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)

Glomerular responses to angiotensin II (AII), arginine vasopressin (AVP), and norepinephrine (NE) were estimated in rabbits recovering from uranium-mediated nephropathy or ischemic acute renal failure (ARF) to examine roles of intraglomerular events in resistance to ARF. Uranyl acetate (UA, 0.8 mg/kg) produced ARF in some animals but did not in others. Rabbits recovering from UA-induced ARF were highly resistant to a rechallenge with a larger dose of the agent (2 mg/kg). Their glomeruli did not respond to AII, AVP and NE in vitro. In animals having not experienced ARF following the initial insult, however, resistance to the rechallenge was lower than in animals recovering from ARF, and the glomerular response to contractile stimuli was well sustained. A two hour clamping of the renal artery induced ARF in uninephrectomized rabbits. These animals were not resistant to an additional ischemia in the recovery phase, despite inhibited glomerular contractile responses to AII. These data indicate a nonspecific inhibition of glomerular responses to contractile stimuli in the recovery phase of ARF. It is unlikely, however, that resistance to ARF can be attributed to the loss of the glomerular contractile response.
 ...
PMID:Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF. 354 13

The relation between lipolysis and glycolysis during ischemia was investigated in isolated perfused rat hearts. In hearts perfused with 11 mM glucose, ischemia caused a marked increase of glycerol release from 10 to 33 nmol/g wt weight/min. Substrate-free perfusion induced an initial stimulation of glycerol release, but lipolysis was subsequently reduced to values comparable to normoxic conditions. Neither did perfusion in the presence of acetate (10 mM) and beta-hydroxybutyrate (10 mM) stimulate lipolysis. Inhibition of glycolysis by pyruvate prevented the increase of glycerol release during ischemia. These data suggest a tight link between glycolysis and lipolysis during ischemia which is probably mediated by the availability of glycolytically produced glycerol-3-phosphate for reesterification. In the absence of glycerol-3-phosphate, the lipolysis is regulated by product inhibition. As a consequence, the tissue triglyceride levels after perfusion remained fairly constant in all groups of hearts. The calculated energy loss by the reesterification cycle during ischemia was found to be approximately 2.5% of the total energy production. These data are inconsistent with the assumption that this energy loss contributes significantly to the negative energetic balance of the heart during ischemia. Removal of fatty acids by reesterification may constitute a protective mechanism in order to prevent excessive intracellular accumulation of fatty acids and derivative esters during ischemia.
 ...
PMID:Relation between lipolysis and glycolysis during ischemia in the isolated rat heart. 380 Aug 43

A case of delayed onset of diabetes insipidus (DI), which developed 27 days after a closed head injury, is reported. The patient sustained only a minor neurological deficit and, except for antidiuretic hormone (ADH) insufficiency, hypothalamic function was intact. This selective damage of posterior pituitary function was total and permanent. Ischemia due to vascular injury may be the most likely etiology. Once the diagnosis of delayed posttraumatic DI is confirmed, the treatment of choice is DDAVP (desmopressin acetate). In contradistinction to DI immediately following minor head injury, most patients with a delayed onset of DI after trauma have permanent ADH deficiency.
 ...
PMID:Unusual delayed onset of diabetes insipidus following closed head trauma. Case report. 402 Apr 75

The angioarchitecture of rat brain with deoxycorticosterone acetate (DOCA)-saline and renal forms of experimental hypertension were studied and compared with those of normotensive rats. The number of pial arteries of the third, fourth, and fifth order of branching was lower and their diameter smaller in hypertensive animals as compared with controls. In the medulla oblongata, pons, and mesencephalon the number of arterioles was lower and the total length of capillaries per unit volume was shorter in the experimental group. Rarefication of the capillary network was observed also in rats with spontaneous hypertension. Rarefication was found to begin at the earliest stage of developing hypertension. It was observed as soon as 24 hr after the ligation of the remaining kidney in rats with unilateral nephrectomy. A substantial decrease was recorded in the number of pial arteries with preserved lumens. The hypothesis that the rarefaction of the vascular net in the brain may lead to the formation of zones of ischemia is presented here.
 ...
PMID:Rarefication of the arterioles and capillary network in the brain of rats with different forms of hypertension. 402 32

The aim of this study was to investigate whether chronic (1, 3, 6, 12, or 16 months) low lead (5 or 25 ppm), administered as lead acetate in the drinking water, commencing either after weaning or from conception, altered the susceptibility of the heart to arrhythmias induced by coronary artery ligation in pentobarbitone anesthetized male Sprague-Dawley rats. The cardiac effects of chronic (3 or 12 months) administration of lead (25 ppm) were also examined in spontaneously hypertensive rats. Treatment from weaning of normotensive rats with 5 or 25 ppm lead for periods of 1, 3, or 6 months had no statistically significant effect on the severity of ischemia-induced arrhythmias. Each of the groups treated from conception with 5 or 25 ppm lead for periods of 1, 12, or 16 months exhibited a higher incidence of ventricular tachycardia than the appropriate control group, but the difference was statistically significant only in the case of animals treated with 25 ppm lead for 12 months. The incidence of ventricular fibrillation was significantly higher in rats treated from conception for 16 months with 5, but not with 25 ppm lead. Spontaneously hypertensive rats treated with 25 ppm lead for 3 but not for 12 months had significantly more ectopic beats than control Sprague-Dawley rats. Lead treatment for the longer exposure periods only caused significant accumulation of lead in the blood whereas all lead treatments resulted in a marked accumulation in the bone. We conclude that chronic exposure to low concentrations of lead does not consistently alter susceptibility of the heart to ischemia-induced arrhythmias in anesthetized rats
 ...
PMID:The effects of chronic low lead treatment and hypertension on the severity of cardiac arrhythmias induced by coronary artery ligation in anesthetized rats. 402 14

Oxidation of acetate, palmitoyl carnitine and palmitoyl-CoA was studied in isolated rabbit heart mitochondria. The highest rate of respiration was found if acetate was used as a substrate, the other substances studied were less effective. Oxidation of these substrates was gradually decreased after permanent coronary artery occlusion within 1, 4 and 24 hrs; the extent of the oxidation decrease was similar for all the substrates used. Incomplete oxidation of palmitoyl carnitine was observed in mitochondria from ischemic heart. Consumption of acetate in the mitochondria of control and ischemic animals exceeded distinctly its production in total respiration and in beta-oxidation of palmitoyl carnitine. The data obtained suggest that the decrease in coupled respiration, observed in mitochondria under conditions of ischemia, caused rather by lowering in respiratory capacity than by impairment of adenine nucleotides transport.
 ...
PMID:[Oxidation of fatty acids in heart mitochondria of the ischemic myocardium]. 409 Mar 85

The influence of transient myocardial ischemia on recovery uridine incorporation into RNA and histone acetylation was investigated in an isolated perfused rat heart. Hemodynamically, hearts recovered from 15 min of ischemic arrest and were stable for at least 60 min of perfusion. Uridine incorporation was reduced (P less than 0.05) in ischemic hearts by 24 and 26% after 30 and 60 min of recovery perfusion. The incorporation of uridine into RNA from purified myocytes was decreased by 50% in the ischemic muscle cells. The covalent acetylation of total nucleohistones was diminished by 37%. Histone fractionation by urea polyacrylamide gel electrophoresis clearly indicated that histones H3 and H4 preferentially incorporated less acetate during ischemic recovery. However, histone acetylation for proteins H2A + H2B was not effected. These data suggest that a brief period of ischemia disrupts nucleotide incorporation during the recovery phase, with marked decrease associated with the muscle cell. The similar change in histone acetylation indicates a possible link between nucleoproteins and chromatin function during ischemic insult to the heart.
 ...
PMID:Effect of myocardial ischemia on uridine incorporation and histone acetylation. 617 4

The effect of 12-0-tetradecanoyl-phorbol-13-acetate (TPA) on cyclic adenosine 3',5'-monophosphate (cyclic AMP) level in adult mouse skin in response to ischemia was examined. The incubation of skin pieces in a buffered salts medium at 37 degrees C resulted in a rapid accumulation of cyclic AMP. In mouse skin pieces maximum accumulation (about 6 times the basal level) occurred after 2 min incubation and was followed by a rapid decline in the cyclic AMP level. This "ischemic" rise in epidermal cyclic AMP was greatly reduced if skin was used 16 hr after a single application of 17 nmoles of TPA. The effect of TPA on cyclic AMP accumulation in response to ischemia was first observed at 1 hr after TPA treatment and was maximal at 4 hr. The lack of "ischemic" response in TPA-treated skin was not related to an increase in the activity of cyclic AMP phosphodiesterase after TPA application. In addition, the accumulation of cyclic AMP in skin in response to both ischemia and exposure to isoproterenol, adenosine, histamine, or prostaglandin E2 (PGE2) was not observed in skin treated with the tumor promoter TPA.
 ...
PMID:Decreased accumulation of cyclic adenosine 3',5'-monophosphate in "ischemic" skin after 12-0-tetradecanoyl-phorbol-13-acetate treatment. 627 33

During permanent coronary artery occlusion (1 and 4 h) the respiratory rate of rabbit heart mitochondria with palmitoyl-CoA, palmitoyl carnitine and acetate was progressively reduced to a similar extent. Oxidation of palmitoyl carnitine was incomplete, whereas beta-oxidation of palmitoyl carnitine was not altered significantly. Postischemic reperfusion (3 h) promoted the recovery of mitochondrial respiration. The data obtained suggest that in both the control and ischemia, palmitate oxidation is limited by outer carnitine palmitoyltransferase but not limited by the tricarboxylic acid cycle and respiratory chain.
 ...
PMID:[Effect of ischemia and postischemic reperfusion on fatty acid oxidation in heart mitochondria]. 672 31

Na+ - Ca2+ exchange was studied in two preparations of dog heart mitochondria isolated from normal and ischemic muscle following occlusion of the circumflex (CFX) coronary artery with or without prior verapamil infusion. Na+ - Ca2+ exchange in mitochondria isolated using polytron homogenization showed sigmoidal kinetics with phosphate, whereas mitochondria isolated using gentle nagarse treatment showed hyperbolic kinetics and a Vmax 60% greater than the polytron preparation. Nagarse did not alter the sigmoidal kinetics or exchange velocities of the polytron mitochondria observed with phosphate. With acetate, both preparations exhibited hyperbolic kinetics, and the sodium required for half-maximum activity was increased. Verapamil inhibited Na+ - Ca2+ exchange in both preparations with phosphate, but not with acetate. Thirty or sixty minutes of acute ischemia following CFX occlusion produced significant epicardial surface S-T elevation in the ischemic area and a decrease in myocardial segment shortening. Na+ - Ca2+ exchange of both ischemic preparations was depressed, and the kinetics of the polytron preparation changed to hyperbolic. Pretreatment of the experimental animals with verapamil (0.3 mg/kg) before 60 min of ischemia protected the exchange rates in both preparations, and the sigmoidicity of the polytron mitochondria was retained.
 ...
PMID:Sodium-calcium exchange in dog heart mitochondria: effects of ischemia and verapamil. 684 51


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