Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of plain ischemia (34 degrees C) and the protective role of hypothermia (20 degrees C) alone or in combination with cardioplegia (St Thomas' Hospital [STH] or glucose-potassium-nifedipine [GPN]) on the intracellular kinetics of the activator calcium of cardiac muscle were quantified and compared from the interval-force behaviour (mechanical restitution) of right and left ventricles of the perfused rat heart. Plain ischemia caused a major depression in the restitution of force of contraction of both ventricles, deranged the mixed linear-exponential functions by significantly increasing the time constants of the fitted mechanical restitution curves (MRC) and altered the control right/left ventricle interval-force relationship. The right ventricle was found to be more susceptible to ischemic damage than the left ventricle, and its inotropic reserve was virtually abolished by 1 h of plain ischemia. Hypothermic preservation during ischemia improved the mechanical restitution, salvaged the inotropic reserve and optimized right/left ventricle interval-force relationship, but the time constants of the fitted MRCs were still prolonged. However, both the cardioplegic formulations were equally effective in normalizing the time constants of the fitted curves. In general, right ventricle functions were better preserved by STH cardioplegia and left ventricle functions were better preserved by GPN cardioplegia. Cardioplegic interventions did not further improve the ventricular inotropic reserve compared with hypothermic preservation. Additional beneficial effects of cardioplegic formulations were directed towards stabilizing the linear-exponential functions and hence restitution of force of contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Intracellular kinetics of the activator calcium of rat heart after ischemic arrest and cardioplegia: quantitative comparison of right and left ventricles. 137 92

A case is presented in which a patient with ischemic heart disease developed episodic, nonsustained ventricular tachycardia (VT) during electroconvulsive therapy for major depression. The VT had a frequency of 200 beats/min and ceased spontaneously after 17 s. Altered autonomic discharge in the presence of ischemia is the probable cause. Predisposing factors, as well as management considerations, are discussed.
 ...
PMID:Ventricular tachycardia with ECT. 964 7

Depression represents a major public health problem. It is estimated that 13-20% of the population has some depressive symptoms at any given time and about 5% of the population is assumed to suffer from major depression. Known pathological processes include ischemia, neoplasia, necrosis, apoptosis, infection, and inflammation. Of those, inflammation is the most compatible with the waxing and waning course of depression, and could explain the biology of this disorder that has a fluctuating course with severe episodes that can be followed by partial or complete remission. Over the years a body of evidence has been accumulated suggesting that major depression is associated with dysfunction of inflammatory mediators. Major depression commonly co-occurs with ischemic heart disease and decreased bone mineral density. Depressive symptoms are known to have a negative impact on cardiovascular prognosis, increasing the mortality rate of coronary artery disease. Several lines of evidence indicate that brain cytokines, principally interleukin-1beta (IL-1beta) and IL-1 receptor antagonist may have a role in the biology of major depression, and that they might additionally be involved in the pathophysiology and somatic consequences of depression as well as in the effects of antidepressant treatment. A particularly unique and novel aspect of the studies and views discussed here is their potential to lead to interventions which may reduce the morbidity and mortality risks for osteoporosis, cardiovascular disease, and behavioral symptoms in patients with major depression. We also discuss the emerging concept of peripheral and central cytokine compartments: their integration and differential regulation is a key element for the optimal functioning of the immune and nervous systems.
 ...
PMID:The role of inflammatory mediators in the biology of major depression: central nervous system cytokines modulate the biological substrate of depressive symptoms, regulate stress-responsive systems, and contribute to neurotoxicity and neuroprotection. 1048 47

Nineteen patients with major depression were alternately given intravenous atropine or saline immediately prior to anesthesia for electroconvulsive therapy (ECT). Atropine increased the heart rate, reduced the number of dropped beats, and reduced the number of premature atrial beats. These features may be advantageous in patients with cardiac hypodynamic states presenting for ECT, that is, with bradycardia, bradyarrhythmia, or hypotension. However, as atropine also increased the cardiac work, we recommend that it not be given to patients with hypertension, tachycardia, or who are at risk for cardiac ischemia.
 ...
PMID:Atropine in Electroconvulsive Therapy. 1194 Sep 94

Signal hyperintensities on magnetic resonance imaging (MRI) are increased in the white matter (WMH) and deep gray matter in dementia and depression and may have similar pathologies. However, no previous study has examined WMH in subjects with major depression. We carried out in vitro MRI on brain tissue from elderly subjects who had suffered major depression and elderly control subjects to identify and rate WMH. The tissue was subsequently prepared for histopathological analysis using a number of conventional and immunohistochemical stains, and the WMH were examined to identify their underlying pathological causes. Cerebral microvessels were also assessed and the findings compared with assessments of atheromatous disease in these subjects. PVH were found to be due to one of three causes: dilated perivascular spaces (with and without ischemia in the perivascular area), oligemic demyelination, and ischemic demyelination. DWMH also showed three types of causes: dilated perivascular spaces (with and without ischemia in the perivascular area), oligemic demyelination, and ischemic demyelination. Cerebral microvascular disease only contributed to a few of the lesions and atheromatous disease did not show associations with WMH in these subjects. These findings are similar to previous reports in other diseases and demonstrate WMH in elderly depression to be a manifestation of cerebrovascular disease. However, since large vessel and small vessel disease were not associated with WMH, our findings suggest hypotensive disease might be an important and unrecognized mechanism underlying WMH in late-life depression.
 ...
PMID:Pathologies and pathological mechanisms for white matter hyperintensities in depression. 1248 Jul 70

The evidence from research studies linking depression to excess risk for coronary heart disease (CHD) is strong and consistent. Depression is a risk factor for new cardiovascular events in individuals initially free of CHD, as well as for recurrent events and mortality among cardiac patients. The risk is not only limited to individuals who meet the criteria for a clinical diagnosis of major depression. Increasing levels of depressive symptoms, even in the absence of a major depressive episode, also carry higher CHD risk. What is less established, however, is the mechanism (or mechanisms) responsible for the effect of depression on CHD risk. Depression might increase CHD incidence by promoting or worsening coronary atherosclerosis (through effects on lipid profile, platelets and inflammatory factors), directly inducing cardiac ischemia, increasing the risk for cardiac arrhythmias and sudden death, and inducing unhealthy behaviors (cigarette smoking, decreased adherence to medications and other lifestyle factors). Depression is common in the U.S. and its prevalence is rising. It is important that individuals with depression are promptly identified and treated. This is likely to result in a reduction of CHD and related disability as well as health care costs among Americans.
 ...
PMID:The association between depression and coronary heart disease incidence. 1284 75

A major focus of attention in structural brain-imaging research in major depression is the increased prevalence of T2-weighted image 'hyperintensities' (T2-WIH). Our aims in this study were to characterize the distribution and magnetic resonance imaging (MRI) presentation of brain hyperintensities in major depression patients compared to healthy control subjects and to explore the association between the presence of T2-WIH and measures of clinical and cognitive state. Thirty-seven patients suffering from major depression and 27 age- and sex-matched healthy controls underwent brain MRI and were evaluated by the Hamilton Rating Scale for Depression, the Mini Mental State Examination and the Haschinsky Ischaemia Index. T2-WIH (at least one) were found in 26 out of 37 major depression patients and 7 out of 27 controls (p=0.0001). The number of brain T2-WIH was significantly and positively correlated with age in depressed (p=0.001) but not in healthy subjects. Mean volume of T2-WIH was significantly greater (p=0.004) in depressed subjects. In the control group T2-WIH were exclusively located in the supratentorial hemispheral white matter while in the depressed group T2-WIH were also found in basal ganglia, temporal lobe, cerebellum and brainstem. More (52 vs. 20%; p=0.018) T2-WIH were demonstrable on T1 in depressed subjects. Depressed patients with T2-WIH in basal ganglia were clearly the most severely depressed and cognitively impaired subjects, and may constitute a clinically distinct subgroup within major depression.
 ...
PMID:T2-weighted image hyperintensities in major depression: focus on the basal ganglia. 1297 87

The concept of vascular depression has recently been reassessed and more clearly delineated. The diagnostic criteria for vascular depression require a major depression associated with evidence of confluent or diffuse vascular lesions in the subcortical regions on MRI. The clinical symptoms are not specific, but they are often associated with mild cognitive decline. Ischemia is probably the main factor for vascular depression, but the relationship between ischemic lesions and clinical symptoms remains not well explained. The apolipoproteine E genotype is not a risk factor for vascular depression, but it is associated with more severe hyperintensities on MRI. A pharmacological resistance has been described in vascular depression, but, in recent studies, clinical improvement has been observed with antidepressants in more than 80% of cases. A neuropsychological follow-up is recommended, because dementia may appear with 25% of patients.
 ...
PMID:[Vascular depression, limits of the concept]. 1568 31

Melatonin is a ubiquitous molecule and widely distributed in nature, with functional activity occurring in unicellular organisms, plants, fungi and animals. In most vertebrates, including humans, melatonin is synthesized primarily in the pineal gland and is regulated by the environmental light/dark cycle via the suprachiasmatic nucleus. Pinealocytes function as 'neuroendocrine transducers' to secrete melatonin during the dark phase of the light/dark cycle and, consequently, melatonin is often called the 'hormone of darkness'. Melatonin is principally secreted at night and is centrally involved in sleep regulation, as well as in a number of other cyclical bodily activities. Melatonin is exclusively involved in signaling the 'time of day' and 'time of year' (hence considered to help both clock and calendar functions) to all tissues and is thus considered to be the body's chronological pacemaker or 'Zeitgeber'. Synthesis of melatonin also occurs in other areas of the body, including the retina, the gastrointestinal tract, skin, bone marrow and in lymphocytes, from which it may influence other physiological functions through paracrine signaling. Melatonin has also been extracted from the seeds and leaves of a number of plants and its concentration in some of this material is several orders of magnitude higher than its night-time plasma value in humans. Melatonin participates in diverse physiological functions. In addition to its timekeeping functions, melatonin is an effective antioxidant which scavenges free radicals and up-regulates several antioxidant enzymes. It also has a strong antiapoptotic signaling function, an effect which it exerts even during ischemia. Melatonin's cytoprotective properties have practical implications in the treatment of neurodegenerative diseases. Melatonin also has immune-enhancing and oncostatic properties. Its 'chronobiotic' properties have been shown to have value in treating various circadian rhythm sleep disorders, such as jet lag or shift-work sleep disorder. Melatonin acting as an 'internal sleep facilitator' promotes sleep, and melatonin's sleep-facilitating properties have been found to be useful for treating insomnia symptoms in elderly and depressive patients. A recently introduced melatonin analog, agomelatine, is also efficient for the treatment of major depressive disorder and bipolar affective disorder. Melatonin's role as a 'photoperiodic molecule' in seasonal reproduction has been established in photoperiodic species, although its regulatory influence in humans remains under investigation. Taken together, this evidence implicates melatonin in a broad range of effects with a significant regulatory influence over many of the body's physiological functions.
 ...
PMID:Melatonin: Nature's most versatile biological signal? 1681 50

This review addresses the role of adult hippocampal neurogenesis and stem cells in some of the most common neurodegenerative disorders and their related animal models. We discuss recent literature in relation to Alzheimer's disease and dementia, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, alcoholism, ischemia, epilepsy and major depression.
 ...
PMID:Changes in adult neurogenesis in neurodegenerative diseases: cause or consequence? 1818 68


1 2 Next >>