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

Tracer kinetic studies on the effect of i.v. infused adrenaline and angiotensin, and a hyperglycemia induced by glucose application, upon glucose metabolism of the rat brain under ischemic and normoxic conditions are reported. in the ischemic brain, the initial glycolytic rate proved dependent on the glucose content being kept at various levels by glucose administration or hormone infusion prior to the onset of ischemia. The typical saturation kinetics revealed a maximal glucose conversion only from a definite initial content of brain glucose, being equivalent to a glucose level of approximately 13 mumole/ml in plasma, and appeared to depend on the presence of glucose in the cellular space. The early cessation of anaerobic lactate formation even with high glucose in the cellular space. The early cessation of anaerobic lactate formation even with high glucose depot in the brain tissue is referred to inhibition of glycolytic key enzymes by increasing tissue azidosis. The aerobic glucose conversion, as calculated from the Cglucose flux in amino acids associated with the citrate cycle was unaffected by the cerebral glucose content (hyperglycemia by hormone or glucose application). During glucose infusion the cerebral levels of NH3, total NH2 and glutamine rose; the Cglucose flux into aspartate and glutamine was increased and almost proportionally reduced in glutamate and gamma-aminobutyrate. These flux shifts are interpreted as a switching of C-chains from pyruvate owing to increased CO2 fixation, and as a biochemical correlate of an increased irritation level of the experimental animals.
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PMID:[Effect of increased plasma levels of glucose, adrenaline, and angiotensin upon glucose metabolism of totally ischemic and normally perfused rat brain]. 123 36

The effects of metabolic accumulation on myocardial metabolism during global heart oxygen deprivation were evaluated in a working in situ swine heart preparation with controlled total coronary blood flow. Myocardial oxygen consumption was depressed to a similar extent by either reducing total coronary flow 60 per cent (ischemia, low coronary perfusion) in 10 swine or by decreasing coronary perfusate PO2 to 30 mm. Hg at normal flows (hypoxemia, high coronary perfusion) in 13 swine. Compared with findings in 13 control hearts, ischemia significantly (p less than 0.05) decreased myocardial oxygen consumption (640 to 390 mumole per hour per gram), glucose uptake (185 to 16 mumole per hour per gram), and free fatty acid consumption (32 to 17 mumole per hour per gram). ttissue levels of glycogen, creatine phosphate, and adenosine triphosphate (tatp) were significantly reduced (p less than 0.005), and tissue lactate, adenosine diphosphate (ADP), and adenosine monophosphate (AMP) were increased (p less than 0.001). During hypoxemia, glucose uptake was increased (240 mumole per hour per gram) and free fatty acid consumption was somewhat less depressed (19 mumole per hour per gram). Creatine phosphate and ATP were higher than with ischemia (p less than 0.01), and lactate, ADP, and AMP accumulations were less (p less than 0.01). Thus, in the period immediately following myocardial oxygen deprivation, inadequate coronary perfusion caused greater metabolic buildup which inhibited myocardial substrate utilization and energy production. High coronary perfusion, even though the perfusate was unoxygenated, was associated with greater preservation of substrate utilization, higher levels of high-energy phosphates, less accumulation of metabolic products, and a longer survival. These data suggest a critical role of coronary perfusion in protecting myocardial metabolism in the immediate period following global heart hypoxia.
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PMID:Effects of coronary perfusion during myocardial hypoxia. Comparison of metabolic and hemodynamic events with global ischemia and hypoxemia. 126 57

Using microfluorometry, effects of acidic fibroblast growth factor (aFGF) on the in vitro ischemia-induced intracellular calcium elevation were investigated in gerbil hippocampal slices at 35 degrees C. When slices were superfused with hypoxic and glucose-free medium, the mean latency of the in vitro ischemia-induced calcium elevation was 209 +/- 51 s. The addition of aFGF in medium (25 micrograms/l) delayed the calcium elevation throughout the experiments: the mean latency was 541 +/- 94 s. This retardation in calcium elevation may be indicative of neuroprotective nature of aFGF.
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PMID:Acidic fibroblast growth factor delays in vitro ischemia-induced intracellular calcium elevation in gerbil hippocampal slices: a sign of neuroprotection. 128 22

The acidic fibroblast growth factor (aFGF) in rat cerebrospinal fluid (CSF) increased 1000 times in the 2 hr period after food intake, or intraperitoneal (IP) or intracerebroventricular (ICV) glucose infusion. It diffused into the brain parenchyma and was taken up into neurons in the hypothalamus, hippocampus, etc.... aFGF is produced in the ependymal cells and released into CSF in response to increased glucose. ICV application of aFGF dose dependently inhibits, and anti-aFGF antibody facilitates food intake. IP injection of glucose 2 hr before a task that combined acquisition with passive avoidance significantly increased retention of avoidance by mice tested 24 hr later. In a Morris water maze task, IP glucose injection 2 hr before a first trial block reduced time to find and climb onto a platform hidden just below the water surface. These facilitation by glucose of affective and spatial memory were abolished by pretreatment with anti-aFGF antibody applied ICV. Continuous ICV infusion of aFGF into rats also significantly increased the reliability of passive avoidance for several days. The memory facilitation by aFGF was significantly attenuated by CA1 neuron death in the hippocampus caused by 5 min ischemia of the brain, in gerbils. After food intake, centrally-released aFGF reaches the hippocampus and facilitates memory, while peripherally released cholecystokinin reaches the endings of the afferent vagal nerves in the portal vein and changes the vagal nerve activity, which modulates hippocampal activity, to lead to memory facilitation. This, however, is blocked by vagotomy below the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiological significance of brain acidic fibroblast growth factor. 128 50

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

This study was designed to determine changes in one of metabolic functions, gluconeogenesis after ischemic renal injury. Right kidneys of SD rats were removed and a vascular clamp was placed across the left renal artery and vein for 0, 10, 30, 60 and 90 min. On 1, 3 and 7 days after the treatment, tubule suspensions were prepared by collagenase treatment of left kidneys and incubated with or without 2 mM pyruvate or malate aerobically. After the incubation, glucose contents were assayed photometrically. Serum creatinine was also determined. In addition, morphological changes were observed under light microscopy to examine the relationship between metabolism and morphology. The tendency of increase of gluconeogenesis was observed on day 1 and 3 after 10, 30, 60 min of ischemic time. On the other hand, gluco-neogenesis decreased significantly on day 1 after 90 min treatment. In contrast, on day 1 and 3 after treatment, serum creatinine levels showed no difference from control at the groups of 10 and 30 min ischemia. Whereas it rose significantly at the group of 60 min ischemia, showing a different tendency from that of the increase of gluconeogenesis. Moreover, morphologic damage was observed on day 1 and 3 after ischemia of 30 and 60 min. The morphologic damage was found more advanced in the corticomedullary region than those of the cortex which has the high gluconeogenic activity and which thus showed relatively limited damage. These results suggest that renal gluconeogenesis is relatively insusceptible to ischemic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Alterations of gluconeogenesis by ischemic renal injury in rats]. 128 6

Effects of ergot alkaloids, nicergoline (NIC), on survival rate, brain water content, local cerebral blood flow (LCBF: 14C-iodoantipyrine) and glucose utilization (LCGU: 14C-2-deoxyglucose) were examined after bilateral carotid artery occlusion (BCAO) in spontaneously hypertensive rats. Two series of study were performed; the permanent BCAO and 3-hr-BCAO study. After permanent BCAO, the survival rate at 24 hrs of 32% (8 mg/kg, i.p.) or 38% (16mg/kg) in NIC group was higher than that in non-treated group (12%). At the end of 3-hr-BCAO, the increase in water content (dry-wet) in di-mesencephalon was less in NIC (100 micrograms/kg/min, i.v.) group than that in non-treated group. The decrease in LCBF in caudate-putamen (CP), parietal cortex (PC), thalamus (TH), hypothalamus (HT), and substantia nigra (SN) were less in NIC group than those in non-treated group. At the 2-hr-reperfusion after 3-hr-BCAO, the decrease in LCBF in TH and HT were less in NIC group than those in non-treated group. The LCGU in sensory motor cortex, CP, PC, HT, inferior colliculus and pons-reticular were higher in NIC group than those in non-treated group. From these results, it is concluded that nicergoline may have ameliorative effects on survival rate related to the prevention of decreased cerebral blood flow and metabolism following brain ischemia.
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PMID:[Nicergoline, an ergot alkaloid, improves ischemic brain damage by ameliorating the decreased cerebral blood flow and metabolism in spontaneously hypertensive rats]. 129 29

The authors examined 56 patients with obliterating diseases (OD) of arteries of the lower extremities and conducted experiments on 97 male albino rats. In patients with OD the lactate content in the regional venous blood of the involved extremity increases proportionally to the severity of ischemia. No essential changes occur in the concentration of ATP and glucose. In rats with transitory ischemia of the extremities the lactate level in venous blood increases in the absence of changes of the ATP and glucose content; reduced concentration of ATP and glycogen was encountered in the ischemic muscles of the extremities. The mechanisms and significance of the disorders of metabolic parameters in ischemia are discussed.
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PMID:[Relationship between metabolic changes in regional blood and tissues in ischemia of the extremities]. 130 25

With the animal model of cerebral ischemia and reperfusion, we conducted experiments on such model to study the effects of Ligustrazine(LZ) and Salvia Miltirrhizae(SM). The results obtained are as follows: (1) The ischemic brain showed hyperperfusion (congestion period) after 10 min reperfusion following 50 min of ischemia, and then entered a delayed hypoperfusion period after 60 minutes reperfusion and afterward the hypoperfusion was remained till the end of 120 min reperfusion. (2) Following 50 min of ischemic insult, ATP and glucose contents in brain tissue were almost depleted and much of lactate accumulated. Although rapid recovery of energy metabolism occurred within 60 min of reperfusion, a secondary deterioration emerged at 120 min of reperfusion. (3) Apparent brain edema occurred after cerebral ischemia and its further development was observed at the early stage of reperfusion owing to congestive response. Despite the degree of brain edema alleviated obviously after 60 min of reperfusion, the condition become worse at 120 min of reperfusion, which was accompanied by secondary metabolic deterioration. (4) Experimental results showed that LZ and SM could significantly elevate rCBF during the delayed hypoperfusion period, and limit the development of secondary deterioration in energy metabolism and brain edema after 120 min of reperfusion. (5) Notably, LZ and SM had no significant effect on MABP when these two Chinese drugs manifested their therapeutic actions in the animal model of cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in gerbil brain tissue following cerebral ischemia and postischemic reperfusion and studies of the effects of the Chinese drugs]. 130 98

Insulin and insulin-like growth factors I and II (IGF-I and IGF-II) have recently been shown to have biological activity in central neurons, but their normal functions and mechanisms of action in the brain are unknown. Since central neurons are particularly vulnerable to hypoglycemia that results from ischemia or other insults, we tested the hypothesis that growth factors can protect central neurons against hypoglycemic damage in vitro. IGF-I and IGF-II (3-100 ng/ml) each prevented glucose deprivation-induced neuronal damage in a dose-dependent manner in rat hippocampal and septal cell cultures. High concentrations of insulin (greater than 1 microgram/ml) also protected neurons against hypoglycemic damage. Epidermal growth factor did not protect against hypoglycemic damage. Both IGFs and insulin were effective when administered 24 hr before or immediately following the onset of glucose deprivation. Direct measurements of intraneuronal calcium levels and manipulations of calcium influx demonstrated that calcium influx and sustained elevations in intraneuronal calcium levels mediated the hypoglycemic damage. IGF-I and IGF-II each prevented the hypoglycemia-induced elevations of intraneuronal free calcium. Studies with excitatory amino acid receptor antagonists and calcium channel blockers indicated that NMDA receptors did, and L-type calcium channels did not, play a major role in hypoglycemic damage. Taken together, these findings indicate that IGFs can stabilize neuronal calcium homeostasis and thereby protect against hypoglycemic damage.
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PMID:IGF-I and IGF-II protect cultured hippocampal and septal neurons against calcium-mediated hypoglycemic damage. 131 98


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