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J Ross

Publications and source records attributed to J Ross.

At least 955 records · Page 53Linked to original sources
PubMedDate not supplied

Alpha 1-adrenergic blockade reduces exercise-induced regional myocardial ischemia in dogs.

The effect of selective alpha 1-adrenoceptor blockade on regional myocardial blood flow and contractile function during exercise-induced myocardial ischemia was determined in nine dogs having chronic single vessel coronary stenosis (ameroid constrictor). Treadmill exercise performed after beta-adrenoceptor blockade (1.0 mg/kg i.v. propranolol), to block potential prejunctional effects recently recognized with alpha-blockade, elicited severe regional myocardial ischemia with a steady-state reduction of regional systolic wall thickening of the post-stenotic myocardium from a resting value of 21.8% to 7.0%. Blood flow to the ischemic subendocardium was reduced from 0.76 to 0.36 ml/min/g (microspheres). Prazosin (80 micrograms/kg i.v.) was administered during continued running, and angiotensin II was simultaneously infused to prevent the decrease in systemic arterial pressure caused by prazosin. During the subsequent steady state, with arterial pressure matched to the pre-prazosin level, regional subendocardial blood flow improved to 0.60 ml/min/g and systolic wall thickening in the post-stenotic region increased modestly to 10.2%. No changes in blood flow to the outer portion of the post-stenotic region or to the remote control region were seen, and prazosin caused no effect on regional function in the control area, indicating effective blockade of prejunctional effects of prazosin (demonstrated in pilot studies). The finding that blockade of alpha 1-adrenoceptors resulted in improved ischemic zone subendocardial blood flow and contractile function are consistent with alpha 1-adrenoceptor-mediated reduction of blood flow to the ischemic subendocardium during exercise-induced ischemia in dogs with beta-blockade.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Effects of a sinus node inhibitor on the normal and failing rabbit heart.

The effects on cardiac function of slowed frequency produced by a sinus node inhibitor (zatebradine, or UL-FS 49) were studied in the conscious rabbit under control conditions (n = 16) and after heart failure was produced by rapid atrial pacing for an average of 18.5 days (n = 8). Echocardiography was used to verify severe left ventricular (LV) dysfunction, and high-fidelity micromanometry and cardiac output measurements (Doppler echo) were performed. Echocardiographic fractional shortening was 40.3 +/- 4.1 % (SD) in controls; in heart failure it was 18.0 +/- 1.6 %, and the LV was enlarged. In controls, as heart rate (HR) was decreased from 279 beats per minute (bpm) by incremental doses of zatebradine (up to 0.75 mg/kg), maximal changes occurred when the heart reached 218 bpm with a maximum decrease of the first derivative of LV pressure (LV dP/dtmax) of 15.9 %; LV enddiastolic pressure (EDP) increased from 4.3 to 8.4 mmHg along with a significant decrease in cardiac index (CI) of 15.2 %, while LV systolic pressure (SP) was stable. In heart failure, LV dP/dtmax and CI were markedly reduced compared to controls and with reduction of HR from 257 to 221 bpm LV dP/dtmax was unchanged, LVEDP increased slightly (NS), LVSP was unchanged and CI fell by 13.5 % at the highest dose. In subgroups (control n = 9, failure n = 6), in order to eliminate the hemodynamic effects of cardiac slowing by zatebradine the sinus rate present before zatebradine was matched by atrial pacing; this procedure eliminated all hemodynamic abnormalities accompanying cardiac slowing in both groups. In conclusion, slowed HR due to a sinus node inhibitor was well tolerated in severe heart failure, and all negative hemodynamic responses in both controls and in heart failure were due entirely to a negative forcefrequency effect, without a direct depressant action of zatebradine on the myocardium.

Animals↗
PubMedDate not supplied

Cyclical coronary flow reductions in conscious dogs equipped with ameroid constrictors to produce severe coronary narrowing.

In conscious dogs equipped with ameroid constrictors to produce gradual coronary occlusion, coronary flow velocity was monitored prior to complete occlusion when coronary constriction was severe (resting flow velocity reduced by 10-50% from control recordings made days after ameroid implantation). In six of the ten dogs, we observed spontaneous cyclical variations in coronary flow velocity, characterized by gradual reduction in flow followed by very abrupt restoration of flow. The cyclic coronary flow reductions were observed between 20 and 31 days after ameroid implantation. These changes in flow bear striking similarity to those observed by previous investigators using anesthetized, open-chest canine preparations, in which the role of platelets was clearly demonstrated. Consequently, we hypothesize that spontaneous platelet aggregation and de-aggregation within the severely narrowed coronary lumen (enclosed by the ameroid constrictors) could account for our observations.

Animals↗
PubMedDate not supplied

Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function.

A two-dimensional framework can be used for considering the characteristics of left ventricular ejection in terms of the appropriateness of the matching between afterload and the level of inotropic state, as modulated by the preload reserve. An afterload mismatch (reduced velocity and extent of shortening) can be induced acutely in the normal heart under controlled conditions if the preload is not allowed to compensate for an increased afterload, or if the limit of preload (Frank-Starling) reserve has been reached. In the intact circulation the normal heart is sensitive to some degree to acute changes in afterload, perhaps due to impaired venous return; but under basal resting conditions the ejection phase measures (such as the ejection fraction and the mean velocity of circumferential fiber shortening or VCF, corrected for heart size) encompass a relatively narrow range. This finding, and the lack of change in ejection phase measures after the normal heart has adapted to a chronic pressure or volume overload, provides justification for the use of ejection phase indices for detecting depressed inotropic state under basal conditions. When there is mild depression of myocardial inotropic state, with or without accompanying mechanical overload, enhanced preload may allow full compensation, but acute pressure loading may allow early detection of a less than normal preload reserve. When the inotropic state is substantially reduced, however, a mismatch between afterload and contractility (a reduction in mean VCF) will become evident even in the basal state (venous return being presumed to be adequate under these conditions). The concept of afterload mismatch with limited preload reserve provides an explanation for the value of ejection phase indices compared to isovolunic phase measures in assessing the basal level of inotropic state: the former may be more reliable because they are sensitive to afterload. The effects and implications of therapeutic afterload reduction as modulated by the preload also are understood within this framework.

Animals↗
PubMedDate not supplied

Mechanisms of regional ischemia and antianginal drug action during exercise.

Several mechanisms involved in the production of regional exercise-induced ischemia are described. Each offers the potential for modification using different types of antianginal drugs operating to alter regional O2 demands, improve regional perfusion, or both, leading to reduced ischemia and increased contractile function in the ischemic zone. Evidence is presented for matching of regional subendocardial myocardial blood flow and flow per beat with regional myocardial contraction at various levels of ischemia at rest, during steady-state exercise, and after antianginal drugs, signifying a particularly important role for heart rate control. In addition to reducing myocardial O2 demand per minute, beta-blockers and bradycardic drugs cause improvement of absolute subendocardial blood flow and particularly flow per beat by producing vasoconstriction in the epicardial region of the ischemic zone, with improvement of transmural blood flow distribution. Vasodilator drugs can act at several locations to increase regional blood flow and also to decrease O2 demands. A recruitable vasodilator reserve has been shown to exist during exercise-induced ischemia either in native resistance vessels, collateral channels, or both, which appears to be due at least in part to reduction of increased alpha-adrenergic constrictor tone to the coronary vessels during exercise, even in the presence of severe ischemia. The potential for additive effects using combinations of bradycardic and vasodilating agents are described within a framework relating regional subendocardial blood flow to regional systolic contraction. The experimental findings described suggest some potential new directions for antianginal therapy and, along with recent clinical observations, support the use of combinations of antianginal agents that act by different mechanisms.

Angina Pectoris↗
PubMedDate not supplied

The role of heart rate in myocardial ischemia and infarction: implications of myocardial perfusion-contraction matching.

The pathophysiology of myocardial ischemia traditionally has been attributed to disturbances of oxygen demand, as observed in classic effort-induced angina pectoris, or to a primary disruption of coronary blood supply, as in unstable angina or acute myocardial infarction. Laboratory research eliciting various types of perfusion-contraction matching has challenged such a historical distinction between supply and demand-induced determinants of myocardial ischemia. A growing number of clinical studies analyzing the role of heart rate in the course of coronary heart disease suggest the possibility that a common perfusion-contraction scheme may underlie these diverse clinical manifestations. During experimental myocardial ischemia, produced by a low coronary blood flow, regional perfusion-contraction matching exists in which the energy demands and regional contraction are reduced to match the diminished myocardial substrate supply. Heart rate is a major factor influencing transmural blood flow distribution and regional function, because when coronary vasodilation is maximal there is an inverse relation between the level of heart rate and subendocardial perfusion. Thus, in experimental regional ischemia, increasing heart rate reduces subendocardial flow and contraction, whereas slowing of heart rate causes improvement of contraction associated with increased subendocardial blood flow, accompanied by a decrease in outer wall blood flow. Also, "interventricular steal" of blood from the left ventricle by the right ventricle during ischemia can be reversed by slowing the heart rate in the presence of regional ischemia. Improvement of contraction by heart rate slowing is more than would be expected on the basis of the increase in subendocardial perfusion alone, reflecting a combination of decreased oxygen demand and increased oxygen supply, and separate curves relating blood flow per minute to contractile function are observed at different heart rates. However, when perfusion is normalized for heart rate by expressing subendocardial blood flow in units per beat, a single relation is observed at different heart rates. This observation supports the concept of a close coupling between subendocardial blood flow per beat and regional performance, or perfusion-contraction matching, during various levels of ischemia. Based on these principles, it can be predicted that exercise-induced regional ischemia in the presence of coronary stenosis will be attenuated by several mechanisms when heart rate is slowed using either a beta-blocking agent, or a specific bradycardic drug.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Catecholamine biosynthesis and vasopressin and oxytocin secretion in the spontaneously hypertensive rat: an in vitro study of localized brain regions.

The in vitro synthesis of catecholamines and the secretion of vasopressin (AVP) and oxytocin (OT) was measured in localized regions of the hypothalamo-neurohypophyseal system in the spontaneously hypertensive rat (SHR). The posterior pituitary (PP), median eminence (ME) and supraoptic (SON) and paraventricular (PVN) nuclear regions were incubated in vitro in media containing 3H-tyrosine. Media and tissue levels of AVP and OT were measured as well as norepinephrine and dopamine content and biosynthesis. There were no differences in peptide release in either the PP, ME or SON. However, there was a marked increase in peptide release from the PVN of the SHR. Media AVP levels were 0.3 pg/ml/micrograms protein in the WKY as compared to 2.1 pg/ml/micrograms protein in the SHR. OT release was increased 2 fold, from 0.85 to 1.7 pg/ml/micrograms protein. PVN content of both AVP and OT was significantly lower in the SHR. ME and SON peptide levels were not changed, while neurohypophyseal AVP levels were increased in the SHR. With regard to the catecholamines appreciable norepinephrine synthesis was measured in the PVN and SON while there was little 3H-norepinephrine in the ME or PP. In the hypertensive rat, there was an increase in norepinephrine synthesis in the PVN with no change in the SON. These results provide further support for fundamental changes in the catecholaminergic and peptidergic systems of the hypothalamo-neurohypophyseal axis of the SHR.

Animals↗
PubMedDate not supplied

Demographics, treatment seeking, and diagnoses of anxiety support group participants.

Two peer-led anxiety disorder support groups were surveyed to ascertain characteristics of individuals seeking the services of these groups. Both groups had received information and consultation from the Anxiety Disorders Association of America. One hundred and eighty-four individuals were interviewed for diagnosis by structured clinical interview; demographics and treatment-seeking behaviors were ascertained by self-report questionnaires. Both groups surveyed were composed of more females than males and were predominantly Caucasian. Treatment was most frequently sought from psychiatrists, psychologists, and family doctors. One fourth of the sample had sought help for anxiety in a hospital emergency room. Eighty-eight subjects (94%) at the Dallas site and 57 subjects (61%) at the Durham site met criteria for at least one current anxiety or affective disorder. More than half of those who met criteria for current panic disorder with agoraphobia also met criteria for at least one other anxiety disorder, or for major depression. Approximately one third of each support group met criteria for current social phobia. Severity of social phobia symptoms was assessed by four scales. An increased risk of substance abuse was noted for individuals with a diagnosis of social phobia, as compared with diagnoses of other anxiety disorders.

Adult↗
PubMedDate not supplied

An acquired interatrial fistula secondary to para-aortic abscess documented by transesophageal echocardiography.

Para-aortic ring abscess and resulting fistulous communication between adjacent structures frequently occur in prosthetic aortic valve endocarditis but are rarely diagnosed preoperatively. We report a patient who had an abscess involving the aortic-mitral intervalvular fibrosa that eroded into the interatrial septum, causing an interatrial communication with a left-to-right shunt. The abscess was detected by transthoracic echocardiography, but the fistula was only seen by the subsequent transesophageal echocardiogram. To our knowledge, this is the first report of an interatrial fistula secondary to a para-aortic valve abscess and its diagnosis preoperatively. Transesophageal echocardiography should be performed in any patient suspected to have complicated aortic endocarditis.

Abscess↗
PubMedDate not supplied

Biosensor-based micro-affinity purification for the proteomic analysis of protein complexes.

A biosensor-based micro-affinity purification method to recover protein binding partners and their complexes for down stream proteomics analysis has been developed using the BIAcore 3000 fitted with a prototype Surface Prep Unit (SPU). The recombinant GST-intracellular domain of E-cadherin or the recombinant GST-beta-catenin binding domain of Adenomatous Polyposis Coli (APC) were immobilized onto the SPU and used to affinity purify binding partners from chromatographically enriched SW480 colon cancer cell lysates. A GST- immobilized surface was used as a control. Samples recovered from the SPU were subjected to SDS-PAGE with sensitive Coomassie staining followed by automated in-gel digestion and LC-MS/MS. The results obtained using the SPU were compared with similar experiments performed using Sepharose beads.

Biosensing Techniques↗
PubMedDate not supplied

Added noise restores recognizability of coarse quantized images.

When a portrait is coarsely quantized into blocks, the block structure hides the face, although lower spatial frequencies of the original image sufficient by themselves for recognition are preserved. Recognition can be recovered by blurring the image, or otherwise attenuating the spurious higher spatial frequency components. Harmon and Julesz claim that high spatial frequencies introduced by quantized blocking mask the lower spatial frequencies which convey information about the face, preventing recognition. Here we show that recognition can be enhanced, without decreasing the amplitude of these spurious higher frequencies, by adding further high-frequency noise to the quantized image. This result is clearly at odds with a theory of high-frequency (or critical band) masking. We suggest that the added noise mutes mechanisms which would otherwise impose a block structure on the image, allowing the alternative perceptual organization of the hidden face to reemerge.

Form Perception↗
PubMedDate not supplied

Comparison of HL-A typing with NIH trays and the NIH technique with typing by the fluorochromasia cytotoxicity assay.

A comparison of HL-A phenotypes determined with plates containing predispensed typing sera supplied by the NIH Serum Bank with phenotypes determined by the fluorochromasia cytotoxicity assay using local reagents showed that the NIH plates (as dispensed in 1972) had an insufficient number and variety of typing sera. Using NIH trays, it was difficult to detect HL-A9 and W19, both of which specificities are now known to have subtypes. The NIH trays also appeared to detect more HL-A antigens than were consistent with the current theory of two segregant series, each expressing a maximum of two antigens. The excess antigens could not be comparatively evaluated in view of the small number of sera defining each. With the NIH technique, it was impossible to interpret the reactions if the preparation had too many dead cells. A high proportion of dead cells was occasionally noted when lymphocytes had been previously frozen or obtained from lymph nodes. When the NIH and fluorochromasia techniques were compared using the same antisera and fresh lymphocytes, they proved equivalent in sensitivity.

Cytotoxicity Tests, Immunologic↗