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)

Despite a fundamental difference in their underlying mechanisms, both postextrasystolic potentiation (PESP) and administration of nitroglycerin (TNG) have been utilized to predict reversibility of abnormal segmental wall motion in patients with ischemic heart disease. To determine whether these interventions induce the same changes in segmental contraction pattern, we analyzed biplane ventriculograms of 14 patients who had an adequately visualized PESP beat on a basal ventriculogram as well as a post-TNG ventriculogram. Four segments in each plane were defined and the area ejection fraction of each segment was calculated for a basal sinus, PESP, and post-TNG beat. To correct for global differences in the response to PESP and TNG, we normalized each segmental ejection fraction (NSEF) by the ventricular ejection fraction for that beat and then compared the differences in NSEF from the basal value after PESP and TNG. Eleven patients demonstrated similar responses to both interventions. The three patients whose responses were discordant had elevated or unchanged left ventricular systolic or end-diastolic pressures at the time of the TNG ventriculogram. Our data suggest that, provided these pressures are lower than basal values at the time of the TNG ventriculogram, PESP and TNG will induce similar changes in segmental contraction patterns. Seven patients with similar responses had a PESP beat on their post-TNG ventriculogram. Changes in NSEF after PESP+TNG were identical to those after either intervention. This implies that the combination of interventions does not induce further changes in segmental contraction pattern beyond that produced by either intervention alone.
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PMID:The similarity of changes in segmental contraction patterns induced by postextrasystolic potentiation and nitroglycerin. 6 Oct 73

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.
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PMID:Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease. 80 82

Effects of nicorandil (NC), a newly synthesized nicotinamide derivative (2 mg i.v.), nitroglycerin (TNG, 0.3 mg sublingual), nifedipine (NF, 10 mg sublingual), and propranolol (PR, 0.1 mg/kg i.v.) on coronary hemodynamics were evaluated in 41 patients with ischemic heart disease. Coronary sinus flow (CSF) was measured using a continuous thermodilution method. NC decreased arterial pressure, cardiac output (CO), and pulmonary artery pressure without changing heart rate. Rate-pressure product tended to decrease. Resting CSF was increased by NC (117-148 ml/min, p less than 0.01) and NF. TNG and PR caused no significant changes. Furthermore, NC revealed the highest CSF/CO ratio among four agents and decreased coronary resistance. During rapid atrial pacing, CSF was slightly increased by TNG, but remained unchanged after NC and NF. Myocardial norepinephrine release was markedly increased by TNG (1.5-6.2 ng/min, p less than 0.01) and slightly increased by NF. No changes were noted after NC and PR. Myocardial lactate extraction varied insignificantly in all agents. NC is a potent coronary vasodilator and seems to reduce both preload and afterload; however, in contrast to TNG and NF, NC did not cause reflex tachycardia or an increase of myocardial sympathetic tone.
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PMID:Effects of nicorandil on coronary hemodynamics in ischemic heart disease: comparison with nitroglycerin, nifedipine, and propranolol. 244 17

A comparative study of venodilating and veno-arterial dilating drugs was conducted for clinical patients and for experimental animals. The subjects were 21 patients with ischemic heart disease associated with left ventricular failure. Fourteen patients received venodilators alone (Group I), and seven were administrated venoarterial dilators alone (Group II). At the time of the maximum effect, the two groups showed similar improvement. In Group I, the left ventricular filling pressure (LVFP) was reduced from 24 to 16 mmHg and the cardiac index (CI) was increased from 2.5 to 2.8 l/min/m2. In Group II, the LVFP was similarily reduced from 27 to 16 and the CI increased from 2.4 to 2.9. The effects of each drug on the total vascular resistance/LVEP were similar in both groups. In animals with partial occlusion of the left anterior descending artery, intravenous administration of nitroglycerin (TNG) or nitroprusside (NPS) lowered the aortic pressure stepwise at intervals of 10 mmHg from a mean of 130 mmHg. As a result, segmental shortening was improved either by TNG or NPS. However, when the systolic aortic pressure was decreased below 100 mmHg, segmental shortening of the ischemic area was aggravated in dogs receiving either drug. The end-diastolic length showed no difference between the dogs administrated TNG and NPS. When the effects of TNG and nifedipine (NFP) were compared to those in dogs with the old infarcted myocardium, both drugs produced improvement in hypokinetic segments. TNG induced a decrease in the end-diastolic length, whereas NFP revealed no changes, reflecting different modes of improvement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vasodilator therapy in ischemic heart disease]. 644 15

When given during acute myocardial infarction (AMI), vasodilators such as nitroglycerin (TNG) and nitroprusside (NP) improve some of the hemodynamic determinants of myocardial oxygen demand. TNG has been shown to reduce ischemic injury during AMI, but variable results have been noted with NP therapy. To compare the effects of these two agents, 8 closed chest sedated dogs with pre-existing multi-vessel coronary constrictions underwent repeated, random-order, acute 15-min balloon occlusions of the left anterior descending coronary artery during the following conditions: (1) saline infusion (control), (2) TNG infusion, and (3) NP infusion. The severity of myocardial ischemia was estimated by summating the ST-segment elevations (xi ST) measured from 7 intramyocardial electrodes; mean left atrial pressure (LAP), heart rate (HR), and mean systemic arterial pressure (SAP) were also measured. No dog had left ventricular failure either before or after occlusion. Since HR and SAP responses to TNG and NP are different, the dogs were randomized into two subgroups: TNG and NP were infused in 4 dogs to produce similar increases in HR (10--20% greater than control), and in the other 4 to produce similar decreases in SAP (15--20% less than control). In each subgroup, xi ST was significantly lower following TNG than following NP. Moreover, in the total group of 8 dogs, xi ST after 10 min of occlusion averaged 38 +/- 10 mV during TNG treatment compared to 46 +/- 10 mV during control occlusion (P less than 0.05). In contrast, xi ST after 10 min of occlusion averaged 57 +/- 11 mV during NP treatment (P less than 0.01 compared to control occlusion). Thus, (1) when given to achieve similar hemodynamic changes following acute coronary occlusion, TNG reduced while NP increased myocardial ischemia, (2) although both 'vasodilators', TNG and NP appear to have different actions on various vascular beds, and (3) the hemodynamic changes induced by vasodilators do not in themselves provide an accurate index of directional alterations in myocardial ischemia.
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PMID:Relative effects of nitroglycerin and nitroprusside during experimental acute myocardial ischemia. 677 Nov 45

Nitroglycerin (TNG) decreases ST-segment elevation accompanying myocardial ischemia, but its effect on morphometrically and enzymatically estimated infarct size (IS) has not been defined. Accordingly, coronary occlusion was produced in 92 conscious dogs; 65 survived for 24 hours. Thirty-three received TNG (200-300 microgram/min i.v. for 8 hours) and the results were compared with those in 32 untreated dogs. Coronary blood flow (CBF) was measured with tracer microspheres (141Ce, 85Sr and 95Nb) 5 minutes after occlusion before TNG, 20 minutes after TNG and again at 8 hours. Mean blood pressure decreased from 103 to 84 mm Hg with TNG, vs 99 to 94 mm Hg in controls (p > 0.02). Nitroglycerin increased CBF in the subendocardium of ischemic areas by 45% (0.09 to 0.13 ml/min/g). The dogs were sacrificed after 24 hours and IS was estimated morphometrically (25 +/- 1% vs 27 +/- 1% of left ventricular weight) and from myocardial CK depletion (23 +/- 1% vs 24 +/- 1%) were similar for the two groups. Thus, despite increased subendocardial CBF, prolonged i.v. TNG did not decrease infarct size, although a 15% difference would have been detected with this sample size. TNG may relieve coronary spasm but does not appear to be beneficial with sustained coronary occlusion.
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PMID:The effects of intravenous nitroglycerin on hemodynamics, coronary blood flow and morphologically and enzymatically estimated infarct size in conscious dogs. 677 71

Nitroglycerin (TNG), based on electrocardiographic evidence, has been shown to reduce myocardial ischemia, but its effect on morphometrically and enzymatically estimated infarct size has not been defined. Accordingly, coronary occlusion was produced in 50 conscious dogs without LV failure. Twenty-five received TNG (200-300 micrograms/min i.v. for 8 h) and the results compared with those in 25 untreated dogs. Coronary blood flow was measured with 141Ce, 85Sr, and 95Nb (9 microns) after occlusion before TNG, 30 min after TNG, and again at 8 h. Mean blood pressure decreased from 103 to 84 mmHg with TNG vs. 99 to 94 mmHg in controls (p < 0.02). Average heart rates were similar [135 +/- 26 vs. 120 +/- 33 beats/min (SD)]. TNG Did not increase total transmural coronary flow in any region but increased subendocardial flow in the central ischemic areas by 45% (0.09 ml/min/g vs. 0.13 ml/min/g). Animals were sacrificed after 24 h. Infarct size estimated morphometrically (25 +/- 1.5 vs. 26 +/- 1.5 of LV weight) and from myocardial CK depletion (23 +/- 2 vs. 23 +/- 2) was similar for the two groups. Thus, despite increased subendocardial flow, prolonged i.v. TNG did not decrease infarct size even though a difference of 15% would have been detected with this sample size. TNG May relieve coronary spasm but does not appear to be beneficial with sustained coronary occlusion.
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PMID:The effect of intravenous nitroglycerin on coronary blood flow and infarct size during myocardial infarction in conscious dogs. 677 4

The exact mechanism or mechanisms by which nitroglycerin exerts its beneficial effect on pacing-induced regional myocardial ischemia has not been ellucidated previously. In an open-chest, anesthetized canine preparation a fixed, flow limiting stenosis was applied to the left anterior descending (LAD) coronary artery and heart rate was increased by atrial pacing. Mass spectrometry was used to measure myocardial oxygen (PmO2) and carbon dioxide (PmCO2) tensions. Myocardial blood flow was measured by the radioactive microsphere technique. Application of the stenosis resulted in regional decreases in PmO2 and increases in PmCO2 of greater magnitude in the subendocardial than in the subepicardial layer. Atrial pacing resulted in a further decrease in PmO2 and increase in PmCO2 as well as a reduction in subendocardial blood flow. Nitroglycerin (TNG) infusion reduced mean arterial pressure 20 mm Hg, resulting in a 14 mm Hg reduction in PmCO2 in the more ischemic subendocardial layer (P less than 0.05). Myocardial blood flow decreased in all regions; however, the magnitude of this decrease was less in the ischemic region. Addition of aortic constriction abolished both the afterload and preload lowering effects of nitroglycerin but improved ischemic zone blood flow. These data demonstrate that nitroglycerin reduces the severity of pacing-induced regional myocardial ischemia primarily by reducing the determinants of myocardial oxygen demand. We found that when these effects are counteracted, improvement in myocardial oxygen supply becomes the dominant mechanism.
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PMID:Effects of nitroglycerin on regional myocardial ischemia induced by atrial pacing in dogs. 678 Feb 31

We report five patients who developed intraoperative myocardial ischemia but were treated successfully with nicorandil. Case 1; An 84 year-old male underwent emergent laparotomy and ileolysis under inhalational plus thoracic epidural anesthesia. During his emergence from anesthesia, arterial pressure and heart rate increased abruptly due to excitement, leading to ST-T depression on V5 lead. Bradycardia and hypotension developed subsequently. Immediately after i.v. injections of nicorandil 4 mg and atropine 0.3 mg, ST-T change and hemodynamics improved dramatically. Case 2; A 67 year-old male underwent esophagectomy under inhalational plus thoracic epidural anesthesia. Following the completion of surgery, elevation of ST-T developed suddenly on lead II, though hemodynamics were not compromised. ST-T elevation disappeared immediately after nicorandil 6 mg and continuous infusion of nitroglycerin (TNG) was initiated. Case 3; A 71 year-old female underwent aortic valve replacement under high-dose fentanyl anesthesia. Shortly after starting cardiopulmonary bypass (CPB), ST-T segment on leads II and V5 was elevated suddenly. This was accompanied by severe pulmonary hypertension suggestive of severe left ventricular failure. Shortly after nicorandil 4 mg via a pulmonary artery (PA) catheter, ST-T segment returned to the baseline and pulmonary arterial pressure was normalized. Case 4; A 61 year-old male underwent coronary revascularization under high-dose fentanyl anesthesia. During weaning from CPB, elevation of ST-T segment occurred on leads II and V5. ST change improved, responding to nicorandil 6 mg en bolus via a PA catheter. Case 5; A 67 year-old male underwent coronary revascularization under high-dose fentanyl anesthesia. He was unable to be weaned from CPB for several hours because of frequent and repeated attacks of ventricular tachycardia and ventricular fibrillation. The arrhythmia did not respond to various kinds of treatments including intra-aortic balloon pumping and continuous infusions of inotropes, anti-arrhythmic drugs and anti-anginal drugs. In spite of repeated intracoronary injections of TNG, graft flow to the left anterior descending branch remained low at 40 ml.min-1. After an intracoronary injection of nicorandil 1 mg, however, blood flow increased to 100 ml.min-1, resulting in a marked reduction in frequency of ventricular arrhythmia. The patient came off bypass successfully. In each case, intraoperative myocardial ischemia was treated successfully with nicorandil. Neither hypotension nor arrhythmia resulted from its bolus injection. Nicorandil might be a useful therapeutic tool for myocardial ischemia during anesthesia.
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PMID:[Successful treatment of intraoperative myocardial ischemia with nicorandil]. 912 27