Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuronal ultrastructure of the frontal and temporal cerebral cortex has been studied in persons 36-, 39-, 50-, 70-year-old, died from the ischemic heart disease and 73-, 83-year-old, whose deaths are not connected with vascular pathology. The neurons can be divided into several groups, depending on osmiophilic degree of their nucleus and cytoplasm: I--electron-light, II--electron-opaque, III--with dark nucleus and light cytoplasm and IV--with light nucleus and dark cytoplasm. The protein-synthesizing apparatus (PSA) is subjected to the earliest and most essential disorders. Its changes in the I group of neurons at the age of 36-50 years are mainly of compensatory-adaptive character, while at the age of 73 and 83 years the dystrophic changes of the PSA result in hollowness of the cell, that evidently makes the base of the cell ageing mechanism. Presence of electron opaque neurons is not a sign of ageing, and depends on various pathology, in the given case on the ischemic heart disease, that causes certain vascular disorders in the brain. Variability of the ultrastructures of the electron opaque neurons and essential changes of some part of them, observed in the brain of the 72-year-old man confirm that the vascular factor is an important one in pathology of neurons. Dependence of lipofuscin appearance in neurons on the manifestation degree of the pathological process and ageing in them is discussed.
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PMID:[Effect of vascular factors and aging on the ultrastructure of neurons of the human cerebral cortex]. 261 68

Neuronal uptake1 constitutes the main elimination process of cardiac norepinephrine under normoxic conditions. Uptake1 may be subject to changes during myocardial ischemia. We therefore studied the regulation of the uptake1 carrier in isolated perfused rat hearts, comparing ischemic and nonischemic conditions. Radioligand binding with [3H]mazindol was used to determine carrier densities and affinities, whereas cardiac clearance of[3H]norepinephrine served as a measure of the transport capacity of the uptake1 carrier. When exocytotic norepinephrine release was induced in nonischemic rat hearts by electrical field stimulations, we observed an increase in the cardiac density of uptake1 carriers (Bmax) to 210 +/- 5 fmol/mg protein (versus 134 +/- 3 fmol/mg in control hearts). Simultaneously, the cardiac clearance of [3H]norepinephrine increased to 41 +/- 4% versus 30 +/- 4% in control hearts. Both carrier density and norepinephrine clearance returned to baseline values within a period of 40 minutes after stimulation. Carrier affinities (Kd values) did not differ between the groups. Stop-flow ischemia induced a substantial overflow of norepinephrine by itself. Additionally, carrier density was increased to 144% after 40 minutes of stop-flow ischemia (P < .005 versus control hearts). When ischemia was followed by 20 minutes of reperfusion, the Bmax of the uptake1 carrier remained significantly elevated. With a further extension of the reperfusion period to 40 minutes, however, carrier density declined to baseline values. Kd values were not influenced by any of these interventions. Clearance of [3H]norepinephrine was suppressed (to 5 +/- 2%) in the first minutes of reperfusion, which may reflect the inverse transport direction of the norepinephrine carrier known to occur in ischemia. After 20 minutes of reperfusion, clearance increased to 39 +/- 5% (P < .005 versus control hearts) and then fell to 29 +/- 5% after 40 minutes of reperfusion (NS). These results demonstrate that after both electrical field stimulation and myocardial ischemia, the density of uptake1 carrier proteins temporarily increases, which may result in an increased transport capacity for norepinephrine.
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PMID:Upregulation of cardiac uptake 1 carrier in ischemic and nonischemic rat heart. 863 34

In myocardial ischemia, adrenergic nerves release excessive amounts of norepinephrine (NE), causing dysfunction and arrhythmias. With anoxia and the concomitant ATP depletion, vesicular storage of NE is impaired, resulting in accumulation of free NE in the axoplasm of sympathetic nerves. Intraneuronal acidosis activates the Na(+)/H(+) exchanger (NHE), leading to increased Na(+) entry in the nerve terminals. These conditions favor availability of the NE transporter to the axoplasmic side of the membrane, causing massive carrier-mediated efflux of free NE. Neuronal NHE activation is pivotal in this process; NHE inhibitors attenuate carrier-mediated NE release. We previously reported that activation of histamine H(3) receptors (H(3)R) on cardiac sympathetic nerves also reduces carrier-mediated NE release and alleviates arrhythmias. Thus, H(3)R activation may be negatively coupled to NHE. We tested this hypothesis in individual human SKNMC neuroblastoma cells stably transfected with H(3)R cDNA, loaded with the intracellular pH (pH(i)) indicator BCECF. These cells possess amiloride-sensitive NHE. NHE activity was measured as the rate of Na(+)-dependent pH(i) recovery in response to an acute acid pulse (NH(4)Cl). We found that the selective H(3)R-agonist imetit markedly diminished NHE activity, and so did the amiloride derivative EIPA. The selective H(3)R antagonist thioperamide abolished the imetit-induced NHE attenuation. Thus, our results provide a link between H(3)R and NHE, which may limit the excessive release of NE during protracted myocardial ischemia. Our previous and present findings uncover a novel mechanism of cardioprotection: NHE inhibition in cardiac adrenergic neurons as a means to prevent ischemic arrhythmias associated with carrier-mediated NE release.
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PMID:Coupling of histamine H3 receptors to neuronal Na+/H+ exchange: a novel protective mechanism in myocardial ischemia. 1122 30

We have shown that electroacupuncture (EA) at the Neiguan-Jianshi (N-J) acupoints over the median nerve reduces myocardial ischemia by modulating the pressor response induced by application of bradykinin on the gallbladder. The present study was designed to investigate the neural substrate underlying the prolonged modulatory effect of EA on visceral afferent input into the rostral ventral lateral medulla (rVLM). Experiments were performed on ventilated anesthetized cats. Neuronal activity was recorded while either stimulating the splanchnic nerve or applying EA at the N-J acupoints. Thirty-three cells responsive to splanchnic nerve and median nerve stimulation were antidromically driven from the intermediolateral columns, T(2)-T(4), indicating their function as premotor sympathetic neurons. These neurons also received baroreceptor input demonstrating that they were cardiovascular sympathoexcitatory cells. Arterial pulse-triggered averaging and coherence analysis demonstrated a correlation between cardiac-related discharge activity with 2.8+/-0.3 Hz rhythms and arterial blood pressure. Stimulation (2 Hz, 1-4 mA, 0.5 ms) of the splanchnic nerve for 30 s evoked excitatory responses. These neuronal responses were reduced during and after 30-min stimulation of EA at the Neiguan-Jianshi acupoints. These splanchnic nerve-induced excitatory responses in neurons subjected to 30 min of EA were reduced by 68%. Iontophoresis of naloxone promptly reversed the EA-induced inhibitory effect by 52%. Neuronal activity in the rVLM induced by splanchnic nerve stimulation was reduced for 50 (or more) min after termination of EA in 7 of 12 rVLM neurons. Our results indicate that rVLM premotor sympathetic cardiovascular neurons receive convergent input from the gallbladder through the splanchnic nerve and N-J acupoints through the median nerves. Through an opioid mechanism, EA inhibits splanchnic nerve-induced excitatory responses of these rVLM neurons. Many of these neurons receiving convergent visceral and somatic input exhibit long-lasting inhibition by EA.
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PMID:Prolonged inhibition of rostral ventral lateral medullary premotor sympathetic neurons by electroacupuncture in cats. 1287 81

Ulinastatin (UTI), a trypsin inhibitor, is isolated and purified from human urine and has been shown to exert protective effect on myocardial ischemia reperfusion injury in patients. The present study was aimed at investigating the effect of ulinastatin on neurologic functions after spinal cord ischemia reperfusion injury and the underlying mechanism. The spinal cord IR model was achieved by occluding the aorta just caudal to the left renal artery with a bulldog clamp. The drugs were administered immediately after the clamp was removed. The animals were terminated 48 hours after reperfusion. Neuronal function was evaluated with the Tarlov Scoring System. Spinal cord segments between L2 and L5 were harvested for pathological and biochemical analysis. Ulinastatin administration significantly improved postischemic neurologic function with concomitant reduction of apoptotic cell death. In addition, ulinastatin treatment increased SOD activity and decreased MDA content in the spinal cord tissue. Also, ulinastatin treatment suppressed the protein expressions of Bax and caspase-3 but enhanced Bcl-2 protein expression. These results suggest that ulinastatin significantly attenuates spinal cord ischemia-reperfusion injury and improves postischemic neuronal function and that this protection might be attributable to its antioxidant and antiapoptotic properties.
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PMID:Neuroprotective Effect of Ulinastatin on Spinal Cord Ischemia-Reperfusion Injury in Rabbits. 2616 Dec 41

Mechanisms for electroacupuncture (EA) in disease treatments are still enigmatic. Here, we studied whether hippocampus was involved in the protection of EA stimulation on myocardial ischemia injury. Acute myocardial ischemia (AMI) model was produced. EA stimulation at heart meridian from Shenmen (HT7) to Tongli (HT5) was applied to rats 3 times a day for continuous three days. Coronary occlusion related tachycardia and hypotension, indicated by heart rate, mean arterial pressure, and rate pressure product, were apparently impaired after AMI injury. By contrast, EA stimulating could ameliorate the impairments of heart function (P < 0.05). Interestingly, lesion of CA1 region of hippocampus abolished the protection of EA. Neuronal activity in CA1 area was affected by AMI. As evidenced, cell counts, cell types, and frequency of the discharged neurons were facilitated after AMI, while EA stimulation attenuated the abnormalities. Furthermore, c-Fos expression was significantly facilitated in CA1 area after AMI, which was reduced by EA stimulation. Correlations were established between c-Fos expression and cell counts of discharged neurons, as well as between heart function and cell counts of discharged neurons. Taken together, EA stimulation at heart meridian protects against heart dysfunction induced by AMI possibly through suppressing the neuronal activity in CA1 region.
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PMID:Electroacupuncture Ameliorates the Coronary Occlusion Related Tachycardia and Hypotension in Acute Rat Myocardial Ischemia Model: Potential Role of Hippocampus. 2622 Nov 81