Search PubMed⌕ Search

Biomedical subjects

J Ross

Publications and source records attributed to J Ross.

At least 721 records · Page 40Linked to original sources
PubMed1977

Innate resistance to myxomatosis in wild rabbits in England.

Wild rabbits (Oryctolagus cuniculus) from one study area in England have been used over a period of 11 years to investigate the possible appearance of innate resistance to myxomatosis. Rabbits of 4-6 weeks old were captured alive, retained in the laboratory until at least 4 months old, and then infected with a type of myxoma virus which kills 90-95% of laboratory rabbits. Observations were made of symptoms, mortality rate and survival times.In the first 4 years of the study (1966-9), mortality rates were not significantly different from those of laboratory rabbits, although survival times of wild rabbits were appreciably longer. In 1970, the mortality rate amongst wild rabbits was 59%, in 1974 it was 17%, and in 1976 it was 20%, thus showing that a considerable degree of inherited resistance to myxomatosis has developed.The types of myxoma virus most commonly isolated from wild rabbits in Great Britain in recent years have been those which cause 70-95% mortality in laboratory rabbits. Therefore, if the degree of innate resistance demonstrated is widespread in Great Britain, there are serious implications regarding the size of the rabbit population, because myxomatosis has been an important factor in holding rabbit numbers at a relatively low level.

Animals↗
PubMed1977

Hyperfunction with normal inotropic state of the hypertrophied left ventricle.

Conscious dogs were instrumented with an inflatable cuff around the ascending aorta, a high-fidelity micromanometer in the left ventricle (LV), and pairs of ultrasonic crystals for measurements of LV wall thickness and internal LV diameter. Wall stress (WSt) and mean velocity of wall shortening (VCF) were calculated. Mean force-velocity relations and WSt-diameter loops in single contractions were then analyzed over a range of matched systolic pressures during acute aortic constrictions both before and after induction of chronic hypertrophy by sustained aortic constriction. At normal LV systolic pressures and at each matched level of systolic LV pressure, wall shortening velocity was increased in the hypertrophied ventricle. However, force-velocity relations obtained by relating mean VCF to mean WSt at various stress levels fell on the same relation as during control. The linear relation between LV diameter and pressure at the end of ventricular ejection was shifted to the left in the hypertrophied ventricle, indicating enhanced shortening. However, linear WSt-diameter relations at end-ejection were not different in control and hypertrophied hearts. These findings indicate that the ventricle hypertrophied by pressure overload exhibited hyperfunction as a pump but that its myocardium had a normal level of inotropic state.

Animals↗
PubMed1977

In situ measurement of papillary muscle dynamics in the dog left ventricle.

In five open-chest dogs, pairs of ultrasonic dimension gauges were implanted in the anterior papillary muscle and in a circumferential subendocardial segment of the anterior left ventricular free wall, and simultaneous recordings were made with intracardiac pressure. The average shortening of the anterior segment in isovolumetric systole was 6% of end-diastolic length (EDL), with a total shortening of 19%. In the papillary muscles, isovolumetric shortening averaged 2%, total shortening was 10%, and shortening velocity was only 0.60 length/s. With acute pressure and volume overload, or inotropic interventions, changes in EDL were relatively less in papillary muscles than in the free wall. During acute occlusion of the anterior descending coronary artery, shortening of anterior segments and papillary muscles was replaced by holosystolic lengthening, and occlussion of the circumflex artery produced augmentation of shortening in both these regions, with lengthening of the posterior papillary muscle. The present study documents shortening of the anterior left ventricular papillary muscle throughout systole that is substantially less than that of the circumferential free wall, and demonstrates severe papillary muscle dysfunction with systolic elongation during regional ischemia.

Animals↗
PubMed1977

Loss of regional ventricular postextrasystolic potentiation after coronary occlusion in dogs.

Postextrasystolic potentiation following coronary artery occlusion was studied serially using pairs of ultrasonic crystals to measure regional myocardial function in control, marginally ischemic, and ischemic segments of the left ventricle in dogs. Prior to coronary occlusion (CO), percent shortening in control (normal) segments increased by an average of 51.4 +/- 4.6% in the beat after a premature ventricular contraction (post-PVC beat), and this response changed little after coronary occlusion. During the 1st min after CO, in ischemic segments, systolic expansion developed but was replaced by active shortening in post-PVC beats; however, after 3 min of CO (average) and thereafter, there was no net positive shortening in post-PVC beats. In marginally ischemic segments early after CO, hypokinesia developed, but there was marked augmentation of percent shortening (208.6 +/- 32.6%) which persisted in post-PVC beats even after 2 h. It is concluded that loss of postextrasystolic potentiation occurs rapidly in ischemic regions after CO and is not indicative of irreversible damage; partially ischemic regions retain this mechanism for prolonged periods.

Animals↗
PubMed1977

Detection of perioperative myocardial damage after coronary artery bypass graft surgery.

In order to evaluate methods for detecting peri-operative myocardial damage we studied 41 patients before and serially following coronary artery bypass graft surgery utilizing the 12-lead ECG, serum MB-CPK measurements, and 99mTc pyrophosphate myocardial scans. Six of the 41 patients (15%) developed persistent new Q waves after surgery. Six other patients demonstrated ischemic ST-T wave changes that persisted for 48 hours or more. Mean total MB-CPK released was highest for the group with new Q waves [1598+/-545 (SE) I.U./L-hr] as compared to the group with ischemic ST-T wave changes 708+/-65 I.U./L-hr) or the group with no ECG changes (262+/-47 I.U./L-hr). Ten patients (24%) has positive postoperative pyrophosphate scans consistent with myocardial infarction. The three techniques were compared in these 41 patients utilizing 465 I.U./L.-hr as the upper limit of normal MB-CPK released after uncomplicated coronary bypass surgery (no ECG changes, negative scan). Five patients with ischemic ECG changes had a positive scan and high MB-CPK; six patients with no ECG changes had high MB-CPK but a negative scan; and one patient with high MB-CPK and new Q wave had a negative scan. We conclude 1) new Q waves on ECG underestimate the incidence of myocardial damage after coronary artery surgery; 2) MB-CPK alone overestimates the incidence of infarction; and 3) a combination of the three techniques is the best means for detecting myocardial damage after coronary artery bypass graft surgery.

Adult↗
PubMed1977

Regional myocardial function and dimensions early and late after myocardial infarction in the unanesthetized dog.

Pairs of ultrasonic dimension gauges and a micromanometer implanted in the subendocardium of the left ventricles of unanesthetized dogs were used to analyze serial changes in hemodynamic status and segmental function for up to 4 weeks after permanent circumflex coronary artery occlusion. Regional function was studied in control segments and in segments identified as marginal (hypokinetic) and ischemic. In three dogs, after transient regional dysfunction, no myocardial infarction developed, whereas in five dogs regional dysfunction at 3 hours after occlusion was followed by the development of persistent dysfunction and infarction. Left ventricular end-diastolic segment length (EDL) changes over time; EDL of the control segments increased progressively, but in marginal segments EDL was 12% below control and in the ischemic segments 30% below control by 4 weeks. Progressive increases in percent active shortening occurred in control segments; but holosystolic bulging was replaced by akinesia in ischemic segments, and persistent reduction in shortening was present in marginal segments at 4 weeks. Correlations were found between percent scar and reductions in percent shortening, EDL, and the ratio of change in diastolic length to change in diastolic pressure. These methods have detected hyperfunction in normal regions and variable segmental loss of contractile function, together with reduction of subendocardial dimensions and changes that may reflect decreased diastolic compliance in ischemic regions. We conclude that this model for the conscious animals may be useful for studying the influence of therapy on the extent of myocardial damage after experimental coronary occlusion.

Animals↗
PubMed1977

Echocardiographic and roentgenographic determination of left ventricular size after coronary arterial bypass graft surgery.

In 38 patients undergoing elective coronary arterial bypass graft surgery, the radiographic dimension of the left side of the heart was determined and echocardiographic studies were performed before and after surgery. On the plain chest x-ray film one week after surgery, all patients showed an increase in the size of the left side of the heart, which usually was not accompanied by an increase in the echocardiographic left ventricular end-diastolic dimension; however, in 25 patients, pericardial fluid was detected soon after surgery, which would explain the enlarged cardiac silhouettes. Several months after surgery, the radiographic size of the heart returned to the preoperative value in most patients, and pericardial fluid was no longer demonstrated on the echocardiogram. Thus, pericardial fluid frequently is found in the first week following coronary arterial bypass graft surgery and may give the impression of increased cardiac size on plain chest x-ray films; however, echocardiographic studies provide a more accurate estimate of left ventricular size and reveal the presence of pericardial effusion.

Adult↗
PubMed1977

Putting it all together.

Outlines an organizational concept that supports the functions and products required of HSAs. Emphasizes the separation of functions with "controlled stresses" designed to produce interdependence of staff sections. Points out the need for tangible products as a basis for tracking staff performance.

Health Systems Agencies↗
PubMed1977

Gonadotropin receptors in experimentally induced ovarian tumors in mice.

Gonadotropic hormones are required for the induction and maintenance of tumors arising in ovaries that have been transplanted to the spleens of gonadectomized mice. The characteristics of gonadotropin receptors for human chorionic gonadotropin (HCG)-luteinizing hormone on cells from these tumors of varying size, age, and morphology have been determined. The specific binding of 125I-labeled HCG to cells obtained by collagenase digestion, 15 to 65 weeks postimplantation from granulosa cell or luteinized cell, or mixed granulosa-luteal tumors was analyzed by Scatchard plot. Neither the size, weight, duration of implantation, nor histological morphology affected the receptor-binding affinity [equilibrium dissociation constant (Kd), 6 X 10(-10) M], and, presumably, the receptor is qualitatively similar. In contrast, the number of HCG receptors per cell increased 17-fold and was related to the degree of morphological luteinization of the tumor. HCG-sensitive adenyl cyclase was also demonstrated and compared to HCG binding in a highly luteinized tumor.

Animals↗
PubMed1976

Coronary arterial reperfusion. III. Early and late effects on regional myocardial function and dimensions in conscious dogs.

Regional myocardial function was studied in five conscious chronically instrumented dogs for 4 weeks after coronary reperfusion following a 2 hour period of occlusion of the left circumflex coronary artery. A cuff and flowmeter were placed around the left circumflex coronary artery, and a micromanometer and three pairs of ultrasonic crystals were implanted 1 cm apart subendocardially in control, marginal and ischemic segments of the left ventricle. Control normal segments showed progressive increases in end-diastolic length and extent of active shortening. Ischemic segments tended to show slight improvement early after reperfusion, but in succeeding weeks, despite some improvement in shortening, they showed progressive decreases in end-diastolic length compatible with subendocardial tissue loss. In marginally ischemic segments, shortening initially remained depressed after reperfusion, but showed late recovery so that shortening and end-diastolic length were not different from control values by 4 weeks. These results contrasted with findings in five similarly studied dogs subjected to permanent coronary occlusion; in that group the data suggested greater tissue loss and less recovery of function in marginal and ischemic segments. The late return of segmental function and reduced loss of subendocardial tissue several weeks after coronary reperfusion suggest that substantial time periods may be required to assess the ultimate effect of therapeutic interventions. The findings further indicate that in this experimental model the usual time constraints for occurrence of irreversible tissue damage do not apply to all of the myocardium within the ischemic zone.

Action Potentials↗
PubMed1976

Favorable effects of orally administered digoxin on left heart size and ventricular wall motion in patients with previous myocardial infarction.

The effects of maintenance oral digoxin therapy on segmental left ventricular wall motion (wall motion videotracking) and left heart size (radiographic left heart dimension) were evaluated in 14 patients with a prior myocardial infarction but without clinical signs or symptoms of congestive heart failure. The left heart dimension decreased in all six patients with cardiomegaly from an average of 55.0 +/- 1.6 (standard deviation) to 52.2 +/- 2.7 mm/m2 body surface area (P less than 0.01) during digoxin therapy. However, there was no significant change in the eight patients with normal heart size. In the resting state, the average extent of shortening in normal segments increased significantly from 3.1 +/- 0.8 to 4.2 +/- 1.2 mm during digoxin therapy. During submaximal handgrip exercise, the extent of shortening averaged 4.0 +/- 1.3 mm and increased further with digoxin therapy to 5.1 +/- 2.1 mm. The effects of digoxin therapy on the maximal velocity of shortening in normal segments at rest and during handgrip exercise were similar. In all 14 patients, there was a decrease in the number of segments with abnormal wall motion at rest or with handgrip exercise during digoxin therapy. With therapy, the number of abnormal sites decreased from 52 to 35 in the resting state and from 84 to 49 during handgrip exercise. Thus, in patients 6 or more months after transmural myocardial infarction, orally administered digoxin decreases cardiomegaly, increases the extent and maximal velocity of shortening in normal left ventricular segments and often reduces the extent of abnormal wall motion at rest or during isometric exercise.

Administration, Oral↗
PubMed1976

Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog.

The thickness of the left ventricular free wall and internal chamber diameter were continuously measured by pairs of ultrasonic crystals together with left ventricular pressure in normal conscious dogs. During the resting state, wall thickness decreased abruptly with the onset of atrial contraction from 10.5 mm to an average end-diastolic valueof9.8 mm. In contrast to most previous studies, there was no change in wall thickness during isovolumic systole, and with ejection the wall thickened by 31.3 percent of end-diastolic wall thickness. Atrial pacing, phenylephrine, isoproterenol and propranolol produced significant changes in chamber size with reciprocal changes in wall thickness. In addition, changes in the extent and velocity of left ventricular chamber shortening in the minor equator were associated with comparable reciprocal changes in the extent and velocity of free wall thickening (correlation coefficients 0.97 to 0.99). During acute coronary occlusion, progressive reductions in the extent and velocity of regional wall shortening with partial ischemia were associated with comparable changes in systolic wall thickening characteristics (r = 0.96 and 0.95), and holosystolic elongation in fully ischemic areas was associated with holosystolic wall thinning. During chronic pressure overload, despite wall thickening, the relation between chamber shortening and wall thickening were retained and direct computation of dynamic wall stress variations was possible. These measurements allowed precise definition of the dynamics of the left ventricular wall during normal and abnormal cardiac states. The demonstration that in the absence of regional dysfunction analysis of wall thickness in a single region of ventricular free wall can be used to describe myocardial and overall left ventricular function, as well as regional function in the presence of ischemia, constitutes a new approach to the assessment of cardiac function that has potential for echocardiographic applications.

Animals↗
PubMed1976

Induction of globin mRNA accumulation by hemin in cultured erythroleukemic cells.

The role of heme in erythroid development is investigated in erythroleukemic (Friend) cells. Exogenous hemin induces the accumulation of globin mRNA and globin protein in T3-C12 erythroleukemia cells to levels comparable to those induced by polar solvents, such as dimethylsulfoxide (DMSO). The hemin concentration required for maximal induction (10(-4) M) is the same as that which stimulates globin message translation in reticulocytes or cell-free reticulocyte lysates. Hemin and DMSO together cause T3-C12 cells to accumulate 8-9 fold more globin mRNA than either inducer individually. The kinetics of globin mRNA induction in hemin as compared to DMSO are very different: globin message accumulation begins 4 hr after hemin addition, but not until 30--40 hr after DMSO addition. Biliverdin induces 20--40 fold less hemoglobin than hemin; delta-aminolevulinic acid and porphobilinogen do not induce.

Aminolevulinic Acid↗