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Biomedical subjects

R L Engler

Publications and source records attributed to R L Engler.

At least 55 records · Page 3Linked to original sources
PubMed1987

Functional significance of alpha-adrenergic receptors in mature coronary collateral circulation of dogs.

There is little information on the functional significance of alpha-adrenergic receptors in the dog's coronary collateral circulation. Accordingly, we investigated the effects of infusion of either norepinephrine (NE) or B-HT 920 (BHT), an alpha 2-adrenergic agonist, on vascular resistance of coronary collaterals in chloralose-anesthetized dogs 2-3 mo after placement of an Ameroid constrictor around the left circumflex coronary (LCX) artery. To accomplish this, the vagotomized left ventricle was autoperfused through the left main coronary ostium using a servo-controlled constant-pressure pump. Pressures of the left anterior descending (LAD) and peripheral LCX arteries were measured, and regional blood flow in LAD and LCX regions were determined with radioactive microspheres before and during NE infusion in the unblocked condition, following beta-adrenergic and beta + alpha 1-adrenergic blockade with the use of propranolol and prazosin, respectively. The same parameters were also measured before and during BHT infusion following beta-adrenergic and beta + alpha 2-adrenergic blockade with the use of propranolol and idazoxan, respectively. In the unblocked condition, NE reduced LAD, LCX, and collateral resistance by 43, 50, and 31%, respectively. After beta-adrenergic blockade, NE increased LAD resistance (29%) but did not alter LCX or collateral resistance. The increase in LAD resistance was abolished following alpha 1-adrenergic blockade. BHT increased vascular resistance in LAD, LCX, and collateral circulations by 35, 29, and 45%, respectively. Selective alpha 2-adrenergic blockade significantly attenuated the vasoconstrictor response to BHT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1987

Granulocytes as active participants in acute myocardial ischemia and infarction.

The classical picture of the polymorphonuclear leukocyte--antimicrobal activities and participation in the inflammatory reaction--appears now to be expanded. It has been recognized that this cell may be highly injurious to other cells, has a propensity to be trapped in the capillary network, and may occlude microvascular pathways. The classical hypothesis that the granulocytes appear in the ischemic or postischemic myocardium as response to the associated inflammatory reaction may have to be revised. Instead, the granulocyte may actually be the key factor causing the inflammation. An array of future studies is needed to clarify the events step by step. Important aspects are the activation and degranulation sequence in the ischemic myocardium, the form and extent of injury caused by the oxygen free radicals and lysosomal enzymes, the source and nature of chemotactic substances, particularly in human forms of myocardial ischemia, and the degree to which granulocytes cause or magnify the injury.

Acute Disease↗
PubMed1986

Accumulation of polymorphonuclear leukocytes during 3-h experimental myocardial ischemia.

Recent evidence indicates that mechanical obstruction of capillaries by leukocytes plays an important role in the "no-reflow" phenomenon in the heart. This entrapment of leukocytes in the microcirculation precedes their recognized role in an inflammatory reaction following ischemia. It is a fundamental rheological mechanism that may be associated with ischemic injury and reflow injury and it has not been elucidated. To explore the accumulation of granulocytes during myocardial ischemia we studied the accumulation of 111Inlabeled autologous granulocytes in acutely ischemic myocardium during 3 h of flow reduction with and without a subsequent period of reflow in open-chest dogs. Granulocytes accumulated in the ischemic endocardium of all animals and, for the majority of dogs, also in the epicardium. Accumulation in the endocardium was enhanced by reperfusion. The entrapped leukocytes may have an influence on the increase in resistance, since regional accumulation of leukocytes in the endocardium inversely correlated with ischemic blood flow during 3 h of ischemia. The tissue water content measured from the wet and dry weights of biopsies showed a significant positive correlation with the number of entrapped granulocytes. These results suggest that collateral flow is an important mechanism of leukocyte arrival early in ischemic myocardium and that reperfusion enhances granulocyte accumulation.

Animals↗
PubMed1986

Role of leukocytes in response to acute myocardial ischemia and reflow in dogs.

Recent evidence indicates that leukocytes (LEU) are large, stiff, viscous cells that naturally adhere to vascular endothelium. Their broad role in the early myocardial microvascular response to acute ischemia was suggested by 1) the role of leukocyte capillary plugging in the no-reflow phenomenon, 2) resistance increases in skeletal muscle with LEU infusions, and 3) salvage of ischemic myocardium by anti-LEU agents. We perfused the coronary circulation under matched, controlled conditions with whole blood or granulocyte-depleted whole blood. During 1 h of ischemia (left anterior descending occlusion) circumflex perfusion pressure was servocontrolled to a constant value. In whole blood-perfused hearts, flow measured by the radiolabeled microsphere method decreased in endocardium from 0.12 +/- 0.05 at 5 min of ischemia to 0.09 +/- 0.04 ml X min-1 X g-1 at 60 min of ischemia and in epicardium from 0.27 +/- 0.17 to 0.21 +/- 0.16 ml X min-1 X g-1, both P less than 0.05. In granulocyte-depleted blood-perfused hearts, flow increased over the same period from 0.18 +/- 0.15 to 0.29 +/- 0.18 ml X min-1 X g-1 in endocardium (P less than 0.05) and did not change significantly in epicardium (0.36 +/- 0.22 to 0.41 +/- 0.24 ml X min-1 X g-1). The LEU-depleted blood perfusate contained less than 33 granulocytes/microliter, whereas control perfusate contained 4,265/microliter. Reperfusion at normal pressures with carbon suspension allowed for histologic evaluation of the no-reflow phenomenon. With whole blood perfusion the no-reflow phenomenon in the endocardium was present with 27% of capillaries occluded, compared with nearly complete reperfusion in LEU-depleted animals (1% of capillaries occluded, P less than 0.05). Furthermore, LEU depletion prevented the increases in tissue water content seen in control hearts and decreased the incidence of ventricular arrhythmias. These studies demonstrate the significant participation of granulocytes in the unfavorable responses of flow, edema formation, and arrhythmias to the 1st h of myocardial ischemia and further document their role in the no-reflow phenomenon.

Acute Disease↗
PubMed1985

Absence of cardioversion-induced ventricular arrhythmias in patients with therapeutic digoxin levels.

To determine the incidence of cardioversion-induced ventricular arrhythmias in patients with therapeutic serum levels of digoxin, 19 patients (average age [+/- standard deviation] 61 +/- 12 years) undergoing elective direct current cardioversion for atrial fibrillation were studied. Only patients with therapeutic serum digoxin levels (range 0.5 to 1.9 ng/ml; mean 1.1 +/- 0.5) at the time of cardioversion were included. Patients with acute myocardial ischemia or unstable angina, serious electrolyte disturbance or those requiring class I antiarrhythmic agents for control of ventricular or supraventricular arrhythmias were excluded. Ambulatory electrocardiograms were recorded for 24 hours before and 6 hours after cardioversion. No patient developed malignant ventricular arrhythmias (ventricular triplets or tachycardia) in the immediate 3 hour period after cardioversion. Furthermore, there were no significant (p less than 0.05) differences in the frequency of ventricular premature beats or couplets before and after cardioversion. To determine whether the level of serum digoxin or the strength of the applied shock had a significant effect on the development of postcardioversion arrhythmias, the change in frequency of single premature ventricular beats after cardioversion was compared with the serum digoxin level (ng/ml) and the applied energy level (joules) by means of linear regression analysis. There was no significant (p less than 0.05) relation between these variables. These findings suggest that patients with therapeutic serum levels of digoxin may safely undergo cardioversion without the concomitant use of class I antiarrhythmic agents.

Adult↗
PubMed1985

Relationship between myocardial fiber direction and segment shortening in the midwall of the canine left ventricle.

Myocardial fiber orientation undergoes an orderly transition from the epicardium to the endocardium in the left ventricle, with circumferential fibers predominating in the middle one-third of the heart wall. How fibers lying at different depths in the myocardium, running in different directions, interact to produce local deformation is not known. To define the relationship between the orientation of uniaxial myocardial fibers and local wall motion, we placed three sets of ultrasonic dimension gauges in the middle one-third of the apex-to-base distance of the left ventricle of nine dogs. One pair was placed in line and two intentionally out of line with the presumed local fiber direction. The relative angle between the gauge and the local myofibers was determined by the use of postmortem radiography and histological techniques. Our results show that in the midwall of the left ventricle, myocardial segment shortening is maximal in the direction of local fibers; the shortening measured by gauges placed out of line with the local fiber axis by more than 30 degrees was significantly less than the actual in-line fiber shortening which occurred. This suggests that functional tethering between midwall fibers and endocardial or epicardial fibers does not play a major role in the pattern of midwall deformation. We also documented that an external reference line can be used to predict midwall myofiber direction. Using this line as a guide, ultrasonic dimension gauges could be placed within an average of 12 degrees (range: 0.5 to 18.5 degrees) from the local fiber axis.

Animals↗
PubMed1983

Changes in plasma renin activity and haemodynamics during vasodilator therapy in conscious dogs with myocardial infarction or chronic volume overload.

The aim of the study was to compare the changes in plasma renin activity induced by a vasodilator in normal dogs and in dogs with an impaired cardiac reserve. In normal conscious dogs, a 60-min nitroprusside infusion increased plasma renin activity from 1.05 +/- 0.26 to 8.35 +/- 1.20 ng, angiotensin I ml-1 h-1 (P less than 0.002) and heart rate from 83 +/- 6 to 149 +/- 15 beats/min (P less than 0.002). In five dogs in which a aortocaval fistula had been created 4 weeks earlier, the same infusion still increased plasma renin activity but significantly less than in normal dogs (0.90 +/- 0.29 to 4.44 +/- 0.64 ng ml-1 h-1; P less than 0.01) and the heart rate was unchanged (134 +/- 4 to 139 +/- 7 beats/min; NS). Similarly, in five dogs with a previous myocardial infarction, the heart rats response to nitroprusside was blunted (108 to 107 beats/min;NS) and plasma renin activity increased less than in normal dogs. Plasma renin activity also increased acutely after hydralazine administration in dogs which myocardial infarction (1.05 +/- 0.26 to 8.99 +/- 0.79 ng ml-1 h-1; P less than 0.05); after 1 week of hydralazine, plasma volume had increased from 54.9 +/- 0.9 ml kg-1 to 74.5 +/- 4.9 ml kg-1 (P less than 0.05) and plasma renin activity remained higher than control (4.66 +/- 0.66 ng ml-1 h-1; P less than 0.01). In conclusion, vasodilator therapy rapidly activates vasoconstrictor forces and fluid retention even in dogs with limited cardiac reserve. Although the regulation of plasma renin secretion appears altered in these models of heart disease, the renin response remains sufficient to seriously limit the beneficial effects of vasodilator therapy.

Animals↗
PubMed1983

Regional venous return: nitroprusside effect in normal and chronically congested dogs.

The venous circulation is a key determinant of cardiac loading conditions. Although it may be altered by chronic congestive heart failure and vasodilating drugs, the mechanisms of these alterations have not been thoroughly studied, and their exact nature is unclear. We used venous return curves characterized by the pressure at zero flow (PZF) and resistance to venous return (RVR) to study the effect of nitroprusside and chronic congestion on regional venous return from the splanchnic and superior vena cava (systemic) venous beds in dogs. Chronic venous congestion was induced by prior creation of tricuspid insufficiency and pulmonic stenosis (TIPS). Nitroprusside lowered splanchnic PZF but not systemic PZF in both normal and TIPS animals. In normal animals systemic RVR increased during nitroprusside infusion but was unchanged in the congested animals. Resting values of PZF and RVR were different in the splanchnic and systemic venous beds in both normal and TIPS animals. We conclude that 1) nitroprusside works to selectively lower PZF in the splanchnic venous bed, 2) the regionally specific site of action of nitroprusside is not altered by TIPS, and 3) the independent behavior of the venous parameters of the two beds represents an important mechanism for the control of cardiac output.

Animals↗
PubMed1983

Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog.

After several hours of ischemia an incomplete return of blood flow has been reported in brain, kidney, skeletal muscle, and heart. The mechanisms responsible for the no-reflow phenomenon have been unclear, and perivascular edema, platelet or red cell plugs, and interstitial hemorrhage have been implicated. In the present study evidence is provided that leukocyte entrapment in capillaries might contribute to no reflow. Leukocytes are large and stiff cells, which adhere to vascular endothelium naturally and are known to alter in their adherence properties under a variety of conditions. Accordingly, 11 open-chest dogs were studied, 1-5 hours after left anterior descending coronary artery occlusion. Reperfusion (9 dogs) at 75 mm Hg arterial pressure was accomplished with Ringer's lactate and carbon suspension as a marker for capillary patency. In non-ischemic tissue, 98% of the capillaries contained carbon, rare leukocytes, and few erythrocytes, whereas tissue from the distribution of the occluded artery was heterogeneous: 60% of the capillaries had no carbon, high hematocrits, and approximately one leukocyte per unbranched capillary; 40% demonstrated reflow and no leukocytes. A significant correlation between capillaries without carbon (no reflow) and the frequency of leukocytes remaining in these capillaries indicated that leukocytes were present in obstructed capillaries. Furthermore, the frequency of leukocytes remaining after the washout with lactate was ten times greater than in normal arrested heart muscle without washout. Our results suggest that progressive leukocyte capillary plugging during myocardial ischemia contributes to preventing full restoration of capillary flow upon reperfusion.

Animals↗
PubMed1982

A simple teaching device for examination of the arterial and venous pulse.

A simple teaching device is described for examination of the cervical arterial and venous pulses. It is a mechanical device that simultaneously generates a visible jugular venous pulsation and a palpable carotid arterial pulsation to train medical students, physicians, and paramedical personnel. Changing of cams allows the observer to appreciate these pulsations in the normal or in a variety of abnormal states. Graphic tracings of wave forms demonstrate the accuracy of reproduction of physiologic tracings. In a test of the device, cardiologists performed significantly better than medical students in the identification of unknown pulsations. The instrument is readily accepted, simple to operate, and fully portable.

Carotid Arteries↗
PubMed1982

Pacemaker spike alternans: an artifact of digital signal processing.

Marked variability in the amplitude or polarity of pacemaker artifacts may be a clue to generator malfunction or partial electrode fracture. We report a case where "pacemaker spike alternans" occurred factitiously as a result of a digital "roll-over" effect. The widespread introduction of digital electrocardiographs into clinical practice makes recognition of such artifacts important.

Aged↗
PubMed1982

Do coronary artery bypass operations prolong life?

Coronary artery bypass operations improve survival in patients with symptomatic left main coronary artery stenosis, but whether or not longevity is improved in other patients has been controversial. Small clinical studies, even when randomized, have not sufficiently controlled for the heterogeneous distribution of risk factors in patient cohorts treated medically and surgically. The first randomized study large enough to overcome such problems, the Veterans Administration Cooperative Study, showed that coronary artery bypass procedures prolonged survival only in the high-risk subgroup. The surgically treated patients suffered more perioperative morbidity and mortality and had worse long-term survival than similar patients operated on in more recent years. The European Coronary Surgery Study Group recently reported that the three-year to five-year survival of symptomatic patients with triple-vessel disease and normal left ventricular function was better if patients were randomly assigned to surgical therapy. The third and by far the largest randomized study, the Coronary Artery Surgery Study (CASS), has not yet reported long-term follow-up results. Large clinical studies, both randomized and nonrandomized, that have subgrouped patients by the number of diseased coronary arteries and by the degree of left ventricular dysfunction all show that survival with single-vessel disease is excellent and not improved by operation. Medically treated patients with double- and triple-vessel disease who have good left ventricular function generally now have a five-year survival greater than 85 percent and only two of the major studies suggest that it is improved by operation. The results of most studies, however, suggest that bypass operation prolongs survival in symptomatic patients when left ventricular dysfunction coexists with double- and triple-vessel disease. Continually improving surgical techniques may potentiate the small survival differences that are now apparent, but until then, because the survival differences are so small, it is recommended that limiting anginal symptoms remain the primary indication for a coronary bypass procedure for an individual patient.

Angina Pectoris↗
PubMed1980

Enhanced left ventricular shortening during chronic volume overload in conscious dogs.

Prior work with the arteriovenous fistula model indicates that left ventricular performance is at least normal and may be enhanced during chronic volume overload. The present study was undertaken in conscious dogs to determine whether ejection-phase indices of ventricular function are enhanced after 1 mo of volume overload, using an experimental design in which loading conditions could be accounted for and animals were used as their own controls before and after volume overload. We also examined the response of the volume-overloaded left ventricle to an afterload stress and the role of adrenergic stimulation in maintenance of function. Both at rest and during hemodynamically matched conditions, percent shortening (ultrasonic dimension gauges) and mean shortening rates were increased during volume overload. This difference was maintained during phenylephrine-induced blood pressure elevation, although diastolic dimensions increased more in control studies during phenylephrine. Propranolol produced significantly larger reductions in these indices during volume overload than in the control state. Thus, ejection-phase function is enhanced during volume overload, at least in part due to increased adrenergic stimulation.

Animals↗