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

A review of the pharmacology of propofol, a new IV anesthetic agent, is presented. Solubilized in a soybean emulsion, propofol is one of a series of sterically hindered phenols that exhibit anesthetic activity. Induction of anesthesia with propofol may be associated with pain on injection, apnea, and a reduction in arterial blood pressure (BP) and cardiac output. Caution should be ascribed to its use in patients with coronary artery disease, where these effects may have the potential for producing myocardial ischemia. The hemodynamic responses to laryngoscopy and intubation are attenuated. The pharmacokinetic profile suggests suitability as an infusion for either maintenance of anesthesia or sedation. Use of propofol as an infusion during surgery may result in a further reduction in cardiac output, particularly with the concomitant administration of adjuvant increments of fentanyl. The ventilatory response to CO2 is depressed during such an infusion. The high clearance of propofol suggests that even after a prolonged infusion, recovery should be rapid. This finding has been confirmed in a series of studies establishing propofol as an ideal agent for use in a total IV anesthetic technique. Both the quality and speed of recovery, together with the absence of emetic sequelae, support the use of propofol in an outpatient setting. Propofol appears to have no long-term effect on adrenocortical function and appears safe for use in patients with acute intermittent porphyria and susceptibility to malignant hyperpyrexia.
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PMID:The pharmacology of propofol. 269 45

The effects of two antianginal drugs, nicorandil and isosorbide dinitrate (ISDN), on metabolism and function of the ischemic myocardium were studied in a preparation of multiple coronary occlusions in barbital-anesthetized dogs. The preparation consisted of three 5 min occlusions of the left anterior descending coronary artery interspersed by 30 min of reperfusion. An equihypotensive dose of nicorandil (7.5 micrograms/kg/min) or ISDN (12.5 micrograms/kg/min) was infused 15 min before and during the second occlusion period. Hemodynamics, myocardial segment shortening (%SS), tissue blood flow, and myocardial oxygen consumption were determined throughout. Uptake of free fatty acids (FFA), glucose, and lactate were determined during control and ischemic periods. At the end of the final 30 min reperfusion period, biopsy samples of transmural tissue were taken for analysis of phosphocreatine, adenine nucleotides, and total tissue water content. No major hemodynamic changes were produced by either drug except for a 5 to 10 mm Hg decrease in mean aortic pressure. Compared with untreated and ISDN-treated hearts, hearts of dogs treated with nicorandil exhibited reversal of a significant increase in FFA uptake during recurrent ischemia. This was accompanied by an attenuation of the increase in oxygen extraction and CO2 production in the ischemic zone by nicorandil, but not by ISDN. Nicorandil, but not ISDN, improved %SS during reperfusion. Endocardial ATP and total adenine nucleotides were preserved in both nicorandil- and ISDN-treated hearts. Tissue edema was also attenuated by both compounds. Thus, nicorandil improved both function and metabolism during recurrent myocardial ischemia independent of a hemodynamic effect, whereas ISDN only attenuated the loss of adenine nucleotides and increase in tissue water.
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PMID:Salutary action of nicorandil, a new antianginal drug, on myocardial metabolism during ischemia and on postischemic function in a canine preparation of brief, repetitive coronary artery occlusions: comparison with isosorbide dinitrate. 295 76

A significant number of patients with ischemic heart disease are not candidates for coronary artery bypass or percutaneous transluminal angioplasty and do not respond to medical management. This group includes those who have diffuse coronary artery disease, those with poor ventricular function, and those who have had poor results from previous surgery. Developing a method to directly revascularize the myocardium by creating channels through the ventricular wall has challenged many investigators. Early methods, including needle acupuncture, were successful in the acute phase, but long-term patency could not be achieved. Closure of the channels was due to fibrosis and scarring. Experiments in our laboratory demonstrated that myocardial channels, made with the CO2 laser, remained patent up to five years. Histopathologic examination of the channels showed minimal damage to the surrounding cells in the acute phase. Studies at intervals of two months to two years showed patent endothelialized channels, with no evidence of fibrosis. Channels created in the myocardium protected the ventricle against an ischemic event when the left anterior descending branch of the coronary artery was ligated. Clinical experience with direct myocardial revascularization by CO2 laser indicates it may be a viable method of treating those patients with ischemic heart disease who are not candidates for other forms of management. The treatment and early postoperative follow-up in one patient are described.
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PMID:Laser myocardial revascularization. 310 Aug 92

The activity of afferent and internuncial neurons of the bulbar cardiovascular centre (BCVC) was evaluated, using microelectrodes, in conditions of serotonin microinjections, altered blood gas composition and sensomotor cortical stimulation, in acute experiments in cats and rabbits. The afferent flow from ischemized myocardium was examined at the level of nodular-ganglion neurons. Cortical stimulation, changed blood O2 and CO2 proportions and the afferent message related to impaired coronary flow are shown to affect primarily the activity of internuncial BCVC neurons. Myocardial ischemia is shown to be much more frequently complicated by idioventricular arrhythmias, including ventricular fibrillations, under sensomotor cortical stimulation. Disintegrated operation of the afferent and internuncial BCVC neurons that precedes the development of severe ischemic arrhythmias may be due to a heavier afferent flow from heart receptors, descending influences from the cortical sensomotor area, and altered blood gas composition and a lower serotonin level in the medulla oblongata, associated with myocardial ischemia.
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PMID:[Central mechanisms of the development of ischemic disorders of heart rhythm]. 311 17

During cardiac arrest (no flow) and CPR (low flow), the onset of myocardial ischemia is followed by myocardial respiratory acidosis. Myocardial contractility is more decreased by respiratory than by metabolic acidosis. We demonstrated in a porcine model of cardiac arrest and in human patients increases in mixed venous PCO2 during CPR, whereas PaCO2 was decreased. Consequently, there was a striking increase in the venoarterial gradients for both [H+] and CO2. Both cardiac output (pulmonary blood flow) and the concentration of expired CO2 were simultaneously decreased. In great cardiac vein blood, even more profound respiratory acidosis with only minor decreases in bicarbonate and only moderate increases in lactate were observed. Intramyocardial pH was profoundly decreased. The severity of respiratory acidosis as a determinant of resuscitability and survival should be further investigated.
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PMID:Incomplete global myocardial ischemia during cardiac arrest and resuscitation. 313 68

The concept of direct revascularization of ischemic myocardium by transmural left ventricular conduits has been investigated by several researchers. Early success was followed by closure of the pathways by fibrosis and scarring caused by mechanical trauma. The CO2 laser was examined as an alternative method of creating channels. Early experiments supported the hypothesis that laser channels would perfuse ischemic areas and would remain patent. Histological examination showed patent, endothelialized channels more than 2 years following operation in the experimental model. A clinical protocol was designed to assess the results of laser revascularization in a series of 12 patients. Patients selected were candidates for bypass grafting, but because of the coronary artery pathology involved, it was thought bypass grafting alone would result in incomplete revascularization. None of the 12 patients have died. Follow-up ranges from 3 to 32 months. Postoperative thallium stress tests and left ventriculography indicate that channels have remained patent and that they perfuse the myocardium. Direct laser revascularization of the myocardium may offer a viable adjunct in the treatment of ischemic heart disease.
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PMID:New concepts in revascularization of the myocardium. 335 83

It is difficult to maintain the long-term patency after conventional anastomosis especially for the small caliber vessels. Since 15 years we have performed aortocoronary bypass with suture materials for the patients with ischemic heart disease. There are some problems in maintaining the long-term patency of the bypass grafts. Low energy CO2 laser was utilized to make vascular anastomosis with a few stay sutures. Vascular anastomoses (side-to-side, end-to-end, end-to-side) were carefully made by CO2 laser in the regions of the femoral arteries and veins, the carotid arteries and jugular veins in dog. A-C bypass was also successfully carried out between the internal mammary artery and the left anterior descending artery under the beating heart in experiment. Outputs of 20-40 mW and irradiation times of 6-12 sec/mm were optimal conditions for anastomosis of the small caliber vessels. There were no problems in the intensity and the healing of the anastomotic sites in comparison with the conventional suture method. On the basis of these excellent experimental results a low energy CO2 laser was employed clinically for vascular anastomosis of the peripheral vessels in 28 patients with angina pectoris or chronic renal failure and cardiac failure. There were no complications such as bleeding and suture line aneurysm after surgery. In conclusion, vascular anastomosis by laser might be recommended in performing with safety and rapidity for small caliber vessels.
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PMID:[A new method of vascular anastomosis by CO2 laser: experimental and clinical study]. 349 23

We examined the effects of preload alteration on global and regional (i.e., non-ischemic and ischemic areas) function in the presence of regional myocardial ischemia and on the degree of ischemia using 18 isolated, metabolically supported canine left ventricles. For this purpose, cardiac output (CO), systolic segment length change (SL), myocardial CO2 tension (PmCO2) and ST level of epicardial ECG were measured at 3 levels of left ventricular end-diastolic pressure (LVEDP), i.e., approximately 7 (low LVEDP), 11 (middle LVEDP), and 16 mmHg (high LVEDP) without and with left circumflex artery (LCx) stenosis under a constant mean aortic pressure (90 mmHg), mean coronary perfusion pressure (90 mmHg) and heart rate. In the Pre-ischemic stage, CO and SL increased significantly when LVEDP was elevated in a stepwise fashion by changing the height of the reservoir connected to the left atrium. There were no significant changes in PmCO2 or ST level. On the other hand, with LCx stenosis, CO did not show a subsequent increase at higher LVEDPs (i.e., from 796 +/- 103 ml/min at middle LVEDP to 931 +/- 153 ml/min at high LVEDP). Furthermore, there was no significant SL response in the LCx area following alterations of LVEDP, although there was considerable lengthening of end-diastolic length. Both increased PmCO2 and ST level of the LCx area, following LCx stenosis, further increased significantly with elevation of LVEDP. These results suggest the possibility that considerable elevation of LVEDP worsens the degree of ischemia and does not significantly augment ischemic regional myocardial function or global function, while mild elevation of preload improves or tends to improve simultaneously regional ischemic and global functions without aggravating the ischemic injury significantly. Therefore, we conclude that the preload level is quite important in managing ischemia induced myocardial dysfunction.
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PMID:Effects of preload alteration on the degree of ischemia and function of ischemic myocardium under constant mean aortic pressure, coronary perfusion pressure and heart rate in isolated perfused canine heart. 382 May 24

Recently, aortocoronary bypass for the patients with ischemic heart disease has been widely performed and excellent operative results have been obtained in Japan. But, there are some problems in coronary artery surgery for the patients with small coronary artery or multiple stenoses of the coronary arteries. For the purpose to resolve of these problems, operative transluminal angioplasty and onlay patch grafting have been routinely done for severely ill cases, and good patency rate of bypass grafts has been confirmed by postoperative angiography in our clinic. Another problem is alternative surgical treatment for these patients whom A-C bypass could not be done, because of diffuse stenosis of the coronary arteries. As a new method of myocardial revascularization for such cases, arterialization of the coronary venous system (Ao-CS bypass, or Ao-LADV bypass) was experimentally performed. Subsequently, improvements of hemodynamics and blood gas analysis during the bypass were obviously recognized in the latter group. Besides, transmyocardial punctures were created by CO2 Laser (output: 60-90 W, irradiation time: 0.15-0.25 sec) in the ischemic myocardium. Newly created myocardial channels were microscopically studied from the stand points of tissue reaction and patency rate. Subsequently, tinned layers of carbonization and coagulation necrosis were observed in the channels and they disappeared gradually, and long-term patency of the channels could be apparently expected from these findings. On the other hand, vascular anastomosis (side-to-side, end-to-end, and end-to-side) by low energy CO2 Laser was experimentally done in which good healing at the site of anastomosis could be microscopically observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Current problems in coronary artery surgery: new methods of myocardial revascularization and vascular anastomosis]. 387 39

The hypothesis that adenosine mediates the coronary vasodilatory response to hypoxia was tested by determining if intracoronary infusion of the adenosine degrading enzyme, adenosine deaminase (ADA), would attenuate this response. Efficacy of ADA was also evaluated by examining its effect on the coronary responses to exogenous adenosine and to 20-s myocardial ischemia. Experiments were conducted in 14 anesthetized, open-chest dogs ventilated 3-5 min with 3% O2-5% CO2-92% N2 to induce systemic hypoxia. Under control, pre-ADA conditions, hypoxia (arterial PO2 19 +/- 2 mmHg) caused left anterior descending (LAD) coronary blood flow to increase from 100 +/- 12 to 382 +/- 47 ml X min-1 X 100 g-1 (+282%). After infusion of ADA (5 U X kg-1 X min-1 for 8-10 min) into the LAD, equally severe hypoxia (arterial PO2 18 +/- 3 mmHg) caused a significantly smaller increase in LAD flow, 79 +/- 9 to 234 +/- 41 ml X min-1 X 100 g-1 (+195%). Oxygen consumption in the LAD perfusion field was unchanged by hypoxia before ADA but fell significantly during hypoxia after ADA. ADA also attenuated significantly the coronary vasodilatory response to exogenous adenosine and to 20-s ischemia. The results of this investigation demonstrate a significant role of adenosine in the coronary vasodilatory response to systemic hypoxia.
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PMID:Adenosine deaminase attenuates canine coronary vasodilation during systemic hypoxia. 396 15


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