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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Even during adequate general anesthesia, hypertension is a common phenomenon in patients undergoing aortocoronary bypass grafting (CABG). In such cases application of vasodilators is recommended in order to decrease myocardial oxygen consumption. This study was performed to compare two commonly used substances, i.e., nitrates and nifedipine, with regard to their influence on hemodynamics, renal blood flow, kidney function, and the requirement for homologous blood transfusions. METHODS. Forty-four patients gave their informed consent to the study. They were randomly divided into 2 groups: group 1 received nitroglycerin (3.0 micrograms/kg.min), group 2 nifedipine (Adalat, 0.5 microgram/kg.min) in order to prevent hypertension in the phase before onset of cardiopulmonary bypass (CPB). Anesthesia was induced by etomidate and succinylcholine and maintained as a modified neuroleptanalgesia with fentanyl (up to 50 micrograms/kg), midazolam (0.3 mg/kg.h), and pancuronium (0.1 mg/kg). Systolic blood pressure was kept within the range of 120-160 mm Hg; in case of higher values boluses of either 0.25 mg nitroglycerin or 0.5 mg nifedipine were administered. Cardiac index, stroke volume index, rate-pressure product, intrapulmonary shunt, and pulmonary and total peripheral resistances were evaluated at five predefined points: (1) after induction of anesthesia; (2) before incision; (3) before cannulating the aorta; (4) after decannulating the aorta; and (5) at the end of operation. Creatinine and free-water clearances as well as sodium and potassium excretion were calculated for three phases of the operation: (A) induction of anesthesia--onset of CPB; (B) during CPB; and (C) end of CPB--end of operation. CPB was performed using a membrane oxygenator (Sorin 51) and a nonpulsatile blood flow of 2.5 1/min.m2, which was reduced during mild hypothermia of 30-32 degrees C to 1.7 l/min.m2. Mean arterial pressure in both groups was kept at approximately 70 mm Hg. In case of lower pressures norepinephrine (50-100 micrograms/bolus) was administered; higher pressures were treated as described above. Volume substitution was performed initially by 500 ml hydroxyethyl starch and continued, if necessary, by homologous blood or 5% human albumin in order to keep the hematocrit greater than 30 in the phases before and after CPB. RESULTS. Group 2 showed significantly higher values of cardiac index and stroke volume index at point 3 while the rate-pressure product was clearly lower, indicating better myocardial performance and lower oxygen consumption than in group 1. Creatinine and free-water clearances in all three phases did not differ. However, sodium excretion during CPB was significantly higher in the nifedipine group while potassium excretion showed no differences. The average requirement for blood and blood substitutes was lower in group 2, but the difference could not be confirmed statistically because of the large dispersion of values. Nevertheless, 4 patients in the nifedipine group but no patient in group 1 did not need homologous blood transfusion. CONCLUSION. In comparison to nitrates, nifedipine showed some advantages in the treatment of hypertension during CABG: (1) it provided better myocardial performance; (2) it had a more reliable but not too long-lasting effect on elevated total peripherial resistance, leading to better hemodynamic stability; and (3) by not affecting the capacitance vessels it may necessitate fewer homologous blood transfusions.
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PMID:[Nifedipine versus nitroglycerin in aortocoronary bypass surgery. The effect on hemodynamics, kidney function and homologous blood requirement]. 153 39

This study presents the results of bypass grafting in 96 patients operated on for triple-vessel coronary artery disease between May 1988 and September 1990. In the first 54 patients a cold crystalloid solution was employed, and in the 42 more recent patients cold blood low-potassium cardioplegia was employed. There were no differences in postoperative cardiac index or left ventricular stroke work index. Yet, in patients with impaired prebypass left ventricular stroke work index, postbypass left ventricular performance correlated negatively with duration of aortic cross-clamping in the cold crystalloid group (r = -0.441, p = 0.045). In contrast, no correlation was found in the cold blood low-potassium group (r = 0.125, p = 0.587). The incidence of myocardial infarction, need for inotropic support, and need for intraaortic balloon counterpulsation were similar among the groups. Release of the myocardial isoenzyme creatine kinase-MB from 12 to 30 hours after operation was significantly less in the low-potassium blood cardioplegia group. The use of low-potassium blood cardioplegia resulted in a marked reduction in the operative administration of fluids (1,527 +/- 87 versus 3,511 +/- 148 mL; p less than 0.001). In conclusion, low-potassium cold blood cardioplegia is a simple and effective method of myocardial protection. The fact that left ventricular stroke work index recovery was not dependent on the duration of aortic occlusion and that release of the MB isoenzyme of creatine kinase was reduced in the low-potassium blood cardioplegia group implies better myocardial protection.
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PMID:Initial experience with low-potassium cold blood cardioplegia: a clinical comparative study. 155 72

To compare the effects of the University of Wisconsin solution with those of an extracellular crystalloid solution, Krebs-Ringer bicarbonate, as cardiac preservation media, we studied 35 adult dogs in an isolated heart preparation. Four groups of seven hearts were preserved in University of Wisconsin solution for 6 or 12 hours or in Krebs-Ringer bicarbonate solution for 6 or 12 hours. An additional group of seven hearts with no ischemia was used for a control group. In the four preservation groups, hearts were arrested by electrolyte solution (Normosol with potassium chloride, 20 mEq/L, added, 4 degrees C), flushed with 200 ml of the preservation solution, and then stored in the same solution at 1 degree to 2 degrees C. The hearts were mounted on an isolated heart preparation equipped with a computer-controlled servo-pump system that used a mock arterial system to modulate the aortic input impedance presented to the left ventricle. Left ventricular pressure-volume loops were measured on-line for 2 hours of reperfusion with autologous warm oxygenated blood. Elastance was derived from the end-systolic pressure-volume relationship, and diastolic compliance was derived from the end-diastolic pressure-volume relationship. The total left ventricular performance was assessed by the preload recruitable stroke work area, the slope, and its x-intercept, all of which derived from the stroke work (pressure-volume area)-end-diastolic volume relationship. Extended global ischemia had more deleterious effects on the end-diastolic than the end-systolic pressure-volume relationship. In confirmation with other studies, elastance did not accurately reflect the level of ventricular contractile dysfunction because of the significant amount of diastolic dysfunction. The preservation of myocardial systolic and diastolic functions, as demonstrated by the preload recruitable stroke work area and diastolic compliance, was better in the University of Wisconsin solution groups than in the Krebs-Ringer bicarbonate solution groups after 6 and 12 hours of preservation. In addition, 6 hours of preservation with University of Wisconsin solution maintained normal systolic and diastolic functions as compared with those of the control group. Preservation with University of Wisconsin solution prevented any myocardial edema formation; by contrast, this was significantly increased after 12 hours in Krebs-Ringer bicarbonate solution. Groups preserved with University of Wisconsin solution had less reperfusion injury as evidenced by the release of coronary sinus creatine kinase during reperfusion; they also had improved oxygen use during reperfusion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Superiority of the University of Wisconsin solution over simple crystalloid for extended heart preservation. A study of left ventricular pressure-volume relationship. 156 79

Age-related changes (e.g., decrease in plasma renin activity and total body potassium, increase in plasma catecholamines, volume depletion) need to be taken into account when selecting an antihypertensive agent for the elderly patient. A number of large scale clinical trials (e.g., Systolic Hypertension in the Elderly Program, Veterans Administration Cooperative Study, European Working Party on High Blood Pressure in the Elderly) have demonstrated that antihypertensive therapy with diuretics substantially reduced cardiovascular mortality and stroke incidence. However, since diuretics, even potassium-sparing agents, may induce hypokalemia, newer antihypertensive agents (angiotensin-converting enzyme [ACE] inhibitors and calcium antagonists) may also be appropriate as first-line monotherapy for this patient population. ACE inhibitors are effective antihypertensive agents and are associated with a lower rate of adverse effects than diuretics, beta blockers, and centrally acting agents. Nevertheless, periodic monitoring of serum potassium, creatinine levels, and renal function is advisable. An important feature of calcium antagonists is that they lower blood pressure with no negative effect on serum lipids or glucose metabolism. Typically, they have few side effects, peripheral edema being the most commonly reported. A recent double-blind randomized study comparing a new sustained release nifedipine formulation and the ACE inhibitor lisinopril found the 2 drugs equivalent in efficacy with no differences in the rate of adverse events.
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PMID:Hypertension in the elderly with a special focus on treatment with angiotensin-converting enzyme inhibitors and calcium antagonists. 157 76

The effect of salt intake on the hypertensive response to long-term infusion of endothelin-1 was investigated. Chronically instrumented male Sprague-Dawley rats (325-375 g) were used in a 15-day protocol that included 3 control days followed by 7 days of endothelin-1 infusion at 5.0 pmol.kg-1.min-1 and 5 days of recovery. Rats were maintained on either a normal sodium chloride intake (2.0 meq Na+ per day; normal sodium) or a high sodium chloride intake (6.0 meq Na+ per day; high sodium) throughout the protocol. Control rats received normal or high sodium intakes but not endothelin-1. In high-sodium rats, endothelin-1 produced a significant increase in mean arterial pressure and total peripheral resistance; a significant bradycardia was observed only on the first day after the start of the endothelin-1 infusion. Cardiac output, stroke volume, water balance, and urinary sodium and potassium excretion remained unchanged. Termination of endothelin-1 infusion resulted in rapid normalization of both arterial pressure and peripheral resistance. In contrast, normal sodium rats exhibited no alteration in mean arterial pressure, heart rate, total peripheral resistance, stroke volume, water balance, or urinary sodium and potassium excretion throughout the endothelin-1 infusion protocol. The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. These results indicate that endothelin-induced hypertension in conscious rats is a salt-dependent model of hypertension.
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PMID:Salt-dependency of endothelin-induced, chronic hypertension in conscious rats. 159 49

High potassium diets greatly reduce intimal and medial thickening in stroke-prone spontaneously hypertensive rats (SHRSP). In vascular smooth muscle cells, transforming growth factor-beta (TGF-beta) inhibits proliferation. To test whether high potassium diets decrease aortic thickening through TGF-beta, we measured TGF-beta-like activity in medium bathing aortas from rats fed either normal potassium or high potassium diets. Five-week-old SHRSP were fed 6% high NaCl diets containing either normal (0.5%) potassium (11 rats) or high (2.1%) potassium (14 rats) for 7 weeks. Aortas were freshly excised and perfused for 3 hours with tissue culture medium at ordinary arterial pressures. TGF-beta-like activity in the acid-activated perfusing medium was assessed using the growth inhibitory action on mink lung cells. Growth inhibition was assessed by [3H]thymidine incorporation. In the medium perfusing the outside of the aorta, the growth inhibitory rates were 2.5 times higher in high potassium SHRSP than in normal potassium SHRSP (-49% versus -20%, p less than 0.03). Antibodies to TGF-beta 1 and TGF-beta 2 were added to other aliquots and did not alter the results whatsoever. Thus, the difference in growth inhibition was not due to differences in TGF-beta. The high potassium aortas released 2.5 times more growth-inhibiting agents than the normal potassium aortas. The same pattern of growth inhibition was also seen using vascular smooth muscle cells rather than mink lung cells (r = +0.818, p less than 0.001, n = 13). The increased growth inhibition of high potassium aortas was not due to an increased release of heparin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High potassium diets greatly increase growth-inhibiting agents in aortas of hypertensive rats. 159 76

During myocardial ischemia there is a drop in high-energy phosphates in the myocardium. Cold potassium cardioplegia decreases but does not altogether prevent this reduction. Supplementation of cardioplegic solutions with the high-energy compound creatine phosphate (10 mmol/L) compared to plain cardioplegic solutions was investigated in this study. Thirty patients scheduled for aortic valve replacement were included. The patients were randomized to group I (creatine phosphate) or group II (control). Postoperative hemodynamic evaluation revealed no significant differences between the groups. However, group I exhibited a tendency toward a better stroke-work index (135 +/- 18% vs. 102 +/- 5% recovery 15 minutes after bypass and 145 +/- 16% vs. 119 +/- 11% recovery 105 min after bypass). There were fewer patients in group I (5/15) needing inotropic support compared to group II (9/14). The myocardial content of ATP and creatine phosphate showed no significant differences during ischemia and reperfusion. It is concluded that the myocardial protection during ischemia was sufficient to prevent significant reductions of myocardial ATP and creatine phosphate irrespective of supplementation with CP.
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PMID:Biochemical and functional effects of creatine phosphate in cardioplegic solution during aortic valve surgery--a clinical study. 163 61

The effect of fish oil on potassium efflux and basal tension in aortas from stroke prone spontaneously hypertensive rats (SHRSP) was evaluated. Four-week-old male Wistar-Kyoto rats (WKY) and SHRSP were divided into two groups: one received a 5% corn oil diet; the other a 5% menhaden oil diet. After 15 weeks, mean systolic blood pressure (mm Hg) was reduced in SHRSP-fish (202 +/- 5) compared to SHRSP-corn (227 +/- 4). Systolic pressure of WKY-fish (146 +/- 3) was not different from WKY-corn (151 +/- 4). Potassium efflux was evaluated with the isotope 86Rb. Basal 86Rb efflux from aorta of SHRSP-corn was evaluated compared to WKY-corn. Diltiazem or sodium nitroprusside decreased 86Rb efflux and basal tension in SHRSP. Basal 86Rb efflux, tension, and the magnitude of this diltiazem- or nitroprusside-induced inhibition were decreased in SHRSP-fish. At maximal diltiazem or nitroprusside concentration, 86Rb efflux from both SHRSP dietary groups was similar but still greater than control aorta. The IC50 values for diltiazem or nitroprusside effects on 86Rb efflux and tension were not altered by diet in SHRSP. Qualitatively similar changes in basal 86Rb efflux and tension were noted in WKY-fish compared to WKY-corn. These experiments demonstrate that dietary fish oil supplementation decreased calcium-sensitive 86Rb efflux and basal tension in vascular smooth muscle and suggest that these changes may contribute to the concomitant antihypertensive effect of dietary fish oil in SHRSP.
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PMID:Effects of dietary fish oil on Rb+ efflux from aorta of stroke prone spontaneously hypertensive rats. 163 20

Evidence from animal stroke models suggests that the proximate cause of neuronal degeneration after ischemia is massive release of glutamate and activation of NMDA receptors. However, in the physiologic presence of oxygen and glucose in the rat hippocampal slice preparation, the neurotoxicity of glutamate, as measured by inhibition of protein synthesis, requires high concentrations and is not prevented by glutamate receptor antagonists. Thus, the NMDA receptor-mediated neurotoxic effects of extracellular glutamate accumulation during ischemia might depend on additional factors, such as neuronal depolarization. In the experiments reported here, slices were exposed to glutamate in a medium intended to mimic the ionic conditions found during ischemia, high potassium (128 mM) and low sodium (26 mM). This depolarizing medium itself inhibited protein synthesis in a manner which was partially mediated by NMDA receptor activation, since it was significantly reversed by the noncompetitive NMDA antagonist, MK-801. Furthermore, the effect of glutamate under depolarizing conditions was also significantly decreased by MK-801, suggesting that glutamate was acting at NMDA receptors. Thus, depolarization appears to enhance the sensitivity of neurons to toxic NMDA receptor activation by glutamate. Under conditions that mimic ischemia, hypoxia plus hypoglycemia, a similar protective effect of NMDA receptor antagonists was observed. Depolarization and ischemia both appeared to attenuate the neurotoxicity of non-NMDA receptor agonists. It appears that under conditions of normal glucose and oxygen, high concentrations of bath applied glutamate inhibit protein synthesis at sites other than the NMDA receptor. However, when the Na+ gradient is decreased, as occurs during ischemia, glutamate's NMDA effects predominate. These findings suggest that ionic shifts may play a central role in permitting NMDA receptor-mediated ischemic neuronal damage.
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PMID:Enhancement of NMDA receptor-mediated neurotoxicity in the hippocampal slice by depolarization and ischemia. 165 99

This study was designed to test the hypothesis that intracoronary administration of esmolol can confer metabolic protection during coronary constriction or occlusion, without affecting hemodynamic parameters, in a canine model. Seventeen anesthetized open-chest dogs underwent direct cannulation of the left anterior descending coronary artery (LADa), its companion vein (LADv), and the distal circumflex vein (CFXv). LADa flow was measured with an electromagnetic flowmeter. Using a micrometer-driven snare around the LADa, flow was reduced by 50%, 75%, and 100% for 15 minutes, with 1 hour of normal flow before each constriction. In 7 dogs (group 1) chosen randomly, esmolol, 15 to 20 micrograms/kg/min, was infused continuously into the LADa; the rate was adjusted to maintain baseline hemodynamic values. The second group (10 dogs) was not treated with esmolol. Heart rate (HR), electrocardiogram (ECG), LADa flow, LV dP/dt, and aorta (Ao), pulmonary artery (PA), LADa, and left ventricular (LV) pressures were recorded continuously. Cardiac output (CO) (thermodilution) was measured and blood was sampled from all catheters before and after constrictions for analysis of glucose, lactate, sodium, potassium, and blood gases. Flow and pressure in the LADa in both groups decreased similarly during each corresponding constriction. Systolic LV pressure, LV dP/dt, and LV stroke work index were affected in both groups only during 100% constriction. HR, Ao, and PA pressures, and total and peripheral pulmonary resistances were affected similarly in both groups during each constriction. Myocardial lactate extraction and consumption were less negative (negative = net production and output) in the LAD perfusion bed during corresponding constrictions with esmolol than without it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased regional lactate production and output due to intracoronary continuous infusion of esmolol during acute coronary occlusion in dogs. 167 24


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