Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The energetic role of inosine (INO) remains controversial. The aim of the present study was first to test whether endogenous INO consumption/production correlates with regional myocardial contractile performance and second to test whether locally increased levels of INO influence contractility and blood flow in severely ischemic myocardium. Fentanyl-anesthetized dogs with implanted sonomicrometry crystals and independently perfused left anterior descending coronary arteries were studied. Two relatively load-independent indexes of regional myocardial contractility derived from left ventricular pressure-segment length loops were used: the regional stroke work-end-diastolic segment length relationship (Wr/L(ed)) and the end-systolic pressure-segment length relationship (Plv/L(es)). Very good correlations between myocardial contractile performance (as measured by the slope of the regional Wr/L(ed) relationship) and endogenous INO consumption/production under both nonischemic and ischemic conditions were found. Ischemia severely depressed contractility, significantly shifting rightward the Wr/L(ed) and Plv/L(es) relationships. INO infused into the left anterior descending bypass, in a concentration of 600 to 800 mumol/L, partially restored contractile performance as evidenced by a significant leftward displacement of both relationships. Wr, measured at a common maximum L(ed), increased significantly by 61 +/- 5%. Border-zone collateral flow (microspheres) increased by 35 +/- 7% within the endocardial segments and by 34 +/- 9% in the epicardial segments, but no increase in flow in the ischemic region was measureable. With the current emphasis on recanalization with thrombolytic therapy and considering the apparent safety of INO, this naturally occurring nucleoside might prove to be a useful adjunctive agent in the treatment of acute myocardial ischemia.
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PMID:Inosine--a natural modulator of contractility and myocardial blood flow in the ischemic heart? 146 98

Myocardial ischemia during surgery can be caused by coronary vasospasm. Neurohumoral mechanisms are involved in this phenomenon, and various substances have been suggested as possible causes, including acetylcholine, histamine, and norepinephrine. The responses of isolated porcine coronary arteries (from 117 pig hearts) with (E+) and without (E-) endothelium to these agents were investigated in the presence of fentanyl, sufentanil, and morphine. Fentanyl significantly shifted to the right, in a concentration-dependent fashion, the concentration-response curve to acetylcholine. This effect was not different between E+ and E- rings. Neither sufentanil nor morphine altered acetylcholine-induced contraction of porcine coronary arteries. Naloxone did not antagonize the suppressive effect of fentanyl on acetylcholine-induced contraction. The response of porcine coronary arteries to norepinephrine was decreased only at very high concentrations of fentanyl. Neither sufentanil nor morphine altered norepinephrine-induced contraction of porcine coronary arteries. Fentanyl, sufentanil, and morphine had no effect on histamine-induced contraction. We conclude that fentanyl antagonized acetylcholine-induced contraction of porcine coronary arteries. This effect of fentanyl seems to be caused by a direct effect on smooth muscle cells and is not opioid-receptor mediated.
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PMID:Effects of opioids on vasoresponsiveness of porcine coronary artery. 153 73

Protecting the patient's airway is of paramount importance in the induction of general anesthesia. For the patient at risk of regurgitation of stomach contents, the rapid-sequence (crash) induction provides protection, but at the expense of increased stress response to laryngoscopy and intubation. This stress response is especially dangerous for the patient at risk for myocardial ischemia. The purpose of this study was to examine the efficacy of using low-dose fentanyl (5 micrograms/kg) to reduce cardiovascular and neuroendocrine stress responses to rapid-sequence induction. Thirty patients were randomly assigned to a rapid-sequence induction protocol either with or without fentanyl preloading. Fentanyl-preloaded patients (fentanyl group) received 2 mg/kg of thiopental whereas patients who were not preloaded with fentanyl (control group) received 4 mg/kg of thiopental. Data collected as indices of the stress response included heart rate, systolic, diastolic, and mean blood pressures, and plasma concentrations of catecholamines (epinephrine, norepinephrine, dopamine) and beta-endorphin. Electrocardiograms (modified V5 lead) were monitored for dysrhythmias and ST segment depression. Control patients had higher systolic, diastolic, and mean blood pressures after intubation than did patients given fentanyl (P less than 0.05). Although the incidence of dysrhythmias was decreased by fentanyl (20% vs 42%), this difference was not statistically significant. Plasma concentrations of beta-endorphin and norepinephrine increased significantly in control patients but not in patients given fentanyl (P less than 0.05). Low-dose fentanyl (5 micrograms/kg) reduces some aspects of the stress response to rapid-sequence induction of anesthesia.
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PMID:Fentanyl preloading for rapid-sequence induction of anesthesia. 631 5

Twenty patients undergoing coronary artery bypass grafting under fentanyl-pancuronium anesthesia were studied. Continuous electrocardiographic (ECG) recording by a Holter Monitor was utilized to determine the incidence of ECG changes of myocardial ischemia during the precardiopulmonary bypass period and to determine the efficacy of an intravenous nitroglycerin (iv NTG) infusion for preventing ischemic ECG changes. Patients in Group 1 (n = 9) received a 0.5 microgram . kg-1 . min-1 iv NTG infusion 20 min prior to induction of anesthesia and throughout the study. Patients in Group 2 (n = 11) received placebo. A randomized double-blind protocol was employed. Anesthesia was induced with fentanyl 3 micrograms . kg-1 . min-1. After fentanyl 25 micrograms/kg and pancuronium 0.1 microgram/kg, the trachea was intubated. After fentanyl 50 micrograms/kg surgery commenced. Prior to induction of anesthesia, iv NTG caused significant decreases in mean arterial pressure and pulmonary capillary wedge pressure, whereas placebo had no effect. However, subsequent to induction of anesthesia, hemodynamics in the two groups were identical. Fifty per cent of patients developed ECG changes of myocardial ischemia during the period from induction of anesthesia to commencement of cardiopulmonary bypass. The incidence of ischemic ECG changes was virtually identical in Group 1 (5/9) and Group 2 (5/11). Ischemic ECG changes were associated with increases in heart rate, mean arterial pressure, and rate pressure product, and decreases in the endocardial viability ratio (DPTI/SPTI). Increases in pulmonary capillary wedge pressure were not associated with myocardial ischemia. Fentanyl-pancuronium anesthesia, as administered in this study, was associated with a high incidence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of intravenous nitroglycerin to prevent intraoperative myocardial ischemia during fentanyl-pancuronium anesthesia. 643 81

Data from the records of 142 patients for carotid endarterectomy at Chugoku Rosai General Hospital between 1983 and 1995, were evaluated concerning perioperative risk factors and anesthetic management. As a preoperative anesthetic risk, the incidence of hypertension was the commonest (76%), and there was a significant incidence of ischemic heart disease (18%). Fentanyl and isoflurane have been used for anesthesia recently and the patients were closely observed and cared in the intensive care unit postoperatively. In order to prevent cerebral ischemia during the occlusion of the internal carotid artery, we measured somatosensory evoked potential as well as jugular venous oxygen saturation, and used near infrared spectophotometry. As a result, postoperative mortality and morbidity were 0% and 2%, respectively. The candidates for CEA have potentially high perioperative risks, and it is important to evaluate the coexisting diseases and to select proper anesthetic technic and monitors.
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PMID:[Perioperative risk factors and anesthetic management of patients for carotid endarterectomy]. 918 70

Spreading of laparoscopic techniques caused changes in anaesthesiological contraindications. In the first period laparoscopy was contraindicated in ischemic heart disease (IHD). Early mobilisation and short postoperative period are positive goals, IHD was taken out of contraindications. Present study compares changes in circulatory, blood gas and acid-base balance values during laparoscopic cholecystectomy (LC) in groups of patients ASA I-II. and ASA III. with IHD. There were 30 patients in group ASA I-II, 30 patients with IHD in category of ASA III. investigated during LC. Fifteen patients of both groups went under Propofol-Fentanyl (TIVA) anaesthesia, others were on Propofol-Fentanyl-N2O (IVA) protocol. All of them got also Atracurium. Pulse rate, mean arterial pressure, O2 saturation and end tidal CO2, blood gases and acid-base state were recorded before induction, after CO2 insufflation, after desufflation, 1 and 3 hours postoperatively. After CO2 insufflation there was a moderate tachycardia in both ASA III. groups (74/min-->88/min). In all groups pCO2 increased (40-->48 mmHg) but normalised till the 3rd postoperative hours (42 mmHg). Ventricular extrasystoles appeared in 3 ASA III. patients in IVA group. Three high risk patients had serious metabolic acidosis postoperatively. Present time the ischaemic heart disease does not contraindicates laparoscopic interventions. TIVA with Propofol is better choice because of its favourable effects on circulation and acid-base balance. Using N2O caused higher grade of intestinal distension. The cardio-respiratory, blood gas parameters and acid-base balance have to be monitorised in perioperative period of laparoscopic surgery.
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PMID:Anaesthesiological indications and contraindications of minimally invasive surgery. 940 93

Long non-coding (lncRNA) MALAT1 can be increased by hypoxia or ischemic limbs. Also, downregulation of MALAT1 contributes to reduction of cardiomyocyte apoptosis. However, the functional involvement of MALAT1 in myocardial ischemia-reperfusion (I/R) injury has not been defined. This study investigated the functional involvement of lncRNA-MALAT1 in cardioprotective effects of fentanyl. HL-1, a cardiac muscle cell line from the AT-1 mouse atrial cardiomyocyte tumor lineage was pre-treated with fentanyl and generated cell model of hypoxia-reoxygenation (H/R). Relative expression of MALAT1, miR-145, and Bnip3 mRNA in cells was determined by quantitative real-time PCR. Cardiomyocyte H/R injury was indicated by lactate dehydrogenase (LDH) release and cell apoptosis. The results showed that fentanyl abrogates expression of responsive gene for H/R and induces downregulation of MALAT1 and Bnip3 and upregulation of miR-145. We found that miR-145/Bnip3 pathway was negatively regulated by MALAT1 in H/R-HL-1 cell with or without fentanyl treatment. Moreover, both MALAT1 overexpression and miR-145 knockdown reverse cardioprotective effects of fentanyl, as indicated by increase in LDH release and cell apoptosis. The reversal effect of MALAT1 for fentanyl is confirmed in cardiac ischemia/reperfusion (I/R) mice. In summary, lncRNA-MALAT1 is sensitive to H/R injury and abrogates cardioprotective effects of Fentanyl by negatively regulating miR-145/Bnip3 pathway.
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PMID:Long non-coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury. 2786 40