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

The acid phosphatase and cathepsin D activities and cAMP and cGMP levels in isolated perfused rat heart were investigated during various periods of ischaemic myocardial injury and postischaemic reperfusion. The effect of phosphodiesterase inhibitor--caffeine was also studied. Free acid hydrolases activities and cyclic nucleotide content were increased under 40 and 60 min ischemia and 20 min postischaemic reperfusion. Addition of 50 microM caffeine to perfusion solution after 30 min of ischaemia resulted in increase of cAMP level, cAMP/cGMP ratio, lysosomal bound activities of acid hydrolase and decrease of free acid hydrolase activities. The obtained results suggested that defect in cAMP synthesis might be present in lysosomal membranes labilization in cardiomyocytes injured during ischaemic conditions. Addition of such agents, as caffeine, which increased heart cAMP level, may be effective in lysosomal membranes stabilization under reversible heart ischaemia and reperfusion.
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PMID:[Acid hydrolase activity and cyclic nucleotide contents in the rat heart during myocardial ischemia and postischemic reperfusion]. 255 45

Short- and long-term effects of intraperitoneally transplanted microcarrier attached liver cells (MAL) have been studied in two experimental models of severe liver insufficiency in the rat: subtotal hepatectomy (HX) and acute liver ischemia. Intraperitoneal transplantation of MAL immediately after subtotal hepatectomy resulted in a significantly lower plasma ammonia level, a higher caffeine clearance, a higher urea production and a significantly smaller loss in body weight in comparison to sham transplanted control rats. Since thymidine kinase activity in the regenerating host liver was only significantly stimulated at t = 48 h it is concluded that the observed metabolic effects are mainly due to the metabolic activity of the transplanted MAL, although a small stimulative effect of MAL-TX on host liver regeneration cannot be excluded. In the course of acute liver ischemia, MAL transplantation results in delayed development of acute hepatic encephalopathy (HE), judged by clinical grading, EEG spectral analysis and Visual Evoked Response (VER) parameters. Furthermore, MAL transplantation is associated with less increased levels of plasma ammonia during acute liver ischemia.
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PMID:Metabolic activity of microcarrier attached liver cells after intraperitoneal transplantation during severe liver insufficiency in the rat. 267 Nov 20

The mechanism of action of coronary vasodilation after dipyridamole may be based on inhibition of cellular uptake of circulating endogenous adenosine. Since caffeine has been reported to be a competitive antagonist of adenosine we studied the effect of caffeine on the outcome of dipiridamole-201Tl cardiac imaging in one patient. During caffeine abstinence dipyridamole induced myocardial ischemia with down-slope ST depressions on the ECG, and reversible perfusion defects on the scintigrams. When the test was repeated 1 wk later on similar conditions, but now shortly after infusion of caffeine (4 mg/kg), the ECG showed no, and the scintigrams only slight signs of ischemia. We conclude that when caffeine abstinence is not sufficient, the widespread use of coffee and related products may be responsible for false-negative findings in dipyridamole-201Tl cardiac imaging.
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PMID:Caffeine reduces dipyridamole-induced myocardial ischemia. 279 13

This study investigates the possible role of oscillatory release of calcium from sarcoplasmic reticulum in the genesis of ventricular arrhythmias during acute myocardial ischemia and reperfusion in isolated rat hearts. We used ryanodine and caffeine, which are known to modulate the oscillatory release of calcium from sarcoplasmic reticulum. During 30 minutes of left main coronary artery ligation, all 13 control hearts developed ventricular premature beats (number of beats, 225 +/- 51) and ventricular tachycardia (duration, 123 +/- 21 seconds); five hearts developed ventricular fibrillation. In a separate series of experiments, reperfusion after 15 minutes of coronary artery ligation caused ventricular fibrillation to occur within 15 seconds in all 12 hearts. Ryanodine (10(-9) to 10(-7) M) abolished ventricular arrhythmias during coronary artery ligation and prevented reperfusion ventricular fibrillation. Ryanodine (10(-9), 10(-8), and 10(-7) M) caused 15%, 23%, and 74% decreases in the maximal rate of rise of left ventricular pressure development and 20%, 32%, and 85% decreases in the maximal rate of fall of left ventricular pressure development, respectively, prior to coronary artery ligation. During acute myocardial ischemia, ryanodine 10(-9) M maintained and 10(-8) M impaired left ventricular function; 10(-7) M caused left ventricular failure. Coronary perfusion rate did not increase during ischemia. Antiarrhythmic activity occurred independent of preservation of high energy phosphates, reduction in tissue lactate, or tissue cyclic adenosine monophosphate in the ischemic myocardium. Caffeine 10(2) M decreased the incidence of ventricular arrhythmias during ischemia and upon reperfusion; protection occurred coincident with development of diastolic contracture. Caffeine increased ischemic tissue cyclic adenosine monophosphate content and worsened tissue energy status.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ryanodine and caffeine prevent ventricular arrhythmias during acute myocardial ischemia and reperfusion in rat heart. 282 12

To elucidate the role of cytosolic calcium, [Ca2+]i, in the physiology of the normal and ischemic heart, we have developed a method for recording [Ca2+]i transients from the epicardial surface of the rabbit ventricle after arterial perfusion with the cell-permeant cytosolic calcium indicator indo-1 AM. Hearts were illuminated at 360 nm, and fluorescence was recorded simultaneously at 400 and 550 nm. The F400/F550 fluorescence ratio was calculated by an analog circuit that allowed cancelation of small movement artifacts that were present at single wavelengths. Clear [Ca2+]i transients were present in the F400/F550 signal and were remarkable for their slow decay. Slow decay of the transients was not due to buffering of [Ca2+]i by indo-1, since there was no associated impairment of contraction or relaxation. The peak amplitude of the [Ca2+]i transients was increased by ouabain, adrenaline, postextrasystolic potentiation, and acetylcholine. The extent to which the transients decayed diminished with shortening of the interbeat interval, but decay of the transients could be further diminished by acetylcholine or caffeine. A major advantage of the intact heart over isolated myocytes is the ability to measure changes in [Ca2+]i during ischemia. Ischemia produced a marked increase in both peak systolic and end-diastolic [Ca2+]i, which was most rapid during the first 30 sec, and approached a plateau value after 90 sec. This increase in [Ca2+]i was associated with a characteristic broadening of the peak of the transient. The increase in [Ca2+]i during ischemia is consistent with a proposed causative role of [Ca2+]i in mediating early electrophysiological abnormalities.
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PMID:Cytosolic calcium transients from the beating mammalian heart. 347 28

We have performed the tourniquet-twitch test of Roberts and Ryan in normal and in malignant hyperthermia (MH) patients and relatives. This test measures the ratio of electrically induced thumb twitches noted after 10 min of ischemia with those noted immediately prior to the ischemia. We found no significant differences in this ratio between normal subjects and those who have had MH reactions, or relatives of such individuals. Furthermore, we have observed no significant differences in tourniquet-twitch ratios between those with normal caffeine-halothane contractures and persons with caffeine-halothane contractures tests positive for MH. These findings do not agree with those of Roberts and Ryan, who reported that tourniquet-twitch ratios were higher in MH patients than in normal patients. We have, however, determined that subjects with tourniquet-twitch ratios greater than or equal to 1.8 are substantially younger than those with tourniquet-twitch ratios less than or equal to 1.0. Therefore we do not believe that the tourniquet-twitch test is useful as a diagnostic, or even as a screening test for MH.
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PMID:Failure of the tourniquet-twitch test as a diagnostic or screening test for malignant hyperthermia. 375 52

Peripheral ischemia, secondary to ergotamine tartrate and caffeine suppositories is reported in a 48-year-old female. Lower extremity pre-gangrenous changes were unresponsive to surgical sympathectomy, calcium channel blockade, intra-arterial vasodilators and systemic anticoagulation. A dramatic clinical and radiological reversal of the vasospasm was obtained with intravenous sodium nitroprusside when surgical amputation appeared inevitable.
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PMID:Rapid reversal of ergotamine-induced vasospasm. 395 57

There is considerable concern over the widespread use of caffeine during and after pregnancy. We have therefore examined the effect of perinatal caffeine use on the vulnerability of the immature brain to hypoxic ischemia (HI). Rat pups were exposed to caffeine during the first 7 d after birth by addition of a low or a high dose (0.3 or 0.8 g/L) of caffeine to the drinking water of their dams. At 7 d the pups were exposed to unilateral carotid occlusion+exposure to 7.70% oxygen for 100 min. The extent of HI brain damage was evaluated 2 wk after the insult. The effects of caffeine on A1 and A2a receptors, A1 mRNA and A2a mRNA, were examined by receptor autoradiography and in situ hybridization. Caffeine, theobromine, theophylline, and paraxanthine were analyzed in plasma of separate animals. Exposure to caffeine reduced HI brain damage from 40.3 +/- 3.2% in controls to 29.8 +/- 4.0% (p < 0.05) in low dose and 33.7 +/- 3.9% (NS) in the high dose group. The A1 receptor density measured as [3H]-1,3-dipropyl-8-cyclopentyl xanthine ([3H]-DPCPX) binding was not significantly affected after low dose caffeine but increased in the brain of rat pups in the high dose group. The A2a receptor density measured as [3H]-2[p-(2-carbonylethyl)-phenethylamino]-5'-N- ethylcarboxamidoadenosine ([3H]-CGS 21680) binding and the expression of A1 mRNA and A2a mRNA were not altered by caffeine treatment. In conclusion, low dose caffeine exposure (plasma levels corresponding to umbilical cord plasma in newborns of coffee-consuming mothers) reduced HI brain damage by 30% in 7-d-old rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of long term caffeine treatment on hypoxic-ischemic brain damage in the neonate. 749 52

The rat hearts isolated and perfused by the Langendorf method were used to examine the effects of caffeine-induced increase in cAMP levels on the contractility, rhythmogenesis, some mechanisms of myocardial autonomic regulation in ischemia and resultant reperfusion. The caffeine-induced elevated intracellular cAMP resulted in normalization of myocardial contractility in reperfusion, as well as in stabilization of norepinephrine levels and cardiac adrenoreactivity during ischemia and reperfusion. The positive action of higher cardiomyocyte cAMP levels on the performance of the heart and its sympathetic and parasympathetic control was followed by a reduction in myocardial sensitivity to the induced lipid peroxidation. The paper discusses that cAMP plays a significant role in the formation of adaptive responses of the heart in its ischemia and in reperfusion.
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PMID:[Effect of caffeine on various regulatory mechanisms, rhythmogenesis and contractile function of the isolated rat heart in ischemia and post-ischemic reperfusion]. 770 Jun 90

Oxygen-derived free radicals (O-Rs) cause alterations in cardiac electrical activity, including sustained depolarization, which may contribute to arrhythmic activity in reperfusion after ischemia. The ionic current(s) and cellular mechanism(s) underlying the sustained depolarization are not well defined. We used the whole-cell variant of the patch-clamp technique to study sustained depolarization in guinea pig ventricular myocytes during the extracellular application of O-Rs (generating system: dihydroxyfumaric acid, 3 to 6 mmol/L; FeCl3/ADP, 0.05:0.5 mmol/L). Myocytes superfused with O-Rs (pipette EGTA, 0.1 mmol/L) showed (1) sustained depolarization to between -40 and -10 mV, (2) oscillations in membrane potential, and (3) triggered activity. The depolarization resulted from an increase in quasi-steady state difference current reversing at approximately -18 mV, and the oscillations were due to transient inward current. The latter were inhibited with ryanodine (10 mumol/L) or high pipette EGTA (5 mmol/L), but the steady state current was unaffected. Nonselective cation current (INSC) (recorded with Cs+, Li+, and Mg2+ replacing K+, Na+, and Ca2+, respectively; 20 mmol/L tetraethylammonium chloride [TEA] and 5 mmol/L BAPTA in the pipette solution and 10 mmol/L TEA, 10 mumol/L tetrodotoxin, and 10 mumol/L nicardipine in the bath solution) was activated by O-Rs; the increase in current was unaffected by preventing changes in [Ca2+]i but was inhibited with dithiothreitol. Oxidizing agents (diamide and thimerosal) or caffeine (pipette EGTA, 0.1 mmol/L) produced a similar increase in membrane conductance. INSC activated with O-Rs, oxidizing agents, or caffeine was sensitive to SK&F 96365. O-R treatment was without effect when INSC was already activated with caffeine. The data suggest that (1) extracellular O-Rs activate a Ca(2+)-sensitive INSC in the absence of changes in [Ca2+]i, (2) oxidative modification of extracellular sulfhydryl groups may be involved, and (3) this mechanism is different from the Ca(2+)-dependent activation of INSC by intracellular O-Rs, indicating that O-Rs may alter ion channel activity by differential mechanisms, depending on the compartment, extracellular or intracellular, in which they are present.
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PMID:Oxygen-derived free radical stress activates nonselective cation current in guinea pig ventricular myocytes. Role of sulfhydryl groups. 772 98


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