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)

Vascular resistance at rest may be normal in humans with borderline or mild hypertension. However, this finding is a facade which can obscure the presence of vascular structural alterations that may have an important influence on resistance and capacitance functions of the circulation. This paper reviews several studies regarding vascular structural changes in borderline hypertension (BHT). First, forearm vasodilator capacity is limited in BHT and in normotensive young men with a family history of hypertension; this suggests the presence of structural changes in forearm resistance vessels. Second, forearm venous distensibility is decreased in BHT. Most of this decrease is caused by nonadrenergic mechanisms--which suggests that there may be structural changes in veins in BHT. Third, the studies of Takeshita and colleagues suggest that sodium intake may influence vascular structural changes. In hypertensive patients who responded to salt loading with increased blood pressure and vascular resistance, salt loading limited vasodilator responses to 10 minutes of ischemia. This effect of salt loading on vasodilator responses occurred in some patients (salt-responders), but not in others (salt-nonresponders). Functional studies support the concept that structural changes in resistance and capacitance vessels occur during the early stages of human hypertension. These changes may not be entirely adaptive responses to elevated arterial pressure, since they occur in capacitance as well as resistance vessels. In addition, the structural changes appear to be responsive to factors such as sodium intake. These observations suggest that vascular structural changes in human hypertension may be related in part to neurohumoral influences or to primary vascular abnormalities.
 ...
PMID:Structural changes in resistance and capacitance vessels in borderline hypertension. 639 93

The effect of dihydroergocristine on energy metabolism was studied in the isolated perfused rat brain affected by ischemia and in cultivated C-1300 neuroblastoma cells deprived of oxygen and glucose. Creatine phosphate, ATP, ADP, AMP, glucose, glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-diphosphate, pyruvate, and lactate were measured enzymatically. After a perfusion period of 30 min, the cortex of the isolated perfused rat brain exhibited an energy state not different from that in vivo. Dihydroergocristine added to the perfusion medium (5 mumol/L) did not influence these substrate levels under normal perfusion conditions. However, this drug was able to retard the breakdown of high-energy phosphates during ischemia and to accelerate the restoration of the energy state during the postischemic reperfusion period. The perfusion rate was not changed by the drug, and therefore it was assumed that dihydroergocristine could act directly on cell metabolism. This view was supported by the results obtained from experiments using cultivated N-2a neuroblastoma cells. These cells were incubated in a buffered salt solution deprived of glucose and oxygen for 15 min. Under these conditions, dihydroergocristine (2 mumol/L) added to the incubation medium caused changes in the concentrations or the high-energy phosphates similar to those in the isolated brain preparation: It increased the ATP concentration and decreased the ADP concentration significantly.
 ...
PMID:Effect of dihydroergocristine on energy metabolism studied in the isolated perfused rat brain affected by ischemia and in neuroblastoma cells deprived of oxygen and glucose. 643 25

[(5Z,13E,9 alpha,11 alpha,15S)-2,3,4-Trinor - 1,5 - inter-m - phenylene - 6,9 - epoxy - 11,5 - dihydroxy - 15 - cyclohexyl - 16,17,18,19,20-pentanor]- prosta-5,13-dienoic acid (sodium salt) (CG 4203) is a new stable epoprostenol (prostacyclin) analogue with a relative platelet antiaggregatory potency of 0.46 (ADP aggregation in vitro) and a hypotensive potency of 0.14 (anaesthetized rat i.v.) as compared to epoprostenol. In isolated perfused rat hearts, CG 4203 (4.64 X 10(-9) mol/l) significantly attenuated arrhythmias and loss of left ventricular creatine kinase (CK) activity observed in control hearts after 30 min perfusion with hypoxic and 30 min reperfusion with oxygenated Krebs-Ringer solution. In anaesthetized rats, CG 4203 (1.0 microgram X kg-1 X min-1 i.v.) significantly reduced incidence of ventricular fibrillation and increase in plasma CK activity after ligation of the left coronary artery. Infusion of 1.0 and 2.15 micrograms X kg-1 X min-1 CG 4203 i.v. in anaesthetized rats dose-dependently inhibited electrocardiographic changes, i.e. ST depression observed after i.v. injection of 1.0 IU X kg-1 vasopressin. In rat models of sustained myocardial hypoxia, myocardial infarction, and transient cardiac ischemia, CG 4203 thus exerts cardioprotective effects which, depending on the model considered, may be ascribed to either its vasodilatory, coronary dilatory, antiaggregatory or epoprostenol-like cytoprotective activity.
 ...
PMID:Cardioprotective action of the new stable epoprostenol analogue CG 4203 in rat models of cardiac hypoxia and ischemia. 644 79

In ischemic impairment of liver tissue the activating effect of the cytoplasmic thermostable fraction on the transport of Ca2+ ions was decreased in liver mitochondria. Fast decrease in the cytoplasmic activity occurred also after preincubation of liver homogenate with salt solutions. Inactivation of the cytoplasmic regulator was prevented by addition of EGTA into the homogenate, but Ca2+ showed the opposite effect. The data obtained suggest that high concentration, of Ca2+ in cytosol under conditions of ischemia is responsible for decrease of the cytoplasmic regulator activity.
 ...
PMID:[Decrease in the activity of the cytoplasmic regulator of mitochondrial function in liver ischemia]. 678 Nov 41

Sixty-three mongrel dogs were exposed to 8-10 min. of complete cerebral ischemia with Aortic occlusion balloon catheter and followed by 120 min. of recirculation. The degree and distribution of post-ischemic reperfusion in 11 different cerebral regions were then assessed using radioactive labelled microspheres (15 +/- 3 micrometers). The animals were divided into 3 groups by the administration of drugs as follows: 1) no additional drugs; 2) Indomethacin (selective inhibitor of cyclooxygenase) 4 mg/kg 5 min. after ischemia; 3) Pyridine deriv. (OKY-1580 Na-salt, selective inhibitor of thromboxane synthetase) infusion 100 gamma/kg/min. beginning 5 min. after ischemia. Animals receiving no additional drugs had low cerebral blood flow rates at 120 min. after ischemia especially in basal ganglia and cerebral cortex. Animals receiving Indomethacin did not differ significantly from the no additional drug group. The significant enhancement and redistribution of post-ischemic reperfusion at 120 min. after ischemia occurred in animals receiving Pyridine deriv. with reversal of the state of poor reperfusion. These observations implicate an imbalance of prostaglandin pathways in platelets and blood vessel walls in the genesis of impaired post-ischemic reflow and suggest the usefulness of Pyridine deriv. in the treatment of local vasoconstriction of the brain after total cerebral ischemia.
 ...
PMID:[Cerebral blood flow after total cerebral ischemia in dog (author's transl)]. 733 24

Three patients developed apparent choroidal ischemia after phacoemulsification. The outer half of the posterior retina appeared white after operation, with confluent lesions in the posterior pole and splotchy white areas in the midperiphery. The separate lesions appeared similar in pattern to the lobular division of the choriocapillaris, and the retinal vessels were not involved. The white lesions resolved in two to three weeks, leaving alterations in the pigment epithelium. Vision was transiently reduced in each eye but returned to a nearly normal level in two of three affected eyes, although paracentral scotomas persisted. In each case of phacoemulsification, the posterior lens capsule was either damaged or was removed. In all three cases, an investigational type of irrigating solution (BSS Plus) containing balanced salt, glutathione, and other constituents was used. Controlled ocular compression was performed before operation using a pneumatic device in two cases. However, the cause of retinal and choroidal damage now described was probably excessively elevated intraocular pressure during the operation.
 ...
PMID:Choroidal ischemia after extracapsular cataract extraction by phacoemulsification. 734 48

The cytoprotective effects of MK-801 and NBQX, selective N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor antagonists, respectively, were compared both singularly and in combination in models of transient severe forebrain and transient focal cerebral ischemia. After 10 minutes of four-vessel occlusion ischemia, the sodium salt of NBQX (30 mg/kg IP) given at the time of reperfusion and, subsequently, 15 and 30 minutes later produced a dramatic reduction in CA1 hippocampal necrosis at 7 days. This effect was not obtained with the intraperitoneal administration of either MK-801 (1 mg/kg x 3) or the combination of both NBQX and MK-801 given at the same time intervals. This effect of intraperitoneal NBQX alone was reproduced in a two-vessel occlusion/hypotension model using this same drug administration. Delayed treatment with both NBQX and GYKI 52466, but neither MK-801 nor the combination of NBQX and MK-801 given after a delay, produced a significant reduction in the mean volume of neocortical infarction after transient focal ischemia. We conclude that the AMPA receptor may play a more important role than the NMDA receptor in both selective ischemic necrosis of hippocampal neurons and in neocortical infarction. AMPA antagonists should be subjected to clinical stroke trials.
 ...
PMID:AMPA antagonists: do they hold more promise for clinical stroke trials than NMDA antagonists? 750 38

Nitric oxide (NO) is a novel biologic messenger with diverse effects but its role in organ transplantation remains poorly understood. Using a porphyrinic microsensor, the first direct measurements of coronary vascular and endocardial NO production were made. NO was measured directly in the effluent of preserved, heterotopically transplanted rat hearts stimulated with L-arginine and bradykinin; NO concentrations fell from 2.1 +/- 0.4 microM for freshly explanted hearts to 0.7 +/- 0.2 and 0.2 +/- 0.08 microM for hearts preserved for 19 and 38 h, respectively. NO levels were increased by SOD, suggesting a role for superoxide-mediated destruction of NO. Consistent with these data, addition of the NO donor nitroglycerin (NTG) to a balanced salt preservation solution enhanced graft survival in a time- and dose-dependent manner, with 92% of hearts supplemented with NTG surviving 12 h of preservation versus only 17% in its absence. NTG similarly enhanced preservation of hearts stored in University of Wisconsin solution, the clinical standard for preservation. Other stimulators of the NO pathway, including nitroprusside, L-arginine, or 8-bromoguanosine 3',5' monophosphate, also enhanced graft survival, whereas the competitive NO synthase antagonist NG-monomethyl-L-arginine was associated with poor preservation. Likely mechanisms whereby supplementation of the NO pathway enhanced preservation included increased blood flow to the reperfused graft and decreased graft leukostasis. NO was also measured in endothelial cells subjected to hypoxia/reoxygenation and detected based on its ability to inhibit thrombin-mediated platelet aggregation and serotonin release. NO became undetectable in endothelial cells exposed to hypoxia followed by reoxygenation and was restored to normoxic levels on addition of SOD. These studies suggest that the NO pathway fails during preservation/transplantation because of formation of oxygen free radicals during reperfusion, which quench available NO. Augmentation of NO/cGMP-dependent mechanisms enhances vascular function after ischemia and reperfusion and provides a new strategy for transplantation of vascular organs.
 ...
PMID:Cardiac preservation is enhanced in a heterotopic rat transplant model by supplementing the nitric oxide pathway. 751 95

Nitric oxide (NO.) plays a central role in the physiology of the gastrointestinal tract and its response to critical illness. Potential sources of NO. in the gut include: intrinsic intestinal tissue (mast cells, epithelium, smooth muscle, neural plexus), resident and/or infiltrating leukocytes (neutrophils, monocytes), reduction of luminal gastric nitrate, and denitrification by commensal anaerobes. The brain and endothelial isoforms of nitric oxide synthase are expressed under resting conditions, whereas inflammatory stimuli are required for the induction of the inducible type. Under resting conditions, mucosal perfusion is regulated by NO. derived from the vascular endothelium of the mesenteric bed. During inflammation, excessive NO. production from the inducible synthase may contribute to mucosal hyperemia. Coordination of peristalsis and sphincteric action is mediated by the release of NO., which acts as the principal neurotransmitter of the nonadrenergic, noncholinergic enteric nervous system. Alterations in bowel motility, such as ileus, result from excessive concentrations of NO. generated during endotoxicosis and inflammatory bowel disease. The role of NO. in the regulation of salt and water secretion is poorly understood. Endotoxin-induced inhibition of gastric acid secretion appears to be mediated by the action of NO. on parietal cells. NO. may protect the gastrointestinal mucosa from a variety of stimuli (caustic ingestion, ischemia, ischemia/reperfusion injury, early endotoxic shock) by maintaining mucosal perfusion, inhibiting neutrophil adhesion to mesenteric endothelium, blocking platelet adhesion, and preventing mast cell activation. Excessive NO., however, may directly injure the mucosa. Barrier function of the intestinal mucosa is protected by NO. in the early stages of injury, when neutrophil adhesion, ischemia, and mast cell activation are relevant. Inhibition of NO. synthesis ameliorates barrier dysfunction during more advanced stages of inflammation, when activation of inducible NOS yields toxic concentrations of NO.. At high concentrations, NO. disrupts the actin cytoskeleton, inhibits ATP formation, dilates cellular tight junctions, and produces a hyperpermeable state. Selective inhibition of the inducible isoform of NOS and maintenance of the constitutive types may be therapeutic.
 ...
PMID:Nitric oxide in the gut. 758 76

Nitric oxide (NO.) plays a central role in the Physioliology of the gastrointestinal tract and its response to critical illness. Potential sources of NO. in the gut include: intrinsic intestinal tissue (mast cells, epithelium, smooth muscle, neural plexus), resident and/or infiltrating leukocytes (neutrophils, monocytes), reduction of luminal gastric nitrate, and denitrification by commensal anaerobes. The brain and endothelial isoforms of nitric oxide synthase are expressed under resting conditions, whereas inflammatory stimuli are required for the induction of the inducible type. Under resting conditions, mucosal perfusion is regulated by NO. derived from the vascular endothelium of the mesenteric bed. During inflammation, excessive NO. production from the inducible synthase may contribute to mucosal hyperemia. Coordination of peristalsis and sphincteric action is mediated by the release of NO., which acts as the principal neurotransmitter of the nonadrenergic, noncholinergic enteric nervous system. Alterations in bowel motility, such as ileus, result from excessive concentrations of NO. generated during endotoxicosis and inflammatory bowel disease. The role of NO. in the regulation of salt and water secretion is poorly understood. Endotoxin-induced inhibition of gastric acid secretion appears to be mediated by the action of NO. on parietal cells. NO. may protect the gastrointestinal mucosa from a variety of stimuli (caustic ingestion, ischemia, ischemia/reperfusion injury, early endotoxic shock) by maintaining mucosal perfusion, inhibiting neutrophil adhesion to mesenteric endothelium, blocking platelet adhesion, and preventing mast cell activation. Excessive NO., however, may directly injure the mucosa. Barrier function of the intestinal mucosa is protected by NO. in the early stages of injury, when neutrophil adhesion, ischemia, and mast cell activation are relevant. Inhibition of NO. synthesis ameliorates barrier dysfunction during more advanced stages of inflammation, when activation of inducible NOS yields toxic concentrations of NO.. At high concentrations, NO. disrupts the actin cytoskeleton, inhibits ATP formation, dilates cellular tight junctions, and produces a hyperpermeable state. Selective inhibition of the inducible isoform of NOS and maintenance of the constitutive types may be therapeutic.
 ...
PMID:Nitric oxide in the gut. 770 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>