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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hemodynamic and electrocardiographic (ECG) effects of pancuronium and vecuronium were compared during high-dose fentanyl anesthesia for coronary artery bypass grafting (CABG) surgery. Forty-eight morphine-scopolamine premedicated patients scheduled for elective CABG were anesthetized with fentanyl (100 micrograms/kg) in divided doses, and either of two muscle relaxants, pancuronium (n = 26; 0.10 mg/kg) or vecuronium (n = 22; 0.09 mg/kg). Hemodynamic data, blood gas samples, and ECG tracings were obtained at the following intervals: (1) control; (2) prior to intubation; (3) 1 minute after intubation; (4) prior to sternotomy; and (5) 1 minute after sternotomy. In the pancuronium group, heart rate (HR), cardiac index (CI), and rate-pressure product (RPP) were increased after induction of anesthesia and following intubation. Eleven patients (42.3%) displayed ischemic ST segment changes. Four patients in this group developed tachycardia and hypertension to an extent requiring pharmacological intervention. Vecuronium-treated patients displayed no increases in HR, MAP, and RPP, and a decrease in CI. Only one patient (5.6%) developed evidence of ischemic ECG changes. Four patients in the vecuronium group, all receiving preoperative beta-blocker therapy, became hypotensive and bradycardic after the induction of anesthesia. The present investigation confirms the increased incidence of myocardial ischemia during high-dose fentanyl-pancuronium anesthesia. Although vecuronium was associated with fewer myocardial ischemic changes, the occurrence of bradycardia and hypotension in some patients receiving preoperative beta-adrenergic blocking drugs remains a concern.
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PMID:Hemodynamic responses to pancuronium and vecuronium during high-dose fentanyl anesthesia for coronary artery bypass grafting. 135 92

The effects of a moderate dose of sufentanil (1 microgram.kg-1 + 0.015 micrograms.kg-1.min-1) plus nitrous oxide (30% O2/70% N2O) anesthesia (group I; n = 8) and of high-dose sufentanil/O2 anesthesia (10 micrograms.kg-1 + 0.15 micrograms.kg-1.min-1) without N2O (group II; n = 8) on cardiovascular dynamics, myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, and hypoxanthine release were studied in two groups of male patients scheduled for elective coronary artery bypass surgery. All patients were on maintenance doses of calcium channel blockers and nitrates with the last doses of medications given the morning of operation. All patients were premedicated with flunitrazepam (2 mg orally), piritramide (7.5 mg IM) and promethazine (25 mg IM). Measurements were performed before the induction of anesthesia with the patients premedicated but awake; 20 min after induction of anesthesia with sufentanil plus pancuronium 0.1 mg.kg-1 for muscle relaxation before surgery; and during sternotomy and sternal spread. Sufentanil at either dose decreased mean arterial pressure, as well as cardiac and stroke volume index while heart rate remained unchanged. Following the induction myocardial blood flow and myocardial oxygen consumption decreased 23% (79 ml.min-1.100 g-1 to 61 ml.min-1.100 g-1 and 28% (9.2 ml O2.min-1.100 g-1 to 6.6 ml O2.min-1.100 g-1) in group I and 14% (78 ml.min-1.100 g-1 to 67 ml.min-1.100 g-1 and 18% (8.7 ml O2.min-1.100 g-1 to 7.1 ml O2.min-1.100 g-1) in group II. Myocardial ischemia was seen in one patient of group II (patient No. 4), as indicated by a hypoxanthine release into the coronary sinus, when after the induction MAP decreased from 93 to 67 mm Hg and heart rate increased from 56 to 71 min-1. During sternotomy 8 of 16 patients (50%) developed hypertension and 9 of 16 patients (56%) showed signs of myocardial ischemia, i.e., a lactate and hypoxanthine release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sufentanil does not block sympathetic responses to surgical stimuli in patients having coronary artery revascularization surgery. 252 78

This study examined the effects of dopamine (DA) and amrinone (AM) on myocardial oxygen demand-supply relationship in coronary artery stenotic areas (40-60% reduction of coronary blood flow by a constrictor) by measuring myocardial oxygen tension (PmO2) after administration of either DA or AM in twelve dogs. The results were as follow; 1) PmO2 showed no significant changes with either DA or AM, but it showed a significant inverse correlation with HR with DA or AM. Thus changes in HR affected the myocardial oxygen balance. 2) AM showed strong coronary vasodilating action in non-stenotic areas and possibly led to 'steal'. 3) Looking at indicators of myocardial ischemia, MAP/HR was significantly correlated with PmO2, and it reflected the myocardial oxygen demand-supply relationship better than RPP or DPTI/TTI. When DA or AM is used in patients with coronary artery disease, both drugs seem to maintain myocardial oxygen balance unless they cause tachycardia. Caution is required in the administration of AM because of the possibility of 'steal'.
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PMID:[The effects of dopamine and amrinone on myocardial oxygen demand-supply relationship in dogs with coronary artery stenosis]. 270 8

Hypertension following aorta-coronary bypass operations can contribute to myocardial ischemia. Nitroprusside therapy will reduce afterload, preload, and coronary perfusion pressure. Since both hypertension and its treatment can result in ischemic injury, nitroprusside must be carefully titrated to optimize cardiac function and metabolism. Thirty-one patients undergoing elective coronary bypass grafting were studied during a hypertensive episode (mean arterial pressure [MAP] = 119 +/- 18 mm Hg) and during nitroprusside therapy at an MAP of 97 +/- 11 mm Hg and at an MAP of 80 +/- 11 mm Hg (normotension). Nitroprusside also produced a significant (p less than 0.05) decrease in left atrial pressure (LAP), left ventricular end-diastolic volume index (EDVI) (stroke index divided by ejection fraction by nuclear angiography), stroke index, and stroke work index (SWI). Cardiac lactate extraction (LEx) and the ratio LEx/SWI increased (p less than 0.05) with the initial nitroprusside therapy, but lactate production resulted when the MAP was lowered to 80 mm Hg. Volume loading studies were performed during hypertension in four patients and during nitroprusside therapy in 15 patients. Neither performance nor compliance was significantly altered at an MAP of 97 mm Hg, but compliance decreased at normotension. Both hypertension and its treatment can result in inadequate myocardial metabolism. Nitroprusside should be titrated to maintain MAP between 90 and 100 mm Hg.
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PMID:Effects of postoperative hypertension and its treatment. 660 14

We have treated 81 patients who had hypertension with slow intravenous infusion of diazoxide (15 mg/min; 5 mg/kg of body weight). Blood pressure was reduced effectively both in patients with severe hypertension (n = 40) and in patients with a hypertensive crisis (n = 34); the decrease of mean arterial pressure (delta MAP) being -17.0% +/- 1.2% (mean +/- SEM) and -19.7% +/- 1.5%, respectively. However, the delta MAP was significantly greater in patients with preeclampsia (-26.0% +/- 3.0%). In all instances BP fell gradually and then decreased only slightly after discontinuation of the infusion. Thus, the potentially hazardous, steep, and exaggerated fall of BP, observed after bolus injections, can be avoided. Electrocardiographic signs of myocardial ischemia were seen in two patients. No other serious side effects were observed. We conclude that, even in patients with a hypertensive crisis, slow infusion is a safe and effective procedure for the reduction of BP.
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PMID:Acute treatment of hypertension with slow infusion of diazoxide. 667 30

The present study was performed to compare hemodynamic effect of intravenous Nitroglycerin (TNT i.v.) in 14 patients developing acute hypertension (Group I) and in 7 non hypertensives after open heart surgery (Group II). In all patients, m.a. 56.6 yrs, (10 mitral and/or aortic prosthetic valve replacements, 9 aorto-coronary bypass, 1 open mitral commissurotomy, 1 closure of atrial septal defect) TNT was infused at doses of 0.5, 1, 2 microgram X kg X min. and subsequently at 2 microgram X kg X min. after volume administration (2 + V.A.) to maintain right and left atrial pressure the same as control (P = N.S.). Mean arterial, right and left atrial pressures (MAP, RAP, LAP), cardiac frequency and index (CF, CI and systemic vascular resistance index (SVRI) were monitorized. TNT i.v. resulted in hypertensive patients (Group I) in reduction vs. control of: a) RAP (--20.17%) and LAP (--20.58%) at 0.5 microgram X kg X min. b) RAP (--26.13%), LAP (--27.50%), MAP (--19.94%) and CI (--12.98%) at 1 microgram X kg X X min. c) RAP (--22.47%), LAP (--26.89%), MAP (--24.68%), CI (--12.6%) and SVRI (--17.34%) at 2 microgram X kg X min. When RAP and LAP was maintained by volume administration TNT i.v. (2 microgram X kg X min.) resulted in an even greater increase in CI and a greater decrease in MAP and SVRI ((--22.04% and --24.88% respectively). No significant hemodynamic modification (P less than or equal to 0.05) were observed in non hypertensive patients (Group II) at all doses of TNT i.v. The results confirm a predominant venodilator effect of TNT at low doses and a good effect on arterial resistances at high doses in hypertensive patients. In view of previous reports of differing effects on ischemia TNT i.v. may be preferable to other vasodilator drugs for control of acute post-ECG hypertension, only on condition to maintain an adequate left ventricular filling pressure to prevent a fall of cardiac index. Moreover the absence of significant (P less than or equal to 0.05) hemodynamic modifications in non hypertensive patients may be a further advantage in the treatment of myocardial ischemia with i.v. TNT.
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PMID:[Effect of intravenous nytroglicerin in hypertensive patients during and after open heart surgery (author's transl)]. 678 Apr 1

Hypertensive emergencies are uncommon and physiologically diverse. Consequently, it is difficult for most physicians to develop a familiarity with all the different hypertensive crises and with all drugs available for treating them (Table 4). Clinicians should not agonize over which is the perfect therapeutic agent for a particular emergency, but instead, they should focus on scrupulous monitoring and familiarize themselves with a few agents that will serve in most situations. Generally, these agents will be sodium nitroprusside and nitroglycerin. Vigilant neurologic monitoring is mandatory in all hypertensive emergencies. The early symptoms and signs of cerebral hypoperfusion can be vague and subtle, but if recognized, serious complications of therapy can be avoided. Remember, the patient may still be hypertensive. Avoid acute (during the first hour) reductions in MAP of more than 20% whenever possible; subsequent reductions should be gradual. In patients known to have markedly elevated ICP and who need acute reductions in their BP, serious consideration should be given to direct monitoring of the ICP so that CPP can be maintained within safe limits. In general, oral agents should not be used for the treatment of hypertensive emergencies. Intravenous Labetalol and intravenous nicardipine are not suitable for general use in hypertensive emergencies. In special situations (e.g., perioperative hypertension and subarachnoid hemorrhage), however, they may be employed. Their role may expand with further study. Trimethaphan may be superior to nitroprusside for hypertension complicated by elevated ICP or cerebral dysfunction. Realistically, most physicians will continue to use nitroprusside. Intense neurologic monitoring is more important than the specific agent used. Nitroglycerin is the agent of choice for acute ischemic heart disease complicated by severe hypertension; if it fails, use nitroprusside. For aortic dissection, the combination of nitroprusside and IV propranolol is the therapy of choice; beta-blockade must be achieved rapidly or the dissection may worsen. Trimethaphan is also an agent for first-line therapy. Esmolol is an alternative to IV propranolol for the treatment of aortic dissection, if prolonged beta-blockade might seriously jeopardize the patient. For eclampsia, unless an expert in hypertension during pregnancy has established an alternative, the therapy of choice is hydralazine and magnesium. The treatment of subarachnoid hemorrhage is in flux; calcium channel blockers are used to prevent spasm, not to lower BP. If the BP must be lowered immediately, use nitroprusside.
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PMID:Hypertensive emergencies. 758 98

The effects of periodic obstructive apneas on systemic and myocardial hemodynamics were studied in nine preinstrumented sedated pigs under four conditions: breathing room air (RA), breathing 100% O2, breathing RA after critical coronary stenosis (CS) of the left anterior descending coronary artery, and breathing RA after autonomic blockade with hexamethonium (Hex). Apneas with RA increased mean arterial pressure (MAP; from baseline 103.0 +/- 3.5 to late apnea 123.6 +/- 7.0 Torr, P < 0.001) and coronary blood flow (CBF; late apnea 193.9 +/- 22.9% of baseline, P < 0.001) but decreased cardiac output (CO; from baseline 2.97 +/- 0.15 to late apnea 2.39 +/- 0.19 l/min, P < 0.001). Apneas with O2 increased MAP (from baseline 105.1 +/- 4.6 to late apnea 110.7 +/- 4.8 Torr, P < 0. 001). Apneas with CS produced similar increases in MAP as apneas with RA but greater decreases in CO (from baseline 3.03 +/- 0.19 to late apnea 2.1 +/- 0.15 l/min, P < 0.001). In LAD-perfused myocardium, there was decreased segmental shortening (baseline 11.0 +/- 1.5 to late apnea 7.6 +/- 2.0%, P < 0.01) and regional intramyocardial pH (baseline 7.05 +/- 0.03 to late apnea 6.72 +/- 0. 11, P < 0.001) during apneas with CS but under no other conditions. Apneas with Hex increased to the same extent as apneas with RA. Myocardial O2 demand remained unchanged during apnea relative to baseline. We conclude that obstructive apnea-induced changes in left ventricular afterload and CO are secondary to autonomic-mediated responses to hypoxemia. Increased CBF during apneas is related to regional metabolic effects of hypoxia and not to autonomic factors. In the presence of limited coronary flow reserve, decreased O2 supply during apneas can lead to myocardial ischemia, which in turn adversely affects left ventricular function.
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PMID:Systemic and myocardial hemodynamics during periodic obstructive apneas in sedated pigs. 951 95

The pathogenesis of hypertension in haemodialyzed uraemic patients is multifactorial. The following are involved: sodium and water retention as a result of the impaired excretory capacity of the kidneys, excessively increased activity of the RAAS and sympathetic nerve, increased levels of the vascular constrictor endothelin-1, cumulation of endogenous inhibitors of NO synthesis and reduced formation of vasodepressor factors. As to other factors in the development of hypertension raised intracellular calcium associated with hyperparathyroidism may participate, the stiffness of calcified arteries, erythropoietin treatment and preexisting essential hypertension. Treatment comprises salt restriction below 5 g/day, systematic control of the volume of extracellular fluid by ultrafiltration during every haemodialysis to the level of so-called dry weight and pharmacological treatment in patients where volume control dos not suffice. All drug groups are used. In their selection contraindications are taken into consideration as well as co-morbidity, the dialyzability of antihypertensive drugs and compelling evidence. In patients with a preserved residual diuresis furosemide is administered--125-750 mg/day. Beta-blockers are indicated in patients with IHD, in particular after IM. Calcium blockers are recommended in ventricular hypertrophy and diastolic dysfunction, when beta-blockers are contraindicated and in elderly patients. ACEI indicated in congestive heart failure and left ventricular hypertrophy with systolic dysfunction. Inhibitors of AT1 receptors are an alternative in case of undesirable effects od ACEI. Alpha-blockers and central alpha agonists are used mainly in combinations. In case of failure the haemodialyzation method can be altered or changing the patients to CAPD may be considered. The relationship between BP and the survival of haemodialyzed patients is bimodal. An adverse effect is exerted by a high as well as low BP and in particular by interdialyzation hypotension. The target BP for the haemodialyzed population has not been defined so far. There is, however, evidence that a high BP is independently associated with the de novo development of IHD and MAP above 106 mm Hg with de novo development of cardiac failure. MAP below 98 mm Hg minimalizes the development and progression of left ventricular hypertrophy and MAP below 106 mm Hg the development of heart failure. Long-term survival for 15 and more years is statistically significantly associated with MAP lower than 99 mm Hg.
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PMID:[Hypertension in hemodialyzed uremic patients]. 1095 54

We recently demonstrated that ischemic preconditioning (IPC) induced by cyclic episodes of short durations of ischemia and reperfusion potentiates a signal transduction cascade involving protein tyrosine kinases and MAP kinases. A rapid activation of janus kinase (JAK) and several signal transducers and activators of the transcription (STATs) including STAT3, STAT5A and STAT6 has been shown to occur during myocardial ischemia and reperfusion. This study sought to examine if JAK/STAT signaling pathway play any role in classical early phase of IPC. Isolated working rat hearts were perfused for 15 min with KHB buffer in the absence or presence of a JAK kinase inhibitor tyrphostin AG490 (5 microm) followed by IPC, 30 min global ischemia and 2 h of reperfusion. The results demonstrated extensive phosphorylation of JAK2 and STAT3 in the IPC hearts which was almost completely abolished by an inhibitor of JAK2, AG490. IPC displayed cardioprotection as evidenced by improved post-ischemic contractile recovery, decreased myocardial infarct size and reduced number of apoptotic cardiomyocytes. AG490 blocked IPC-mediated cardioprotection by altering the IPC-mediated survival signal into death signal. Thus, IPC-induced upregulation of antiapoptotic gene bcl-2 and downregulation of pro-apoptotic gene bax are decreased and increased, respectively, in the AG490 treated hearts. The results suggest that early phase of IPC potentiates JAK/STAT signaling by activating STAT3 which transmits a survival signal to the myocardium.
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PMID:Role of STAT3 in ischemic preconditioning. 1170 38


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