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)

The low predictive value of the signal averaged ECG (SAECG) at rest may be due to the absence of any physiological perturbation. This study assessed changes of late potentials (LP) in the SAECG due to acute ischemia in five susceptible (S) and five resistant (R) dogs for sudden cardiac death. SAECGs were measured at rest prior to and during the last 3 min of 4 min transient occlusion of the left circumflex artery (CAO). At rest no significant differences were seen in the QRS duration (QRSD), the low amplitude signal duration (LAS40) and the root mean square voltage (RMS20) between S and R dogs. However, acute ischemia caused significant increases in QRSD and LAS40, but only in the S dogs. These results indicate differences in the ischemic modulation of the arrhythmogenic substrate in S and R group. Analysis of LP during acute ischemia may provide an important increase in the positive predictive value of the SAECG.
 ...
PMID:Differences in the effect of acute ischemia on late potentials in susceptible and resistant dogs for sudden cardiac death. 855 Nov 81

The effects of exogenous superoxide dismutase (SOD) on acute myocardial ischemia (MI) was investigated in isolated electrically-driven rabbit hearts (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca++ 1.8 mmol/l, 37 degrees C). Acute regional ischemia (MI) was induced by occlusion of a coronary artery branch (CAO) and quantitated from epicardial NADH-fluorescence photography. SOD (48 U/ml) was applied either 30 min after CAO in a single coronary occlusion model (treatment) or 30 min before the 2nd CAO in a repetitive coronary occlusion model (pre-treatment). SOD had no significant influence on the left ventricular pressure or the global coronary flow (p > 0.05). MI was significantly diminished in hearts pre-treated with SOD before CAO (-25%)(p < 0.05), but remained unaffected when SOD was applied after CAO (p > 0.05). The results suggest that superoxide anion radicals contribute to ischemic tissue injury. SOD shows cardioprotective properties only if present in the ischemic zone, requiring the application of SOD before CAO in poorly collateralised rabbit hearts.
 ...
PMID:Comparison of the cardioprotective efficacy of superoxide dismutase in a single and a repetitive coronary occlusion model in rabbit hearts. 859 59

To determine whether myocardial stunning differs among dogs, pigs, and baboons and is reproducible within species, we examined the effects of 10-min coronary artery (CA) occlusion (CAO) on 9 conscious dogs, 12 minipigs, and 6 baboons. During 10-min CAO, systolic wall thickening in the ischemic zone fell similarly in dogs (-108 +/- 5.6%), pigs (-102 +/- 1.8%), and baboons (-107 +/- 5.7%), but blood flow fell more (P < 0.05) in the subepicardium in pigs (0.07 +/- 0.01 ml.min-1.g-1) and baboons (0.07 +/- 0.02 ml.min-1.g-1) than in dogs (0.18 +/- 0.03 ml.min-1.g-1). At 1 h after CA reperfusion (CAR), wall thickening was reduced more (P < 0.05) in dogs (-40 +/- 4.2%) than in pigs (-22 +/- 2.1%) and baboons (-4 +/- 2.4%). In five dogs and five pigs, three separate 10-min CAO, each 2 days apart, were also examined. In dogs, reductions in wall thickening after CAR were significantly less following the second (-26 +/- 4.2%) or third (-30 +/- 3.2%) CAO, compared with the first CAO (-47 +/- 4.9%). In contrast, repetitive CAO did not induce differences in recovery of wall thickening in pigs. These results indicate that myocardial stunning is less severe in conscious pigs and baboons, compared with conscious dogs, despite more intense transmural ischemia. The dogs demonstrated a "preconditioning-like effect" with serial brief CAO, which was not exhibited in pigs.
 ...
PMID:Differences in myocardial stunning following coronary artery occlusion in conscious dogs, pigs, and baboons. 896 71

The mechanism underlying interorgan preconditioning of the heart remains elusive, although a role for adenosine and activation of a neurogenic pathway has been postulated. We tested in rats the hypothesis that adenosine released by the remote ischemic organ stimulates local afferent nerves, which leads to activation of myocardial adenosine receptors. Preconditioning with a 15-min mesenteric artery occlusion (MAO15) reduced infarct size produced by a 60-min coronary artery occlusion (60-min CAO) from 68 +/- 2% to 48 +/- 4% (P < 0.05). Pretreatment with the ganglion blocker hexamethonium or 8-(p-sulfophenyl)theophylline (8-SPT) abolished the protection by MAO15. Intramesenteric artery (but not intraportal vein) infusion of adenosine (10 microg/min) was as cardioprotective as MAO15, which was also abolished by hexamethonium. Whereas administration of hexamethonium at 5 min of reperfusion following MAO15 had no effect, 8-SPT at 5 min of reperfusion abolished the protection. Permanent reocclusion of the mesenteric artery before the 60-min CAO enhanced the cardioprotection by MAO15 (30 +/- 5%), but all protection was abolished when 8-SPT was administered after reocclusion of the mesenteric artery. Together, these findings demonstrate the involvement of myocardial adenosine receptors. We therefore conclude that locally released adenosine during small intestinal ischemia stimulates afferent nerves in the mesenteric bed during early reperfusion, initiating a neurogenic pathway that leads to activation of myocardial adenosine receptors.
 ...
PMID:Sites of action of adenosine in interorgan preconditioning of the heart. 1206 71

Myocardium undergoes functional changes in the infarcted region primarily due to ischemia. Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronary artery occlusion (CAO, n=5) and intracoronary endothelin-1 (ET-1, n=3) administration during a 6-month period. In 3 dogs, the CAO was repeated 6 months after the first occlusion. Signal-averaged ECG (SA ECG) was recorded before the operation and 10 days, 1 month, 3 months and 6 months after myocardial infarction (MI). The modified Wigner distribution was used for spectrotemporal analysis of the SA ECG. Eight-hour Holter monitoring was performed in each dog before and after experimental MI. Spectrotemporal representations of the QRS complex were stabilized after the first 1-month period in the group of dogs after CAO. The same results were also observed after the repeated CAO. No arrhythmias were recorded 9 days after CAO. The spectrotemporal representations of the QRS complex after intracoronary ET-1 administration were not stabilized during the whole observed period. Very few arrhythmic events were recorded by Holter monitoring already 3 days after intracoronary ET-1 injection. Experimental MI induced by CAO caused a changed ECG image, which was stable from 1 month after MI induction till the end of the monitoring. However, the ECG image after ET-1 administration was not stable during the whole observed period. No arrhythmic events were recorded in either group 3 months postoperatively that could be caused by healthy myocardial status before the experimental MI induction. In clinical practice, however, ischemic heart disease usually precedes the MI. Arrhythmogenic substrate could thus be a consequence of combination of healthy status of the myocardium before MI and MI itself.
 ...
PMID:Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs. 1585 64

Postconditioning, i.e., brief intermittent episodes of myocardial ischemia-reperfusion performed at the onset of reperfusion, reduces infarct size after prolonged ischemia. Our goal was to determine whether postconditioning is protective against myocardial stunning. Accordingly, conscious chronically instrumented dogs (sonomicrometry, coronary balloon occluder) were subjected to a control sequence (10 min coronary artery occlusion, CAO, followed by coronary artery reperfusion, CAR) and a week apart to postconditioning with four cycles of brief CAR and CAO performed at completion of the 10 min CAO. Three postconditioning protocols were investigated, i.e., 15 s CAR/15 s CAO (n=5), 30 s CAR/30 s CAO (n=7), and 1 min CAR/1 min CAO (n=6). Left ventricular wall thickening was abolished during CAO and similarly reduced during subsequent stunning in control and postconditioning sequences (e.g., at 1 h CAR, 33+/-4 vs. 34+/-4%, 30+/-4 vs. 30+/-4%, and 33+/-4 vs. 32+/-4% for 15 s postconditioning, 30 s postconditioning, and 1 min postconditioning vs. corresponding control, respectively). We confirmed this result in anesthetized rabbits by demonstrating that shortening of left ventricular segment length was similarly depressed after 10 min CAO in control and postconditioning sequences (4 cycles of 30 s CAR/30 s CAO). In additional rabbits, the same postconditioning protocol significantly reduced infarct size after 30 min CAO and 3 h CAR (39+/-7%, n=6 vs. 56+/-4%, n=7 of the area at risk in postconditioning vs. control, respectively). Thus, contrasting to its beneficial effects on myocardial infarction, postconditioning does not protect against myocardial stunning in dogs and rabbits. Conversely, additional episodes of ischemia-reperfusion with postconditioning do not worsen myocardial stunning.
 ...
PMID:Differential effects of postconditioning on myocardial stunning and infarction: a study in conscious dogs and anesthetized rabbits. 1656 17

Asymptomatic carotid artery stenosis (CAS) and occlusion (CAO) disrupt cerebral hemodynamics. There are few studies on the brain network changes and compensation associated with the progression from chronic CAS to CAO. In the current study, our goal is to improve the understanding of the specific abnormalities and compensatory phenomena associated with the functional connection in patients with CAS and CAO. In this prospective study, 27 patients with CAO, 29 patients with CAS, and 15 healthy controls matched for age, sex, education, handedness, and risk factors underwent neuropsychological testing and resting-state functional magnetic resonance (rs-fMRI) imaging simultaneously; graph theoretical analysis of brain networks was performed to determine the relationship between changes in brain network connectivity and the progression from internal CAS to CAO. The global properties of the brain network assortativity (p = 0.002), hierarchy (p = 0.002), network efficiency (p = 0.011), and small-worldness (p = 0.009) were significantly more abnormal in the CAS group than in the control and CAO groups. In patients with CAS and CAO, the nodal efficiency of key nodes in multiple brain regions decreased, while the affected hemisphere lost many key functional connections. In this study, we found that patients with CAS showed grade reconstruction, invalid connections, and other phenomena that impaired the efficiency of information transmission in the brain network. A compensatory functional connection in the contralateral cerebral hemisphere of patients with CAS and CAO may be an important mechanism that maintains clinical asymptomatic performance. This study not only reveals the compensation mechanism of cerebral hemisphere ischemia but also validates previous explanations for brain function connectivity, which can help provide interventions in advance and reduce the impairment of higher brain functions. This trial is registered with Clinical Trial Registration-URL http://www.chictr.org.cn and Unique identifier ChiCTR1900023610.
 ...
PMID:Brain Functional Network in Chronic Asymptomatic Carotid Artery Stenosis and Occlusion: Changes and Compensation. 3302 29