 9 beating (ejecting left heart preparation) canine hearts. Using an EMI cranial unit, scanning was performed in hearts under in vitro conditions with a lactated Ringer's interface. The tomographic scans obtained were later compared with comparable 8 mm thick sections of the heart. At physiologic levels of hematocrit (range 36 to 45%) external structures were well defined, but because of the lack of a differential between cavitary and myocardial densities, it was not possible to distinguish intracardiac structures. With very small amounts of iodinated contrast material (remotely administered in the case of the beating hearts) or with anemia (hematocrit less than 33%), the right and left ventricular cavities became clearly visible in both horizontal and longitudinal tomographic scans. It was possible to distinguish readily the boundaries of the ventricular and atrial cavities, the papillary muscles, the major trabeculae and the aorta. Rhythmic motion of the beating heart, suspended in its pericardium, did not eliminate structural definition. Thus, computerized tomography provides a new approach to the definition of cardiac structure with a relatively high degree of resolution. These observations point to the potential usefulness of this noninvasive technique for the evluation of both cardiac function and ventricular wall abnormalities.

Anemia↗