Ovid Technologies (Wolters Kluwer Health)
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Sắp xếp:
Blood Capillaries of the Heart and Other Organs The article is a review of work recently carried out on blood capillaries by the author in collaboration with Drs. M. G. Farquhar, G. Majno, and S. L. Wissig.
It reviews the morphology of these vessels at the electron-microscope level and confirms the existence of at least 3 distinct types of blood capillaries in small laboratory mammals. It shows that the capillary wall consists of 3 concentric layers (endothelium, basement membrane, and adventitia), and indicates that the basement membrane forms a continuous layer in all capillaries so far studied.
Experiments in which colloidal gold particles were used as a tracer have shown that, in capillaries with a continuous endothelium (muscle capillaries), the particles are transported across it by "pinocytic" vesicles. At the end of this step they must still transverse the basement membrane.
Experiments on glomerular capillaries, which typically have a discontinuous s endothelium, were carried out on normal and nephrotic rats using ferritin as a tracer. By its accumulation on the luminal side of the basement membrane, the ferritin has identified this layer as the main filtration barrier.
A similar function of the basement membrane was demonstrated in muscle venules and venous capillaries by experiments in which the endothelium was rendered discontinuous by local treatment with histamine and serotonin.
Ovid Technologies (Wolters Kluwer Health) - Tập 24 Số 2 - Trang 368-384 - 1961
Association of Coronary Heart Disease Risk Factors With Microscopic Qualities of Coronary Atherosclerosis in Youth
Background
—This study examined whether atherosclerosis in young people is associated with the risk factors for clinical coronary heart disease (CHD).
Methods and Results
—Histological sections of left anterior descending coronary arteries (LADs) from 760 autopsied 15- to 34-year-old victims of accidents, homicides, and suicides were graded according to the American Heart Association (AHA) system and computerized morphometry. Risk factors (dyslipoproteinemia, smoking, hypertension, obesity, impaired glucose tolerance) were assessed by postmortem measurements. Approximately 2% of 15- to 19-year-old men and 20% of 30- to 34-year-old men had AHA grade 4 or 5 (advanced) lesions. No 15- to 19-year-old women had grade 4 or 5 lesions; 8% of 30- to 34-year-old women had such lesions. Approximately 19% of 30- to 34-year-old men and 8% of 30- to 34-year-old women had atherosclerotic stenosis ≥40% in the LAD. AHA grade 2 or 3 lesions (fatty streaks), grade 4 or 5 lesions, and stenosis ≥40% were associated with non-HDL cholesterol ≥4.14 mmol/L (160 mg/dL). AHA grade 2 or 3 lesions were associated with HDL cholesterol <0.91 mmol/L (35 mg/dL) and smoking. AHA grade 4 or 5 lesions were associated with obesity (body mass index ≥30 kg/m
2
) and hypertension (mean arterial pressure ≥110 mm Hg).
Conclusions
—Young Americans have a high prevalence of advanced atherosclerotic coronary artery plaques with qualities indicating vulnerability to rupture. Early atherosclerosis is influenced by the risk factors for clinical CHD. Long-range prevention of CHD must begin in adolescence or young adulthood.
Ovid Technologies (Wolters Kluwer Health) - Tập 102 Số 4 - Trang 374-379 - 2000
Intravenous pretreatment with A1-selective adenosine analogues protects the heart against infarction.
BACKGROUND
Recent data from this laboratory indicate that pretreatment with adenosine can protect the heart against infarction via A1-receptors, but because of systemic hypotension, adenosine had to be given into the coronary circulation.
METHODS AND RESULTS
In this study, we tested whether the protection could be achieved by intravenous administration of the A1-selective adenosine agonists N6-(phenyl-2R-isopropyl)-adenosine (PIA) and 2-chloro-N6-cyclopentyladenosine (CCPA). Nine groups of open-chest anesthetized rabbits were subjected to 30 minutes of regional coronary ischemia and 3 hours of reperfusion. Infarct size was determined by tetrazolium staining. Control hearts receiving no treatment had 38 +/- 4% of the risk zone infarcted. Preconditioning with 5 minutes of ischemia and 10 minutes of reperfusion before ischemia limited the infarct to 8 +/- 4%. Intravenous PIA 15 minutes before 30-minute ischemia also limited infarct size to 6 +/- 2% at the highest dose. CCPA offered similar protection. When the PIA was given at reperfusion, infarct size was 46 +/- 6%, indicating that receptor activation must precede ischemia to protect. Pretreatment with CGS 21680, a selective A2-receptor agonist, caused identical hypotension but failed to limit infarct size (43 +/- 3%), indicating again that the A1-receptor is involved. When rabbits pretreated with PIA were paced at 220 beats per minutes, PIA still limited infarct size (16 +/- 4%), indicating that protection was not the result of bradycardia.
CONCLUSIONS
These results indicate that stimulation of adenosine A1-receptors causes the heart to become resistant to ischemia and that this protection can be achieved with intravenous administration of A1-selective agents.
Ovid Technologies (Wolters Kluwer Health) - Tập 85 Số 2 - Trang 659-665 - 1992
Variables predictive of survival in patients with coronary disease. Selection by univariate and multivariate analyses from the clinical, electrocardiographic, exercise, arteriographic, and quantitative angiographic evaluations. A progression of univariate followed by multivariate analyses was applied to 46 variables selected from the clinical examination, exercise test, coronary arteriography, and quantitative angiographic assessment of left ventricular function in patients with coronary disease to determine those variables most predictive of survival. For the 733 medically treated patients, the final Cox's regression analysis showed that the left ventricular ejection fraction was most predictive of survival, followed by age, number of vessels with stenosis(es) greater than or equal to 70%, and ventricular arrhythmia on the resting electrocardiogram. For the 1870 surgically treated patients, ventricular arrhythmia on the resting electrocardiogram was most predictive of survival followed by ejection fraction, heart murmur, left main coronary artery stenosis greater than or equal to 50%, and use of diuretic agents.
Ovid Technologies (Wolters Kluwer Health) - Tập 59 Số 3 - Trang 421-430 - 1979
Arrhythmogenesis and ventricular dysfunction after myocardial infarction. Is anomalous cellular coupling the elusive link?
Ovid Technologies (Wolters Kluwer Health) - Tập 87 Số 5 - Trang 1742-1745 - 1993
Relationship Between TIMI Frame Count and Clinical Outcomes After Thrombolytic Administration
Background
—The corrected TIMI frame count (CTFC) is the number of cine frames required for dye to first reach standardized distal coronary landmarks, and it is an objective and quantitative index of coronary blood flow.
Methods and Results
—The CTFC was measured in 1248 patients in the TIMI 4, 10A, and 10B trials, and its relationship to clinical outcomes was examined. Patients who died in the hospital had a higher CTFC (ie, slower flow) than survivors (69.6±35.4 [n=53] versus 49.5±32.3 [n=1195];
P
=0.0003). Likewise, patients who died by 30 to 42 days had higher CTFCs than survivors (66.2±36.4 [n=57] versus 49.9±32.1 [n=1059];
P
=0.006). In a multivariate model that excluded TIMI flow grades, the 90-minute CTFC was an independent predictor of in-hospital mortality (OR=1.21 per 10-frame rise [95% CI, 1.1 to 1.3], an ≈0.7% increase in absolute mortality for every 10-frame rise;
P
<0.001) even when other significant correlates of mortality (age, heart rate, anterior myocardial infarction, and female sex) were adjusted for in the model. The CTFC identified a subgroup of patients with TIMI grade 3 flow who were at a particularly low risk of adverse outcomes. The risk of in-hospital mortality increased in a stepwise fashion from 0.0% (n=41) in patients with a 90-minute CTFC that was faster than the 95% CI for normal flow (0 to 13 frames, hyperemia, TIMI grade 4 flow), to 2.7% (n=18 of 658 patients) in patients with a CTFC of 14 to 40 (a CTFC of 40 has previously been identified as the cutpoint for distinguishing TIMI grade 3 flow), to 6.4% (35/549) in patients with a CTFC >40 (
P
=0.003). Although the risk of death, recurrent myocardial infarction, shock, congestive heart failure, or left ventricular ejection fraction ≤40% was 13.0% among patients with TIMI grade 3 flow (CTFC ≤40), the CTFC tended to segregate patients into lower-risk (CTFC ≤20, risk of adverse outcome of 7.9%) and higher-risk subgroups (CTFC >20 to ≤40, risk of adverse outcome of 15.5%;
P
=0.17).
Conclusions
—Faster (lower) 90-minute CTFCs are related to improved in-hospital and 1-month clinical outcomes after thrombolytic administration in both univariate and multivariate models. Even among those patients classified as having normal flow (TIMI grade 3 flow, CTFC ≤40), there may be lower- and higher-risk subgroups.
Ovid Technologies (Wolters Kluwer Health) - Tập 99 Số 15 - Trang 1945-1950 - 1999
Macrophage Migration Inhibitory Factor Deficiency Impairs Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice
Background—
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine expressed widely by vascular cells. However, scant in vivo evidence supports direct participation of MIF in atherogenesis. Therefore, we investigated whether deficiency of MIF modulates atherosclerotic lesion formation and composition in low-density lipoprotein receptor-deficient (LDLr
−/−
) mice.
Methods and Results—
MIF
−/−
LDLr
−/−
and LDLr
−/−
mice were generated and consumed an atherogenic diet for 12 or 26 weeks. MIF
−/−
LDLr
−/−
mice had significantly reduced abdominal aorta lipid deposition and intimal thickening from aortic arch throughout the abdominal aorta compared with LDLr
−/−
mice. Marked retardation of atherosclerosis over time in MIF-deficient mice accompanied decreased lesion cell proliferation. At 26 weeks, 20% of MIF-deficient mice developed only early, fatty streak-like lesions, whereas >80% of LDLr
−/−
mice developed advanced lesions containing calcification and lipid cores. Analysis of smooth muscle cells from mouse aortae demonstrated that MIF deficiency reduced smooth muscle cell proliferation, cysteine protease expression, and elastinolytic and collagenolytic activities.
Conclusions—
Deficiency of MIF reduces atherogenesis in LDLr
−/−
mice. These results provide novel insight into inflammatory pathways operating in atheromata and identify a new potential target for modulating atherogenesis.
Ovid Technologies (Wolters Kluwer Health) - Tập 109 Số 25 - Trang 3149-3153 - 2004
Cytokine and murine coxsackievirus B3 myocarditis. Interleukin-2 suppressed myocarditis in the acute stage but enhanced the condition in the subsequent stage.
BACKGROUND
It has been shown that the development of coxsackievirus B3 (CB3) myocarditis is regulated by T cells and not by B cells. Interleukin-2 (IL-2) is a T-cell-derived cytokine that stimulates the growth of T cells. This study was carried out to determine the effects of IL-2 on CB3-infected BALB/c mice.
METHODS AND RESULTS
In two separate experiments, recombinant human IL-2 (5 x 10(4) U) was administered subcutaneously to 30 mice early (days 0 to 7) and 30 mice late (days 7 to 14) after infection with CB3. Each experiment had a control group of infected animals that did not receive IL-2. On days 7 and 10, splenic natural killer (NK) cell activity determined by 51Cr release assay and the distribution of myocardial lymphocyte subsets were compared in the treated and untreated groups. In the early treatment experiment, survival at 7 days was higher in treated compared with control animals, myocardial virus titers were lower, inflammatory cell infiltration was less (as was the severity of necrosis at the time the mice were killed), and NK cell activity was higher. However, in the late treatment experiment, survival at 14 days was lower in treated compared with control animals, and there was more infiltration, more severe necrosis, and more T-cell infiltration, but the NK cell activity did not differ significantly. In a third experiment similar to the late experiment described above but involving infected athymic nude mice, we confirmed the lack of effect of late in vivo administration of IL-2 on outcome.
CONCLUSIONS
IL-2 has the capacity to limit CB3 myocarditis by enhancing NK cell activity in the acute viremic stage, resulting in a reduction of cardiac pathology. However, in the subacute aviremic stage, in contrast, IL-2 exacerbates the course and severity of the disease by increasing the number of T cells infiltrating the myocardium. That is, IL-2 has differential effects on acute CB3 myocarditis. IL-2 is beneficial if treatment is given early but later in murine CB3 myocarditis.
Ovid Technologies (Wolters Kluwer Health) - Tập 89 Số 6 - Trang 2836-2842 - 1994
Control of rapid ventricular response by radiofrequency catheter modification of the atrioventricular node in patients with medically refractory atrial fibrillation.
BACKGROUND
Pharmacological control of rapid ventricular response to atrial fibrillation may be difficult in some patients. Alternative treatments, including curative surgery or atrioventricular (AV) node ablation with pacemaker implantation, have significant potential morbidity. In view of evidence that dual AV nodal physiology may exist in a significant percentage of the population, even in those without AV nodal reentrant tachycardia, we postulated that control of ventricular response might be achieved by radiofrequency (RF) catheter ablation in the region of the AV nodal slow pathway with its short refractory period.
METHODS AND RESULTS
Ten patients underwent attempted AV node modification using a 4-mm-tipped electrode catheter positioned in the middle or posterior septum, between the His bundle and coronary sinus ostium on the tricuspid valve annulus. RF energy was applied at 16 to 30 W for up to 60 seconds, until average ventricular response fell below 100 beats per minute. Reduction of maximal ventricular response below 120 beats per minute was confirmed with atropine 1 mg IV. If required, additional ablations were performed progressively more posteriorly up to the coronary sinus ostium. Patients with successful AV node modification were discharged off AV node-blocking drugs and followed in the clinic at regular intervals. Twenty-four-hour ambulatory ECG recordings and/or treadmill stress tests were obtained before and after ablation for statistical comparison of maximum ventricular rate. Resting average ventricular rate was determined during electrophysiology study before and after ablation. In 7 of 10 patients (70%), maximum ventricular rate was reduced from a mean of 164 +/- 12 to 123 +/- 16 beats per minute (P < .01) and average ventricular rate from a mean of 128 +/- 11 to 83 +/- 10 beats per minute after ablation. Mean minimum ventricular rate was 54 +/- 11 beats per minute after ablation. These 7 patients have remained symptom free from rapid ventricular response for a mean of 14 +/- 8 months (range, 1 to 22). Three remain off all AV node-blocking drugs, 3 remain on digoxin alone, which was previously ineffective, and 1 remains on a beta-blocker for angina. In the 3 patients who did not respond to AV node modification, complete AV node ablation and permanent pacemaker implantation was performed in 2 and DC cardioversion after amiodarone loading was performed in 1.
CONCLUSIONS
RF catheter modification of AV node conduction is effective in controlling rapid ventricular response to atrial fibrillation in a significant percentage of medically refractory patients. A possible mechanism of RF modification of AV node conduction is AV nodal slow pathway ablation. Large-scale clinical trials will be needed to determine the overall efficacy and safety of this technique.
Ovid Technologies (Wolters Kluwer Health) - Tập 90 Số 5 - Trang 2299-2307 - 1994
ACC/AHA 2002 Guideline Update for Exercise Testing: Summary Article
Ovid Technologies (Wolters Kluwer Health) - Tập 106 Số 14 - Trang 1883-1892 - 2002
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