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

Preferential blocks of peripheral nerves have shown that myelinated nerves are more susceptible to local compression and less resistant to asphyxia than unmyelinated fibers. Since two groups of functionally different nociceptors exist in the dental pulp, it is of theoretical and clinical interest to determine the influence of ischemia on the sensitivity of human dental pulp, using standard means for testing tooth vitality and at the same time investigating the intensity coding in one pathway of the afferent trigeminal system. Adrenaline was used to study the differential effect of adrenaline-induced ischemia on intradental A-delta nerve activity (INA) and the concomitant sharp pain, as well as on the detection threshold for monopolar electrical stimulation. Cold (ethyl chloride) and heat (heated gutta-percha) stimulation was applied to the tooth surface. In accordance with the hydrodynamic theory of dentin sensitivity the rapid fluid flow induced in the dentinal tubuli by these thermal stimuli is an adequate stimulus for selectively activating the A-delta nerves in healthy pulps. Consistency plots of the magnitude of the perceptual experience of sharp pain against the neural population response in linear coordinates yielded a high product-moment correlation, implying linearity for the intensity coding relationship. In contrast to the significant reduction of INA and its perceptual correlate of sharp pain after adrenaline administration, the electrical detection threshold remained constant during the full test period, suggesting that electrical threshold measurements have their limitations as a diagnostic tool or criterion for assessing the sensitivity of the dental pulp. The absence of A-delta activity was parallelled by no sensation of sharp pain. These findings suggested that the integrated neural A-delta activity constituted the underlying peripheral neurophysiological mechanism of the sensory intensity of sharp dental pain.
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PMID:Pulpal ischemia in man: effects on detection threshold, A-delta neural response and sharp dental pain. 1021 48

Neovascular glaucoma is a dreadful pathology with a rapid spontaneous evolution responsible for painful and blind eye. The main cause is an anterior neovascular proliferation following a broad retinal ischemia. Early diagnosis and treatment are required in order to maintain a good visual status and a satisfactory IOP control with medical, surgical or cylodestructive procedures. In any case, the treatment of the retinal ischemia has to be performed. One must keep in mind that the most efficient way to avoid the incidence of neovascular glaucoma is a strict control of clinical situations potentially responsible for retinal ischemia, namely VRO in elderly patients and diabetic retinopathy in younger patients.
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PMID:[Consensus on neovascular glaucoma]. 1074 59

The hippocampus is an important structure for declarative, spatial, and contextual memory and is implicated in the perception of chronic pain. The hippocampal formation is vulnerable to damage from seizures, ischemia, and head trauma and is particularly sensitive to the effects of adrenal glucocorticoids secreted during the diurnal rhythm and chronic stress. Adrenal steroids typically have adaptive effects in the short run, but promote pathophysiology when there is either repeated stress or dysregulation of the HPA axis. The damaging actions of glucocorticoids under such conditions have been termed "allostatic load", referring to the cost to the body of adaptation to adverse conditions. Adrenal steroids display both protective and damaging effects in the hippocampus. They biphasically modulate excitability of hippocampal neurons, and high glucocorticoid levels and severe acute stress impair declarative memory in a reversible manner. The hippocampus also displays structural plasticity, involving ongoing neurogenesis of the dentate gyrus, synaptogenesis under control of estrogens in the CA1 region, and dendritic remodeling caused by repeated stress or elevated levels of exogenous glucocorticoids in the CA3 region. In all three forms of structural plasticity, excitatory amino acids participate along with circulating steroid hormones. Glucocorticoids and stressors suppress neurogenesis in the dentate gyrus. They also potentiate the damage produced by ischemia and seizures. Moreover, the aging rat hippocampus displays elevated and prolonged levels of excitatory amino acids released during acute stress. Our working hypothesis is that structural plasticity in response to repeated stress starts out as an adaptive and protective response, but ends up as damage if the imbalance in the regulation of the key mediators is not resolved. It is likely that morphological rearrangements in the hippocampus brought on by various types of allostatic load alter the manner in which the hippocampus participates in memory functions and it is conceivable that these may also have a role in chronic pain perception.
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PMID:Plasticity of the hippocampus: adaptation to chronic stress and allostatic load. 1200 27

Although a tourniquet is frequently used in penile surgery there is still no consensus on safe application time. The aim of the present study is to investigate the effect of malondialdehyde (MDA) levels and histological changes in skin flaps after penile tourniquet application and epinephrine injection. A total of 36 male white New Zealand rabbits were randomly divided into six groups each containing six animals. A Mathieu-like flap was raised in all of the groups and a tourniquet was applied and the penis was subjected to ischemia for 10, 20 and 40 min in groups 1, 2 and 3, respectively. The flaps were then allowed to reperfuse for 5 min. Biopsies for MDA measurement were harvested in these groups. Subcutaneous 1/200,000 epinephrine was injected into penile skin in group 4 and 5 rabbits and biopsies for MDA measurement were harvested 10 and 40 min after injection. The control group was anesthetized without tourniquet usage or epinephrine injection. Specimens taken from the harvested flaps of all groups were submitted for histological evaluation. The mean MDA levels in all experimental groups were higher than in the control group and the difference was statistically significant. Edema, congestion and extravasation were observed in groups 1, 2 and 3. Minimal congestion and edema were observed in group 4 and severe edema and extravasation in group 5. Tourniquet usage for a duration of less than 10 min is clearly safer than prolonged usage. Epinephrine injection to penile skin may show a deleterious effect on wound healing.
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PMID:Tourniquet application and epinephrine injection to penile skin: is it safe? 1220 46

The objective of this research was to compare the effects of an alpha- and beta-adrenergic agonist, epinephrine, a selective alpha(2)-adrenergic agonist, alpha-methylnorepinephrine (alpha-MNE), and a non-adrenergic vasopressin on post-resuscitation myocardial function and duration of survival. Epinephrine continues to be the primary adrenergic agent for advanced cardiac life support. However, its major inotropic actions and especially its beta-adrenergic and, to a lesser extent, its alpha(1)-actions increase the severity of global ischemia during cardiac arrest and adversely affect post-resuscitation myocardial function and survival. We had previously observed significantly better outcomes with a selective alpha(2)-adrenergic agonist when compared with epinephrine. Non-adrenergic vasopressin also has promise of more favorable actions. The present study was, therefore, undertaken to compare a selective alpha(2)-adrenergic vasopressor drug with vasopressin, epinephrine, and saline placebo. Ventricular fibrillation (VF) was induced in 20 Sprague-Dawley rats. Mechanical ventilation and precordial compression were initiated after 8 min of untreated VF. About 2 min later, alpha-MNE in a dose of 100 microgram/kg, vasopressin in a dose of 0.4 U/kg, epinephrine in a dose of 30 microgram/kg, or saline control was administered. Defibrillation was attempted after 6 min of CPR. Left ventricular pressure, dP/dt(40), -dP/dt, and cardiac index were measured for an interval of 240 min after resuscitation. Except for saline controls, comparable increases in coronary perfusion pressure (CPP) were observed after each drug intervention. All animals were successfully resuscitated. Post-resuscitation myocardial function and survival were significantly better in animals treated with alpha-MNE. Both post-resuscitation myocardial function and survival were most improved after administration of the selective alpha(2)-adrenergic agonist, intermediate after vasopressin and least after epinephrine and saline placebo.
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PMID:A comparison of alpha-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation. 1266 5

Epinephrine is known to be rapidly oxidized during sepsis. Ischemia and acidosis, which often accompany sepsis, are associated with the release of weakly bound cupric ions from plasma proteins. We investigated whether copper promotes oxidation of epinephrine at both physiological and acidic pH and whether D-Asp-D-Ala-D-His-D-Lys (D-DAHK), a human albumin (HSA) N-terminus synthetic peptide with a high affinity for cupric ions, attenuates this oxidation. Epinephrine alone [100 microM] or with CuCl(2) [10 microM], and with CuCl(2) [10 microM] and D-DAHK [20 microM] at pH 7.4, 7.0, 6.5, and 6.0 were incubated for 1h at 37 degrees C. Epinephrine oxidation was measured by the spectrophotometric quantification of its oxidation product, adrenochrome. We found that adrenochrome increased, suggesting copper-induced oxidation of epinephrine. At pH 7.4, 7.0, 6.5, and 6.0, adrenochrome increased by 47%, 53%, 24%, and 6% above baseline, respectively. D-DAHK attenuated the copper-induced oxidation of epinephrine to baseline levels. These in vitro results indicate that copper-induced epinephrine oxidation is greatest at the physiological pH 7.4 as well as in severe acidosis, pH 7.0, and that D-DAHK completely inhibits this oxidation.
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PMID:Copper-induced oxidation of epinephrine: protective effect of D-DAHK, a synthetic analogue of the high affinity copper binding site of human albumin. 1272 20

The goal of neuroprotection in glaucoma treatment is to employ agents that prevent or delay apoptosis of retinal ganglion cells (RGC) and facilitate regeneration of already damaged calls. The following contribution discusses the mechanisms of RGC death and current status of neuroprotective in vivo studies and investigations on cell cultures and animal models. Discussions on the etiopathogenesis of PCOAG center on elevated IOP and ocular disorders of vascular function. The mechanisms of axonal damage induced by ischemia are explained and the resultant possible neuroprotective effect mechanisms are discussed (Na(+) or Ca(2+) channel blockers, role of reactive astrocytes). Substitution of axonal survival factors and especially the role of BDNF are described. Glutamate excitotoxicity also plays a role in glaucomatous antegrade RGC death. Relevant questions and possible therapeutic approaches are discussed. The three phases of apoptosis cascade and the key role of mitochondria in the insult-induced apoptosis are considered as well as the still relatively unexplored possibilities of RGC regeneration. Finally, perspectives of neuroprotective treatment of PCOAG are presented.
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PMID:[Mechanisms of neuroprotection against glaucoma]. 1549 Jan 84

Brief ischemic episodes that induce myocardial and coronary endothelial dysfunction may alter the responses to inotropic drugs. To determine the effects of inotropic drugs in stunned myocardium, the coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and regional mechanical function in response to intracoronary dobutamine, epinephrine, amrinone, and calcium chloride (CaCl2) were measured before (normal) and 30 min after a 15-min-period occlusion of the left anterior descending artery (stunned) in an open-chest canine model. Percent segment shortening (%SS) and post-systolic shortening (%PSS) were determined. Myocardial extraction of oxygen (EO2) and lactate (E(lac)) was calculated. The inotropic drugs increased %SS, CBF, and MVO2 in normal myocardium. Epinephrine and amrinone decreased, while dobutamine and CaCl2 did not affect EO2. The ischemia and reperfusion itself significantly reduced %SS and E(lac), and increased %PSS. In stunned myocardium, the responses to inotropic drugs were not significantly altered, except that they progressively reduced %PSS and epinephrine did not affect EO2. These findings indicate that a brief episode of ischemia does not affect the mechanical and metabolic coronary flow responses to inotropic drugs, although it abolishes direct vasodilator responses to epinephrine.
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PMID:Effects of inotropic drugs on mechanical function and oxygen balance in postischemic canine myocardium: comparison of dobutamine, epinephrine, amrinone, and calcium chloride. 1622 44

A 75-year-old man with a past history of bilateral thalamic hemorrhage was scheduled for cholecystectomy and cholelithotomy under general anesthesia. Although the preoperative ECG showed a complete right bundle branch block, the echocardiogram revealed no abnormality. Anesthesia was induced with thiopental and vecuronium, and maintained with sevoflurane in oxygen. Soon after changing to the left decubitus position for the insertion of an epidural catheter, ECG showed complete atrioventricular block, which did not respond to atropine. Adrenalin was transiently effective, but arrhythmia continued. After administration of dopamine, norepinephrine and isoproterenol, we inserted a temporary transvenous pacemaker catheter, and the hemodynamics became stable by ventricular pacing. The operation was postponed. Subsequent cardiologic examination showed no ischemia. The atrioventricular block disappeared 7 hours after the induction of general anesthesia. We should be very careful with the anesthetic management of a patient with a complete right bundle branch block.
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PMID:[A case of complete atrioventricular block after induction of general anesthesia]. 1629 74

Historically, the use of regional anesthetic techniques in patients with preexisting central nervous system (CNS) disorders has been considered relatively contraindicated. The fear of worsening neurologic outcome secondary to mechanical trauma, local anesthetic toxicity, or neural ischemia is commonly reported. We examined the frequency of new or progressive neurologic complications in patients with preexisting CNS disorders who subsequently underwent neuraxial blockade. The medical records of all patients at the Mayo Clinic from the period 1988 to 2000 with a history of a CNS disorder who subsequently received neuraxial anesthesia or analgesia were retrospectively reviewed. One-hundred-thirty-nine (n = 139) patients were identified for study inclusion. Mean patient age was 60 +/- 17 yr. Gender distribution was 86 (62%) males and 53 (38%) females. An established CNS disorder diagnosis was present a mean of 23 +/- 23 yr at the time of surgical anesthesia, with 74 (53%) patients reporting active neurologic symptoms. Spinal anesthesia was performed in 75 (54%) patients, epidural anesthesia or analgesia in 58 (42%) patients, continuous spinal anesthesia in 4 (3%) patients, and a combined spinal-epidural technique in 2 (1%) patients. Bupivacaine was the local anesthetic most commonly used in all techniques. Epinephrine was added to the injectate in 72 (52%) patients. There were 15 (11%) technical complications, with the unintentional elicitation of a paresthesia and traumatic needle placement occurring most frequently. A satisfactory block was reported in 136 (98%) patients. No new or worsening postoperative neurologic deficits occurred when compared to preoperative findings (0.0%; 95% confidence interval, 0.0%-0.3%). We conclude that the risks commonly associated with neuraxial anesthesia and analgesia in patients with preexisting CNS disorders may not be as frequent as once thought and that neuraxial blockade should not be considered an absolute contraindication within this patient population.
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PMID:Neuraxial anesthesia and analgesia in patients with preexisting central nervous system disorders. 1679 Jun 57


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