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

Leg muscles were occluded (33 kPa) prior to exercise to determine whether the induced metabolic changes, and reactive hyperaemia upon occlusion release just prior to the exercise, would accelerate the subsequent oxygen consumption (VO2) response. Eight subjects performed double bouts (6 min duration, 6 min rest in-between) of square wave leg cycle ergometry both below and above their lactate threshold (LT). Prior to exercise, large blood pressure cuffs were put around the upper thighs. Occlusion durations were 0 min (control), 5 min and 10 min. Ischaemia was terminated within 5 s prior to exercise onset. Heart rate, VO2, ventilatory rate (V(E)), electromyogram (EMG) and haemoglobin/myoglobin (Hb/Mb) saturation were recorded continuously. Single exponential modelling demonstrated that, compared to control (time constant = 53.9 +/- 13.9 s), ischaemia quickened the VO2 response (P < 0.05) for the first bout of exercise above LT (time constant = 48.3 +/- 14.5 s) but not to any other exercise bout below or above LT. The 3-6 min integrated EMG (iEMG) slope was correlated to the 3-6 min VO2 slope (r = 0.73). Hb/Mb saturation verified the ischaemia but did not show a consistent relation to the VO2 time course. Reactive hyperaemia induced a faster VO2 response for work rates above LT. The effect, while significant, was not large considering the expected favourable metabolic and circulatory changes induced by ischaemia.
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PMID:Effects of ischaemia on subsequent exercise-induced oxygen uptake kinetics in healthy adult humans. 1185 67

Ischemia reperfusion injury (IRI) model of rat heart was prepared by preperfusion for 15 min, then a suspension for 45 min and recycling reperfusion for 15 min with 30 ml KH buffer. The leakage of lactate dehydrogenase(LDH),protein, myoglobin and nitrite (NO2-) in the circular perfusion fluid were measured. Myocardial nitric oxide synthase(NOS) activity and L-arginine transport were observed. In the IR group, the leakage of LDH,protein, myoglobin and NO2- were increased respectively by 4.1,5.4,1 and 1.2 times(P<0.01) and NOS(tNOS, iNOS, cNOS) activity by 48.2%,43.2% and 52.1%,(P<0.01,respectively) as compared with the control group. L-arginine transport might be mediated by either high- or low-affinity transport system in cardiac tissue. In the IR group, L-arginine transport increased significantly with the V(max) being increased by 48% and 2 times respectively for the low-affinity and the high-affinity transport as compared with control. Michaelis constant (km) was decreased by 47.4% for low-affinity transport (P<0.05),but not significantly changed for the high-affinity transport. These results suggest that the increase of nitric oxide generation might result from the increased myocardial NOS activity and L-arginine transport during IRI.
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PMID:[Effects of myocardial ischemia reperfusion injury on L-arginine/nitric oxide system in rat heart]. 1197 71

Patients with chronic heart failure (HF) have a reduced skeletal muscle blood flow which can in part explain reduced exercise tolerance and increased ventilation. All the techniques commonly employed to measure skeletal muscle blood flow have limitations that reduce their accuracy and clinical application. Near infrared spectroscopy (NIRS) is a noninvasive, inexpensive, and reproducible technique able to monitor muscle oxygenation both at rest and during exercise, providing information about tissue perfusion. The principle of NIRS is based on the observation that the light absorption characteristics of hemoglobin (Hb) and myoglobin (Mb) in the near infrared region (700-1000 nm) change depending on their relative saturations. In humans, NIRS has been employed to monitor skeletal muscle oxygenation during exercise and/or after cuff-induced limb ischemia in normal subjects as well as patients with chronic HF. Patients with chronic HF have a reduced Hb/Mb oxygenation at any matched work rate and a more rapid deoxygenation above the anaerobic threshold than normal subjects. More recently, NIRS has been used to determine the kinetics of muscle oxygenation in recovery after constant work rate exercise, providing evidence of an inverse relation with cardiac function as assessed by peak oxygen uptake. In conclusion, NIRS appears to be a new promising noninvasive technique for studying muscle oxygenation in a variety of experimental models. (c)1999 by CHF, Inc.
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PMID:Monitoring skeletal muscle oxygenation during exercise by near infrared spectroscopy in chronic heart failure. 1218 15

Neuroglobin is a newly identified vertebrate globin that binds O(2) and is expressed in cerebral neurons. We found recently that neuronal expression of neuroglobin is stimulated by hypoxia and ischemia and protects neurons from hypoxic injury. Here we report that, like hemoglobin and myoglobin, neuroglobin expression can also be induced by hemin. Induction was concentration dependent and time dependent, with maximal (about 4-fold) increases in neuroglobin mRNA and protein levels occurring with 50 microM hemin and at 8 to 24 hours. The inductive effect of hemin was attenuated by the protein kinase G inhibitor KT5823 and the soluble guanylate cyclase inhibitor LY83583, was mimicked by treatment with 8-bromo-cyclic guanosine 3',5'-monophosphate, and was accompanied by a greater than 10-fold increase in cGMP levels, suggesting that it is mediated through protein kinase G and soluble guanylate cyclase. In contrast, hypoxic induction of neuroglobin was blocked by the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor PD98059, indicating that hemin and hypoxia regulate neuroglobin expression by different mechanisms. These results provide evidence for regulation of neuroglobin expression by at least 2 signal transduction pathways.
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PMID:Hemin induces neuroglobin expression in neural cells. 1223 61

Near-infrared fibre-optic single point spectroscopy has been widely exploited to provide information regarding blood volume and oxygenation in vivo, but it does not provide any information on regional differences in perfusion. We have combined the chemical sensitivity of spectroscopy with the spatial sensitivity of imaging to generate maps of regional cardiac oxygenation. Spectroscopic images were acquired for isolated, arrested, blood-perfused porcine hearts (n=4) over the wavelength range 650 and 1050 nm. Spectroscopic images were acquired during normal perfusion, regional ischemia (occlusion of left anterior descending artery) global ischemia, and reperfusion. Hemoglobin (Hb) and myoglobin (Mb) content and oxygenation were determined by reconstructing the tissue spectra measured at each pixel as weighted sums of water, oxy- and deoxy-Hb (and -Mb) absorptivity spectra. The spectroscopic images acquired during regional ischemia clearly revealed increased deoxy-(Hb+Mb) levels and decreased oxy-(Hb+Mb) levels in the ischaemic regions relative to the normally-perfused regions. Global ischemia produced a dramatic decrease in oxy-(Hb+Mb) levels and a moderate increase in deoxy-(Hb+Mb). These images confirm that blood oxygenation can be mapped in cardiac tissue by near-infrared spectroscopic imaging.
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PMID:Regional variations in myocardial tissue oxygenation mapped by near-infrared spectroscopic imaging. 1239 93

To shed light on cardiac effects of the potent vasoconstrictive peptide urotensin II (U II), Langendorff-perfused isolated rat hearts were consecutively perfused with 0.1, 1 and 10 nmol/L U II, for 5 min at each dose, followed by 5-min washout. Moreover, isolated hearts subjected to 20-min global no-flow ischemia were reperfused with U II (1 or 10 nmol/L) for 20 min. Heart function parameters including heart rate, left ventricular pressure and dP/dt were monitored; content of protein and myoglobin, and activity of lactate dehydrogenase (LDH) in coronary effluent were determined; malondialdehyde (MDA) in myocardium and [(125)I]-U II binding sites in plasma membrane were measured after the completion of perfusion. The results showed that: (1) In normal rat hearts, the coronary flow was decreased and the heart function was suppressed by U II dose-dependently, and these changes were not abolished by washout. The leakage of cardiac protein, myoglobin and LDH increased with the increment of U II, but it diminished rapidly after washout. In contrast, MDA content in U II -treated myocardium was not statistically different from that in normal myocardium. (2) Ischemia-reperfusion caused significant decreases in coronary flow, suppression of heart function, and leakage of protein and LDH. In U II -reperfused hearts, all these disorders were significantly aggravated and myocardial MDA content significantly increased (P<0.01), to a greater extent in the presence of higher dose of U II. (3) The maximal binding capacity (B(max)) of U II receptors in plasma membrane from ischemia-reperfusion myocardium increased significantly as compared with that of normal myocardium (20.53+/-1.98 vs 14.65+/-1.78 fmol/mg pr, P<0.01), while Kd remained unchanged. These results indicate that U II caused injury to the isolated rat hearts under normal perfusion, and worsened the injury of the hearts under ischemia-reperfusion, in which U II receptors were up-regulated.
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PMID:[Effects of urotensin II on isolated rat hearts under normal perfusion and ischemia reperfusion]. 1293 25

The coupling of mitochondrial ATP synthesis and oxygen consumption (ratio of ATP and oxygen fluxes, P/O) plays a central role in cellular bioenergetics. Reduced P/O values are associated with mitochondrial pathologies that can lead to reduced capacity for ATP synthesis and tissue degeneration. Previous work found a wide range of values for P/O in normal mitochondria. To measure mitochondrial coupling under physiological conditions, we have developed a procedure for determining the P/O of skeletal muscle in vivo. This technique measures ATPase and oxygen consumption rates during ischemia with 31P magnetic resonance and optical spectroscopy, respectively. This novel approach allows the independent quantitative measurement of ATPase and oxygen flux rates in intact tissue. The quantitative measurement of oxygen consumption is made possible by our ability to independently measure the saturations of hemoglobin (Hb) and myoglobin (Mb) from optical spectra. Our results indicate that the P/O in skeletal muscle of the mouse hindlimb measured in vivo is 2.16 +/- 0.24. The theoretical P/O for resting muscle is 2.33. Systemic treatment with 2,4-dinitrophenol to partially uncouple mitochondria does not affect the ATPase rate in the mouse hindlimb but nearly doubles the rate of oxygen consumption, reducing in vivo P/O to 1.37 +/- 0.22. These results indicate that only a small fraction of the oxygen consumption in resting mouse skeletal muscle is nonphosphorylating under physiological conditions, suggesting that mitochondria are more tightly coupled than previously thought.
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PMID:Mitochondrial coupling in vivo in mouse skeletal muscle. 1452 19

Cause-effect relationships (CER) between development of ischemia and ischemic damage to hypertrophic myocardium were studied in 128 hypertensive patients (23 females, 105 males aged 35 to 58 years, mean age 52.3 +/- 1.2 years). CER were assessed basing on clinical condition of the patient, results of functional stress tests (transesophageal atrial pacing-TAP), Holter ECG and arterial pressure monitoring, changes in serum myoglobin levels. The analysis of correlations between development of left-ventricular myocardial hypertrophy, frequency and duration of painless ischemic episodes, severity of ischemic damage has established that duration of painless ST depression directly and significantly correlated with left ventricular myocardial mass (r = 0.88, p < 0.01). It was found that hypertensive patients with elevated serum myoglobin and its normal values differed significantly both by after-TAP number of episodes of painless ST depression (12.5 +/- 2.69 vs 5.66 +/- 0.86; p < 0.002) and by their duration (4.1 +/- 1.02 min vs 2.45 +/- 0.41 min, respectively; p < 0.001). Clinical implications of elevated concentration of serum myoglobin in hypertensive patients with unaffected coronary arteries were defined.
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PMID:[Phenomenon of myocardial ischemia in patients with essential arterial hypertension with unaffected coronary arteries]. 1468 4

In addition to the generation from specific nitric-oxide (NO) synthases, NO formation from nitrite occurs in ischemic tissues, such as the heart. Although NO binding to heme-centers is the basis for NO-mediated signaling as occurs through guanylate cyclase, it is not known if this process is triggered with physiologically relevant periods of sublethal ischemia and if nitrite serves as a critical substrate. Therefore electron paramagnetic resonance studies were performed to measure nitrosylheme formation during the time course of myocardial ischemia and reperfusion and the role of nitrite in this process. Rat hearts were either partially nitrite-depleted by nitrite-free buffer perfusion or nitrite-enriched by preinfusion with 50 microm nitrite. Ischemic hearts loaded with nitrite showed prominent spectra of six-coordinate nitrosyl-heme complexes, primarily NO-myoglobin, that increased as a function of ischemic duration, whereas in nonischemic-controls these signals were not seen. Total nitrosyl-heme concentrations within the heart were 6.6 +/- 0.7 microm after 30 min of ischemia. Nitrite-depleted hearts also gave rise to NO-heme signals during ischemia, but levels were 8-fold lower. Nitrite-mediated NO-heme complex formation during ischemia was associated with activation of guanylate cyclase. Upon reperfusion, the levels of NO-heme complexes decreased 3-fold by the first 15 min but remained elevated for over 45 min. The decrease in NO-heme complex levels was paralleled by the formation of nitrate, suggesting the oxidation of heme-bound NO upon reperfusion. Thus, nitrite-mediated NO-heme formation occurs progressively during ischemia, with these complexes serving as a store of NO with concordant activation of NO signaling pathways.
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PMID:Nitrosyl-heme complexes are formed in the ischemic heart: evidence of nitrite-derived nitric oxide formation, storage, and signaling in post-ischemic tissues. 1470 51

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been reported to have beneficial effects on cardiac function. The authors used the Langendorff model of ischemia/reperfusion (I/R) injury in isolated rat heart to determine whether ghrelin exerts direct cardioprotective effects. Also, the capacity of ghrelin to bind to sarcolemmal membrane fractions before and after ischemia and reperfusion was examined. Compared with vehicle administration, administration of ghrelin (100-10,000 pM) during the reperfusion period resulted in improvement in coronary flow, heart rate, left ventricular systolic pressure, and left ventricular end-diastolic pressure. Ghrelin also enhanced the rates of left ventricular contraction and relaxation after ischemia following reperfusion. Administration of ghrelin during reperfusion reduced myocardial release of lactate dehydrogenase and myoglobin, indicating protection against cardiomyocyte injury. In addition, ghrelin attenuated the depletion of myocardial ATP resulting from ischemia and reperfusion. A receptor-binding assay demonstrated that maximum binding capacity of ghrelin to sarcolemmal membranes was significantly increased after ischemia and was further increased after I/R. However, Scatchard analysis showed that the affinity of ghrelin for its receptor was not altered. The authors have concluded that administration of ghrelin during reperfusion protects against myocardial I/R injury. The cardioprotective effects are independent of growth hormone release and likely involve binding to cardiovascular receptors, a process that is upregulated during I/R.
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PMID:Protective effects of ghrelin on ischemia/reperfusion injury in the isolated rat heart. 1471 1


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