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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

White matter lesions (WMLs) detected by cerebral magnetic resonance imaging (MRI) are putatively a consequence of cerebral hypoperfusion or ischemia. We investigated the prevalence, severity and correlates of WMLs in a population-based sample of 1,920 African-American and European-American men and women aged 55-72 years, during the second follow-up examination of the Atherosclerosis Risk in Communities Study. The spin density images from 1.5-tesla MRI scans were used to define WMLs using a 0-9 scale with 0 for normal and 9 for most severe WMLs. Age was positively associated with the prevalence (percent) and severity of WMLs. African-Americans had lower overall prevalence of WMLs, but a higher prevalence of relatively more severe WMLs, than European-Americans. After adjusting for age, sex, and ethnicity, WMLs were significantly associated with smoking, lower education, hypertension, systolic blood pressure, and pulse pressure, and weakly associated with diastolic blood pressure. The associations of smoking, alcohol intake, systolic and diastolic blood pressure, pulse, pressure, and hypertension were stronger in African-Americans than in European-Americans (p < 0.15 for interactions by ethnicity). This population-based MRI study documents significant relationships between several cardiovascular disease risk factors and WMLs. The findings suggest that such factors play a role in the pathogenesis of WMLs, an elements linked to hypoperfusion and/or fluid accumulation, which presumably lead to WMLs. African-Americans exhibited both a higher proportion of normal white matter and a higher proportion of relatively more severe WMLs than European-Americans.
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PMID:The prevalence and severity of white matter lesions, their relationship with age, ethnicity, gender, and cardiovascular disease risk factors: the ARIC Study. 915 70

Morbidity in the diabetic population is primarily a result of cardiovascular dysfunction and failure. Ischemic heart disease is a serious complication in the diabetic population. Recent data indicate that hearts from insulin-dependent models of diabetes differ significantly in their response to ischemia from hearts of models of non-insulin-dependent diabetes. Intrinsic cardiac factors may be responsible for the altered sensitivities to ischemia in the different types of diabetes. However, vascular dysfunction is also clearly present in the diabetic animal models. Endothelial cell damage and dysfunction play a prominent role in the contractile abnormalities and lesion formation during diabetes. The present treatise focuses upon insulin as a causative factor in cardiovascular disease and the differences between insulin-dependent and non-insulin-dependent models of diabetes.
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PMID:Cardiovascular dysfunction in insulin-dependent and non-insulin-dependent animal models of diabetes mellitus. 919 61

Experiments were conducted to determine the effect of chronic elevations in corticosterone on myocardial infarct size. Male Sprague-Dawley rats were treated for 7-22 days with corticosterone. Plasma corticosterone concentrations averaged 0.8 +/- 0.3 in control and 14.9 +/- 1.2 micrograms/dl in corticosterone-treated conscious rats. Experiments were performed in anesthetized rats. After a 30-min control period, myocardial ischemia (30 min)-reperfusion (3 h) was performed in control and corticosterone-treated rats. Mean arterial pressure (+/-SE) in control rats during control, ischemia, and reperfusion periods averaged 111 +/- 4, 100 +/- 5, and 94 +/- 4 mmHg (n = 6), respectively. Chronic treatment with corticosterone increased mean arterial pressure in all three periods 128 +/- 6, 117 +/- 7, and 109 +/- 7 mmHg; n = 8; P < 0.05). Infarct size (as % area at risk) was significantly larger in rats with chronic elevations in corticosterone compared with control rats (77 +/- 2 vs. 51 +/- 5%, P < 0.05). Acute (2 h) blockade of the glucocorticoid type II receptors with mifepristone antagonized the increases in arterial pressure and infarct size produced by chronic administration of corticosterone. Neither mifepristone nor acutely administered corticosterone affected arterial pressure or infarct size in rats without chronic corticosterone treatment. The effect of chronic elevations in plasma corticosterone concentration to increase infarct size could contribute to the increased risk of cardiovascular disease in clinical conditions associated with elevated glucocorticoid levels.
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PMID:Chronic corticosterone treatment increases myocardial infarct size in rats with ischemia-reperfusion injury. 922 23

Cardiovascular disease is excessive in diabetes, and blood cell function is altered. It is not clear, however, if alterations in the blood contribute to the excessive cardiovascular complications of this disease. In this study, we compared the contribution of nondiabetic and diabetic blood to myocardial reperfusion injury. The recovery of cardiac contractile function following no-flow ischemia was studied in isolated diabetic and nondiabetic rat hearts perfused with diabetic or nondiabetic diluted whole blood. Hearts were isolated from 10- to 12-week-old diabetic (streptozotocin, 65 mg/kg, i.v.) and nondiabetic rats and perfused with a Krebs-albumin-red cell solution (K2RBC, Hct 20%). After a 30-min pre-ischemic control period, during which cardiac pump function was evaluated, diabetic and nondiabetic hearts were perfused for 5 min with diluted whole blood (DWB; Hct 20%) collected from either diabetic or nondiabetic donor animals. Coronary flow was then stopped and the hearts subjected to 30 min of no-flow ischemia. Following ischemia, the hearts were reperfused with the K2RBC perfusate. Cardiac contractile function was evaluated throughout the 60-min reperfusion period. Six groups were studied: diabetic and nondiabetic hearts perfused before ischemia with either K2RBC, nondiabetic DWB (NDDWB), or diabetic DWB (DDWB). Perfusion with DWB prior to ischemia impaired the recovery of contractile function in all cases. The impairment to recovery was greater with DDWB than with NDDWB. Although diabetic hearts perfused with K2RBC throughout recovered quite well, the effect of DDWB perfusion in the diabetic hearts was dramatic. In an effort to determine why diabetic blood impaired functional recovery, measures of blood filterability and the generation of reactive oxygen species (ROS) were made. We found that diabetic blood was less filterable than nondiabetic blood; that is, the diabetic blood cells tended to plug the 5-microm filter pores more readily than the nondiabetic blood cells. Also, we found that the diabetic blood was capable of generating significantly greater ROS (oxygen free radicals) than nondiabetic blood (P < 0.05). These findings suggest that the blood contribution to myocardial reperfusion injury is amplified in diabetes. A tendency for diabetic blood cells to plug capillary-sized pores and show enhanced oxygen free radical production may account for the excessive contribution of diabetic blood to reperfusion injury in the heart.
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PMID:The blood contribution to early myocardial reperfusion injury is amplified in diabetes. 935 37

There is a strong relation of carotid atherosclerosis to coronary artery disease and left ventricular hypertrophy. In addition, abnormalities of carotid structure are strongly associated with abnormal left ventricular geometry and structure. However, little is known regarding the relation of exercise-induced ST depression to carotid atherosclerosis, carotid, or left ventricular structure in the absence of apparent coronary disease. The relationship of exercise ECG myocardial ischemia to the presence of carotid atherosclerosis and to carotid and left ventricular structure was assessed in 204 asymptomatic subjects free of clinical evidence of cardiovascular disease. Myocardial ischemia on the exercise ECG, defined by a chronotropically adjusted ST/HR slope of >3.47 microV/bpm, was associated with a nearly threefold greater likelihood of discrete carotid atherosclerosis (50% [6 of 12] versus 17% [29 of 192], P=.007) and with older age, male sex, higher systolic and diastolic blood pressures, greater left ventricular mass and mass index, and greater common carotid artery intimal-medial thickness and cross-sectional area index. Stepwise logistic regression analyses, including standard risk factors, revealed that only carotid artery cross-sectional area index (P=.0007) and systolic blood pressure (P=.005) independently predicted an abnormal chronotropically adjusted ST/heart rate slope. Moreover, among 132 subjects with > or = 10 microV of ST-segment depression, only left ventricular mass index and carotid artery cross-sectional area index were significant predictors of the chronotropically adjusted ST/heart rate slope response. Subendocardial ischemia on the exercise ECG is strongly associated with the presence of carotid atherosclerosis and is related to systolic blood pressure, carotid artery cross-sectional area index, and left ventricular mass index, independent of age, sex, and other cardiac risk factors. These findings provide additional insights into the relation between coronary and carotid atherosclerosis and suggest that an association among ischemia and left ventricular and carotid structural abnormalities may contribute to the pathogenesis of coronary events.
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PMID:Relation of exercise-induced myocardial ischemia to cardiac and carotid structure. 940 57

This case study describes myocardial ischemia and stunning after the topical application of phenylephrine-soaked pledgets (0.25%) in a 63-year-old female undergoing elective endoscopic sinus surgery. The patient had no previous history of cardiovascular disease or illicit drug use. Transient myocardial ischemia was associated with acute hypertension, chest pain, and S-T segment changes 4 minutes after pledget placement. Angiography revealed normal coronary blood flow and severe left ventricular systolic and diastolic dysfunction. Follow-up echocardiography demonstrated improved left ventricular function within 1 week and total resolution of dysfunction by 4 weeks after ischemia.
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PMID:Myocardial ischemia and stunning induced by topical intranasal phenylephrine pledgets. 943 94

The heart is a tumor necrosis factor (TNF)-producing organ. Both myocardial macrophages and cardiac myocytes themselves synthesize TNF. Accumulating evidence indicates that myocardial TNF is an autocrine contributor to myocardial dysfunction and cardiomyocyte death in ischemia-reperfusion injury, sepsis, chronic heart failure, viral myocarditis, and cardiac allograft rejection. Indeed, locally (vs. systemically) produced TNF contributes to postischemic myocardial dysfunction via direct depression of contractility and induction of myocyte apoptosis. Lipopolysaccharide or ischemia-reperfusion activates myocardial P38 mitogen-activated protein (MAP) kinase and nuclear factor kappa B, which lead to TNF production. TNF depresses myocardial function by nitric oxide (NO)-dependent and NO-independent (sphingosine dependent) mechanisms. TNF activation of TNF receptor 1 or Fas may induce cardiac myocyte apoptosis. MAP kinases and TNF transcription factors are feasible targets for anti-TNF (i.e., cardioprotective) strategies. Endogenous anti-inflammatory ligands, which trigger the gp130 signaling cascade, heat shock proteins, and TNF-binding proteins, also control TNF production and activity. Thus modulation of TNF in cardiovascular disease represents a realistic goal for clinical medicine.
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PMID:Tumor necrosis factor in the heart. 953 Feb 22

Angiogenic cytokines constitute a potentially novel form of therapy for patients with cardiovascular disease. The feasibility of using recombinant formulations of angiogenic growth factors to expedite and/or augment collateral artery development in animal models of myocardial and hindlimb ischemia--'therapeutic angiogenesis'--has now been well established. These studies have suggested that two angiogenic growth factors in particular--basic fibroblast growth factor and vascular endothelial growth factor--are sufficiently potent to merit further investigation. More recently, experiments performed in our laboratory have indicated that, in the case of vascular endothelial growth factor--a secreted protein--similar results may be achieved by percutaneous arterial gene transfer. Further laboratory and clinical studies may yield promising insights into the fundamental basis for native as well as therapeutic angiogenesis, and at the same time more explicitly define the manner in which therapeutic angiogenesis may be successfully incorporated into clinical practice.
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PMID:Therapeutic angiogenesis: a new frontier for vascular therapy. 954 20

Heart-rate reduction is an important element of patient management during cardiac bypass surgery and in therapeutic measures for combating ischemia and relieving pain in patients with angina. UL-FS 49 is a novel bradycardic agent that purportedly acts solely on the sinoatrial node without potentially deleterious effects on arterial pressure and cardiac inotropism. However, little is known about influences of this agent on neuronal tissue and cardiovascular reflexes. Moreover, left ventricular hypertrophy, which often accompanies cardiovascular disease, is known to attenuate the arterial baroreflex and could have effects interactive with those of UL-FS 49. In this study, the effects of UL-FS 49 on the arterial baroreflex were tested in normal rats (N), rats with left ventricular hypertrophy 14 days after abdominal aortic constriction (AC), and sham-operated controls (SH). Arterial baroreflex sensitivity (BRS) was estimated as the slope of the relation between mean arterial pressure (independent variable) and the RR interval (dependent variable). At the time of study, the AC group had significantly greater mean arterial pressure than either SH or N (159 +/- 2, 122 +/- 3, and 124 +/- 3 mm Hg, respectively; mean +/- SEM, p < 0.01) and significantly greater left ventricular mass to body mass ratio than did SH (3.73 +/- 0.11, 2.33 +/- 0.11 mg/g; p < 0.01). As expected, BRS was significantly depressed in AC, compared with either SH or N (0.52 +/- 0.16, 1.48 +/- 0.12, 1.69 +/- 0.25 ms/mm Hg, respectively; p < 0.01). Despite its potent dose-dependent bradycardic effects in all three groups, UL-FS 49 did not affect BRS significantly in any group. These results show that the arterial baroreflex is largely unaffected by UL-FS 49 in both normal rats and rats with systemic hypertension and left ventricular hypertrophy.
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PMID:UL-FS 49 (zatebradine) does not affect arterial baroreflex in conscious normal or aortic-constricted rats. 955 94

Therapeutic angiogenesis constitutes a fundamental survival mechanism that acts to preserve the integrity of tissues subjected to ischemia. Supplemental administration of angiogenic cytokines--as recombinant protein or plasmid DNA--have been shown to augment collateral development when endogenous angiogenesis is suboptimal for organ function, and thus constitute a novel therapeutic option for the treatment of cardiovascular disease. These angiogenic cytokines, all of which share in common the ability to act as mitogens for endothelial cells, do not promote angiogenesis in an indiscriminate fashion; thus angiogenic cytokines selectively produce neovascularization in the ischemic tissues. The purpose of this review is to consider the mechanisms responsible for therapeutic angiogenesis which develops endogenously as well as strategies which have been devised to augment this response. The development of blood vessels is considered from the context of the embryonic paradigm; certain principles which have emerged from studies of pathologic neovascularization; and, principally, the development of collateral blood vessels supplying ischemic tissues, either endogenously or in response to administered growth factors.
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PMID:Therapeutic angiogenesis. 956 5


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