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

The possibility of differences between crystalloid-perfused and blood-perfused hearts in their vulnerability to ischemia and responsiveness to protective interventions has been investigated in isolated rabbit hearts perfused with bicarbonate buffer or arterial blood. In preliminary studies with 165 minutes of aerobic perfusion at constant perfusion pressure (55 +/- 3 mm Hg), the stability of left ventricular developed pressure was significantly better in blood-perfused hearts. In subsequent studies, hearts were subjected to 20 minutes of aerobic perfusion (coronary flow, 2.0 +/- 0.3 ml/min/gm wet weight in blood-perfused hearts versus 11.3 +/- 3.0 ml/min/gm wet weight in crystalloid-perfused hearts; left ventricular developed pressure, 90 +/- 4 and 91 +/- 2 mm Hg, respectively) followed by 30, 45, 60, 75, 90, or 105 minutes of normothermic global ischemia and 40 minutes of reperfusion (n = 4 per group). In the buffer-perfused groups the postischemic recoveries of left ventricular developed pressure were 74% +/- 6%, 45% +/- 7%, 39% +/- 6% 32%, +/- 5%, 27% +/- 4%, and 12% +/- 3% of preischemic control, respectively. In blood-perfused groups they were consistently greater (91% +/- 3%, 55% +/- 5%, 46% +/- 5%, 45% +/- 1%, 33% +/- 2%, and 19% +/- 3%, respectively). In further studies, hearts (n = 5 per group) were perfused with buffer (groups 1 and 2) or blood (groups 3 and 4), and each was subjected to 60 minutes of normothermic global ischemia, with (groups 2 and 4) or without (groups 1 and 3) a 3-minute preischemic infusion of St. Thomas' Hospital cardioplegic solution. After 60 minutes of reperfusion, the postischemic recoveries of left ventricular developed pressure in groups 1, 2, 3, and 4 were 32% +/- 3%, 44% +/- 4%, 43% +/- 7%, and 72% +/- 6%, respectively, with coronary flow recovering to 64% +/- 7%, 82% +/- 4%, 82% +/- 4%, and 110% +/- 5%, respectively. Left ventricular end-diastolic pressures were 20 +/- 5, 24 +/- 7, 15 +/- 4, and 4 +/- 3 mm Hg, and tissue water contents were 4.76 +/- 0.11, 4.87 +/- 0.55, 3.93 +/- 0.05, and 3.68 +/- 0.02 ml/gm dry weight, respectively. In conclusion, compared with crystalloid perfusion, the blood-perfused rabbit heart has a greater resistance to ischemia, a superior response to cardioplegic protection, and a lower tissue water content.
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PMID:Comparison of ischemic vulnerability and responsiveness to cardioplegic protection in crystalloid-perfused versus blood-perfused hearts. 156 77

The extraction of reliable and useful relaxation time data for tissue characterization by NMR requires strict protocols, optimized for each type of biological tissue, which include parameters like storage duration and temperature as well as measurement parameters. Spin-lattice relaxation times in liver tissue vary not only with NMR frequency but also with their "time-after-excision characteristics," while spin-spin relaxation times are almost independent of most parameters which influence T1 at 20 MHz in normal liver tissue (e.g., species, sex, circadian rythm, starvation). T2, however, being more sensitive to water content and pH changes, is well suited for detecting nonspecific tissue alterations (e.g., due to ischemia, chemical toxins). Following the suggestions outlined herein, investigation of at least 120 min of time-after-excision (storage) effects allows the significant distinguishing of various physiological differences in normal liver tissue as well as improvement of early detection of liver pathologies.
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PMID:Liver tissue characterization by in vitro NMR: tissue handling and biological variation. 156 62

Rats were subjected to either right proximal middle cerebral artery (MCA) occlusion or sham operation, and examined for an extended period on a battery of tests designed to measure simple motor function, sensorimotor integration and cognitive function. Rats with MCA occlusion showed extensive neuronal loss in the dorsolateral striatum and variable neuron loss in the parietal, temporal and frontolateral neocortex. MCA occluded animals exhibited significant impairments in tests of postural reflex, visual and tactile forelimb placing, locomotor coordination, and a test of simultaneous bilateral tactile extinction. The reflex and sensorimotor function deficits recovered to pre-operative levels by Day 30 post-ischemia. Five weeks following surgery, rats were tested in 2 versions of the Morris water task. Rats with MCA occlusion demonstrated significant impairments in their ability to navigate to a hidden platform, but were not significantly impaired on the visible (cued) version of the task. This general pattern of transient sensorimotor and reflex deficits, but with more persistent cognitive impairments, is similar to that seen in humans following MCA infarcts.
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PMID:Sensorimotor and cognitive consequences of middle cerebral artery occlusion in rats. 157 83

Outcome following stroke is difficult to measure because the behavioral response to infarction is variable. We hypothesized that cognitive function, such as spatial learning, may be a reproducible and sensitive outcome variable. We developed an animal model of multifocal cerebral ischemia in order to study the effects of infarction on learning. To cause ischemia, several hundred microspheres were injected into the internal carotid arteries of rats. After ischemia, behavior was measured using a global rating and a Morris water maze. Postmortem serial brain sections were stained and the size of the infarctions was measured. We found that intracerebral microspheres caused cortical infarction and an impairment of spatial learning. This impairment was not due to occlusion of the internal carotid artery and was not found in animals who received a sham injection of saline. The degree of learning impairment was not correlated with the volume density of the infarctions or with the volume density of the remaining cerebral hemisphere. The learning impairment clearly differentiated normal from lesioned animals, and the impairment was probably due to a delay in acquisition of spatial information rather than a defect in retention or retrieval. Measurement of learning deficit after cerebral ischemia is an efficient and sensitive method for evaluating new stroke treatments and possibly for exploring structure function relationships.
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PMID:Quantitative effects of cerebral infarction on spatial learning in rats. 157 20

Stress gastritis frequently occurs in association with shock or sepsis. Gastric mucosal ischemia appears to be a key feature in these critically ill patients. The University of Wisconsin cold preservation solution (UWS) is an isoosmolar, nonglucose-based perfusate that minimizes hypothermia-induced cell swelling and prevents intracellular acidosis and oxygen-free radical injury, while providing high energy substrates for donor organs. In a prospective, single-blind study, 18 similar Sprague-Dawley rats were randomly divided to receive only 5 per cent dextrose and water (D5W) (Group 1) or a 50 per cent solution of D5W+UWS (Group 2) for 72 hours. At the end of 72 hours the animals were stressed by the cold-restraint model. The mean number of ulcers for Group 2 was nearly half that of Group 1. Also, Group 2 had a significantly lower mean total ulcer length (P less than 0.005) and ulcer index (P less than 0.05). Most of Group 2 had mild gastritis changes (grade 0 to 1), while more than half of Group 1 had severe gastritis (grade 3). Gastric mucosal pH was similar for both groups. Topically applied UWS appears to reduce the severity and incidence of stress gastritis in this experimental model. Because mucosal pH values were similar, it is thought that UWS may alter the effects of gastric mucosal ischemia at a cellular level.
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PMID:Prevention of stress gastritis with tissue preservation solution. 158 84

Burn injury causes acute thrombosis and occlusion of vessels in the dermis directly killed by thermal energy. A vascular response also occurs in the uninjured dermis bordering the site of injury. Diminished blood flow leads to progressive ischemia and necrosis in the dermis beneath and surrounding the burn. If blood flow is maintained or restored in this area, the tissue survives. A noninvasive technique for studying dynamic changes in blood flow in this transitional dermis in rats is presented. A rectangular brass bar 19 mm wide with 5-mm transverse notches was heated in boiling water and applied to the skin surface for 20 seconds, making a "comb" burn composed of a row of four rectangular 10 x 19-mm full-thickness burns. Between the burns were 5 x 19-mm bands of uninjured skin, called "interspaces." After burning, blood flow near the surface of both the burn sites and the interspaces was monitored with a laser Doppler perfusion monitor for 24 hours. The vascular patency of blood vessels was directly visualized by latex vascular casts made 24 hours after burn. The possible prevention of progressive ischemia by injecting systemic ibuprofen was examined in this new model. Normal skin has a surface blood flow reading of 80 +/- 16 mV, burn sites have a reading of 11 +/- 4 mV, and interspaces have a reading of 21 +/- 4 mV at 24 hours postburn in untreated rats. Systemic ibuprofen given IM immediately postburn at 12.5 mg/kg increased blood flow to 80 +/- 28 mV within the interspaces, to 17 +/- 12 mV in the burn site, and to 80 +/- 9 mV in normal skin. The vascular casts showed an absence of patent vessels within both the burn sites and interspaces in untreated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elucidating the vascular response to burns with a new rat model. 158 42

Although calcium antagonists produce salutary effects after shock and ischemia, it is unknown whether such agents restore the depressed cardiac output (CO) and renal function in a nonheparinized model of trauma-hemorrhage and resuscitation. To study this, rats underwent a midline laparotomy (i.e., trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of the maximum bleedout was returned in the form of Ringer lactate (RL). They were then resuscitated with four times the volume of shed blood with RL over 60 min. Diltiazem (400 micrograms/kg body wt) or an equal volume of saline was infused intravenously over 95 min. This infusion was started during the last 15 min of resuscitation. CO was determined by indocyanine green dilution. Glomerular filtration rate (GFR) was assessed with [3H]inulin clearance, and cortical microcirculation was examined by laser Doppler flowmetry. Results indicate that crystalloid resuscitation alone transiently restored but did not maintain CO after hemorrhage. Diltiazem infusion in conjunction with crystalloid resuscitation, however, restored and maintained CO and cortical microcirculation. Although GFR decreased in both groups, the values in diltiazem-treated animals were significantly higher than those in the sham-operated animals. Furthermore, diltiazem markedly decreased tissue water content. Thus diltiazem appears to be a promising adjunct in the treatment of hemorrhagic shock even in the absence of blood resuscitation.
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PMID:Diltiazem restores cardiac output and improves renal function after hemorrhagic shock and crystalloid resuscitation. 159 Apr 48

1. We investigated the effect of a novel vinca alkaloid derivative, vinconate, against brain damage after focal ischemia induced by a middle cerebral artery (MCA) occlusion in rats. 2. Persistent focal ischemia was induced by 6 hr, and vinconate (50 and 100 mg/kg) was given intraperitoneally twice 10 min and 3 hr after MCA occlusion. 3. Focal ischemia produced the disturbance of glucose metabolism, the increase of water content and the impairment of protein synthesis in the surrounding occluded MCA territory. 4. Vinconate was effective in preventing marked reduction of cerebral glucose utilization in the areas surrounding the occluded MCA territory. 5. Vinconate significantly reduced an increase of water content in the surrounding the occluded MCA territory. 6. Preliminary L-[methyl-14C]methionine autoradiographic study also indicated that vinconate can partly prevent a severe impairment of protein synthesis after focal ischemia. 7. The results indicate that vinconate may ameliorate the disturbance of glucose metabolism, brain edema and the impairment of protein synthesis after persistent focal ischemia, and they also suggest that vinconate has a beneficial effect against brain damage.
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PMID:Protective effect of vinconate, a novel vinca alkaloid derivative, on glucose utilization and brain edema in a new rat model of middle cerebral artery occlusion. 159 23

The spin-lattice relaxation time (T1) of water protons and the cross-relaxation time (TIS) between irradiated protein protons and observed water protons were measured in order to study water-macromolecular interactions in ischemic rat brain tissues. Tissues were obtained by bilateral common carotid artery occlusion from stroke-prone spontaneously hypertensive rats. Water, Na, and K contents were measured in ischemic brain tissue at the same time. Water and Na content increased while the TIS value and K content decreased following ischemic insults. The T1 value did not change until 180 min after ischemia had been induced. Changes in the TIS value occurred earlier than changes observed for the T1 value, water, and electrolyte contents. Results indicate that the value of TIS may be useful for detecting cerebral ischemia and that the physical structure of water-macromolecular interaction may be altered soon after ischemic onset in brain tissue.
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PMID:Proton NMR studies on ischemic rat brain tissue. 159 59

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
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PMID:The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction. 159 96


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