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

It has been suggested that rapid cooling before the induction of arrest may be harmful to the newborn myocardium. The objective of this study was twofold: (1) to evaluate whether prearrest rapid cooling is indeed detrimental to myocardial recovery and (2) if so, to evaluate whether the adverse effect of prearrest hypothermia is dependent on the rate of cooling or the total duration of cold perfusion. After an initial stabilization period isolated Langendorff hearts (n = 5 per group) from neonatal piglets (5 to 7 days old) were randomized to four groups: group 1, 5 minutes of rapid cooling to 15 degrees C; group 2, 20 minutes of slow cooling to 15 degrees C; group 3 and group 4, rapid and slow cooling, respectively, with the addition of St. Thomas cardioplegic solution. All groups were then subjected to 2 hours of ischemia at 15 degrees C followed by 30 minutes of reperfusion at 38.5 degrees C. Post-ischemic recovery of left ventricular developed pressure was significantly greater in group 1 versus group 2 (80% +/- 3% versus 61% +/- 2%; p less than 0.05) and in the presence of cardioplegia, group 3 versus group 4 (72% +/- 3% versus 57% +/- 3%; p less than 0.05). The increase in left ventricular end-diastolic pressure was significantly less in group 1 versus group 2 (8% +/- 5% versus 33% +/- 7%; p less than 0.01). Myocardial adenosine triphosphate content recovery correlated with ventricular recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse effect of prearrest hypothermia in immature hearts: rate versus duration of cooling. 154 65

Aortic and renal vascular reconstruction often involve significant renal ischemia. Profound hypothermia during renal ischemia preserves renal tissue. However, in the clinical setting of vascular reconstruction specific attempts at cooling the kidney are often impractical, and renal ischemia frequently occurs at physiologic temperatures. This study demonstrates that minimal temperature changes during renal ischemia alter the functional and morphologic outcome. Rats anesthetized with halothane underwent a right nephrectomy and placement of a snare around the left renal pedicle for 45 minutes to produce renal ischemia. Seventy-five adult male Sprague-Dawley rats, weighing 250 to 350 gm were divided into three groups based on the body temperature maintained during renal ischemia (35 degrees C, 37 degrees C, 39 degrees C). Body temperature was continuously monitored with a rectal thermistor and maintained by adjustment of a heating pad and lamp. Two postischemic protocols were followed including a creatinine assessment protocol with blood samples collected at 24, 48, and 72 hours and a histologic assessment protocol with biopsy of the kidney at 30 hours. At 24 hours after ischemia plasma creatinine concentrations were increased in rats with elevated body temperatures (35 degrees C vs 37 degrees C; [p = 0.001], 37 degrees C vs 39 degrees C; [p = 0.150]). The 30-hour histologic assessment indicated a difference in morphologic outcome (35 degrees C vs 37 degrees C; [p = 0.063], 37 degrees C vs 39 degrees C; [p = 0.016]), with proximal tubular morphology being better maintained at lower temperatures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Minimal physiologic temperature variations during renal ischemia alter functional and morphologic outcome. 156 May 50

We investigated the effect of moderate post-ischemic hypothermia on neuropathological outcome and cerebral high energy phosphate metabolism, intracellular pH and Mg2+ concentration in the rat. Three groups of animals were investigated: (1) Wistar rats subjected to 12 min of forebrain ischemia under normothermic conditions (n = 17), (2) rats subjected to the identical procedure of ischemia, except that 30 degrees C hypothermia was induced post-ischemia and maintained for 2 h of reperfusion (n = 6), and (3) control hypothermic rats not subjected to ischemia (n = 4). In vivo 31P NMR spectroscopy was performed prior to ischemia, and at intervals up to 168 h after ischemia. Histological analysis of brain tissues was performed 7 days after ischemia. No significant differences in cortical and hippocampal neuronal damage was detected between the two experimental groups. Significantly lower pH values were detected in the hypothermic ischemic animals at 24 h (P = 0.0001) and 48 h (P = 0.018) post-ischemia compared to the normothermic ischemic animals. Normothermic ischemic animals exhibited significantly lower [Mg2+] at 72 h (P less than 0.006) compared to the pre-ischemia level. Our data indicate that post-ischemic hypothermia modifies the profiles of post-ischemic brain tissue pH and Mg2+ concentration, and this modification is not associated with histopathological outcome 7 days after ischemia.
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PMID:The effects of post-ischemic hypothermia on the neuronal injury and brain metabolism after forebrain ischemia in the rat. 156 17

The purpose of this study was to determine the effect of selective modulation of brain temperature in the experimental settings of permanent and reversible middle cerebral artery (MCA) occlusion in Sprague-Dawley rats. Three models of proximal MCA occlusion were used, in which the effect of brain-temperature modulations could be studied. These included (a) permanent MCA occlusion with an initial 30-min period of hypotension (30 or 36 degrees C x 4 h), (b) permanent MCA occlusion alone (30, 36, or 39 degrees C x 2 h), and (c) 2 h of reversible MCA occlusion (30, 36, or 39 degrees C x 2 h). In the transient MCA occlusion series, intra- and postischemic cortical blood flow was assessed using a laser-Doppler flowmeter placed over the dorsolateral cortex. After a 3-day survival, all rats were perfusion fixed for histopathological analysis and the determination of infarct volume. In animals with permanent MCA occlusion plus hypotension, no significant difference in infarct volume was demonstrated between the 30 and 36 degrees C groups. In rats with permanent MCA occlusion without hypotension, significant differences in infarct volume were again not demonstrable, but an interaction between infarct area and temperature class was shown by repeated-measures analysis, indicating that hypothermia altered the topographic pattern of the cortical infarct. With 2 h of reversible MCA occlusion, there was a statistically significant reduction in infarct volume in the 30 degrees C group compared to 39 degrees C rats. Although intra- and postischemic CBF were not significantly different among the three temperature groups, the cortical infarct volume was positively correlated with postischemic CBF. The postischemic CBF, in turn, was positively correlated to the intraischemic brain temperature and was negatively correlated to CBF during the ischemic period. These findings demonstrate that moderate manipulations of brain temperature have a greater influence on the resulting cortical infarction in the setting of transient focal ischemia than in the context of permanent vascular occlusion.
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PMID:The significance of brain temperature in focal cerebral ischemia: histopathological consequences of middle cerebral artery occlusion in the rat. 156 34

The ideal level of hypothermia during myocardial preservation for cardiac transplantation remains unknown. Therefore 31P-NMR spectroscopy was applied to assess the effect of different preservation temperatures (15 degrees C in group 1, 4 degrees C in group 2) on time dependent changes of myocardial high energy phosphorous compounds during prolonged global ischemia (5 hours in group 1, 8 hours in group 2) and subsequent reperfusion of isolated rat hearts preserved with modified St. Thomas Hospital solution. ATP-depletion during ischemia was slower in group 2 leading to a significant difference in myocardial ATP-concentrations between both groups after 3 hours of ischemia. The drop of intracellular pH during ischemia was significantly less pronounced in hearts preserved at 4 degrees C compared to 15 degrees C. Postischemic recovery of both left ventricular (LV) peak systolic pressure and its +dP/dt max. was superior in group 2, although the ischemic time was 3 hours longer than in group 1. Hypothermia at 4 degrees C appears favourable for prolonged myocardial protection compared to 15 degrees C with regard to preservation of ATP, prevention of intracellular acidosis and postischemic hemodynamic recovery.
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PMID:[31-phosphor-NMR spectroscopy for determining optical preservation temperature during long-term myocardial ischemia]. 158 63

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

The temporal constraints of protection of neuronal damage by post-ischemic hypothermia was investigated in the gerbil model of global ischemia. Three experimental paradigms were used: 1) Hypothermia was initiated prior to ischemia followed by warming to normothermia immediately post ischemia; 2) Hypothermia of different durations was initiated immediately after reflow and 3) Six hours of hypothermia was initiated at various times following reperfusion. Hypothermia during 5 minutes of ischemia followed by warming to normal body temperature immediately post ischemia resulted in near complete protection of the hippocampus from CA1 cell loss. Hypothermic durations of 1/2, 1, 2, 4, and 6 hours beginning immediately following reperfusion resulted in progressively increased protection from ischemic damage (6 +/- 6%, 21 +/- 10%, 34 +/- 15%, 75 +/- 16% and 77 +/- 12%, respectively). Six hours of hypothermia delayed for 1 hour after reperfusion resulted in 49 +/- 9% protection. No reduction of ischemic damage was observed if 6 hours of hypothermia was delayed for 3 hour after reflow. These data suggest that: 1) Hypothermia during ischemia protects the brain from damage; 2) Hypothermia initiated immediately following reperfusion must have a duration of 2 hours or more to be effective and 3) Six hours of hypothermia is effective if initiated within 1 hour of reperfusion.
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PMID:Protection against hippocampal CA1 cell loss by post-ischemic hypothermia is dependent on delay of initiation and duration. 160 65

Early investigations involving central nervous system (CNS) temperature lowering to protect against the detrimental effects of hypoxia and ischemia were based on the observation that hypothermia reduces brain metabolism and energy consumption. The protective effects of hypothermia have been demonstrated in numerous experimental models of cerebral ischemia and recently in models of brain trauma. These observations also led to the application of hypothermia, in the form of local spinal cord cooling (LSCC), in animal models of experimental spinal cord injury (SCI). Although some investigators have reported negative results in studies of LSCC following traumatic SCI, the majority of studies have noted beneficial effects. The favorable results in animal experimentation led to a limited number of cases where LSCC was used in the treatment of human SCI. However, results are difficult to interpret because (1) most investigators report only a small number of cases, (2) the studies lack a control population, (3) the time interval from injury to the application of cooling has been highly variable, and (4) several investigators combined drug treatments with LSCC. In these experiments, LSCC was achieved via perfusion with a cold solution or an epidural heat exchanger and the aim was to lower cord temperatures significantly (about 10 degrees C). The application of the technique itself is fraught with difficulties. It requires acute surgery in a traumatized patient, a wide multilevel laminectomy, and minimizing the time interval between injury and the application of spinal cord cooling. Recent studies in experimental brain ischemia strongly suggest that a drastic lowering of CNS temperature may be unnecessary to lessen the degree of tissue damage occurring following an ischemic brain injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothermia in spinal cord injury. 161 9

The present report reviews the biochemical and physiological responses to adenosine receptor activation and how these responses underlie the ability of adenosine to couple energy demand with energy supply. In addition, activation of adenosine receptors pharmacologically is shown to initiate various reactions which could be responsible for the observed adenosine-mediated attenuation of the neuropathological consequences of brain ischemia. Also reported is the extent to which side effects such as hypothermia can contribute to the observed efficacy of adenosine agonist administration in the small animal model of ischemia. Data from various in vitro and in vivo ischemia studies is presented showing that neuroprotection can be achieved following pharmacological activation of adenosine receptors either through agonists with high affinity for A1 adenosine receptors or drugs which potentiate endogenous adenosine levels. In general the data support utilization of adenosine receptor activation as a means of attenuating ischemic brain damage.
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PMID:Therapeutic potential for adenosine receptor activation in ischemic brain injury. 161 14

Infrarenal circumaortic occlusion devices were operatively placed in 74 New Zealand white rabbits. Two days after operation the animals were randomly assigned to one of seven treatment groups: I, control, n = 23; II, halothane, n = 8; III, thiopental, n = 12; IV, ketamine (30 mg/kg intravenously), n = 6; V, halothane+hypothermia, n = 8; VI, thiopental+hypothermia, n = 12; VII, ketamine+hypothermia, n = 5. In each group, the infrarenal aorta was occluded for 21 minutes. Final neurologic recovery after restitution of blood flow was graded as acute paraplegia, delayed paraplegia (neurologic deficit developing after initial recovery), or normal. Halothane alone was of no benefit. Hypothermia with any anesthetic was completely protective and reduced neurologic deficits to 0% compared with 91% in controls (p less than 0.05). Thiopental and ketamine treatment each reduced acute paraplegia to 17% (as compared with 61% in controls) and increased delayed paraplegia from 30% in controls to 75% and 50%, respectively (p less than 0.05 for thiopental, p = 0.10 for ketamine). The authors interpret the increase in delayed deficits and decrease in acute deficits as being the result of partial spinal cord protection. These findings document that this model of spinal cord ischemia is sufficiently sensitive to identify interventional treatments that protect the ischemic spinal cord.
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PMID:Protecting the ischemic spinal cord during aortic clamping. The influence of anesthetics and hypothermia. 161 78


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