UMLS:C0038454 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

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

We have studied haemodynamic responses to 0, 0.25, 0.5, 0.75 and 1 MAC isoflurane administration in 10 patients during a zero-order propofol infusion and normocapnia. Isoflurane reduced mean arterial pressure (MAP), systemic vascular resistance and left ventricular stroke work in a dose-dependent manner (29%, 38% and 33%, respectively, at 1 MAC), while cardiac output (CO), stroke volume (SV) and heart rate were not affected significantly. Mean pulmonary artery pressure, pulmonary vascular resistance and right ventricular stroke work decreased by 13%, 10% and 17%, respectively (not significant). Pulmonary capillary wedge pressure and central venous pressure were affected minimally, while intrapulmonary shunting and PaO2 remained constant. It is concluded that administration of isoflurane during infusion of propofol caused a dose-dependent decrease in MAP as a result of afterload reduction without modification in CO or SV.
...
PMID:Haemodynamic effects of isoflurane during propofol anaesthesia. 163

The cardiovascular actions of three concentrations of desflurane (formerly I-653), a new inhalation anesthetic, were examined in 12 unmedicated normocapnic, normothermic male volunteers. We compared the effects of 0.83, 1.24, and 1.66 MAC desflurane with measurements obtained while the same men were conscious. Desflurane caused a dose-dependent increase in right-heart filling pressure and a decrease in systemic vascular resistance and mean systemic arterial blood pressure. As measured by echocardiography, left ventricular end-diastolic area did not change except for a small increase at 1.66 MAC desflurane, and systolic wall stress was less at all concentrations of desflurane than during the conscious state. Desflurane did not change cardiac index or left ventricular ejection fraction. Heart rate did not change at 0.83 MAC, but progressively increased with deeper desflurane anesthesia. Stroke volume index was less at all concentrations of desflurane than while the men were conscious, but desflurane did not alter the velocity of ventricular circumferential fiber shortening. Mixed venous blood PO2 and oxyhemoglobin saturation were higher during all concentrations of desflurane anesthesia than during the conscious state. No volunteer developed a metabolic acidosis. We conclude that desflurane with controlled ventilation and constant PaCO2 causes cardiovascular depression, as indicated by the increased cardiac filling pressure and decreased stroke volume index and by no change in the velocity of circumferential fiber shortening in the presence of decreased systolic wall stress. However, cardiac output is well maintained, and heart rate does not increase at light levels of anesthesia. The cardiovascular actions of 0.83 and 1.66 MAC desflurane were also reexamined in 6 of the 12 men during the seventh hour of anesthesia. Prolonged desflurane anesthesia resulted in lesser cardiovascular depression than was evidenced during the first 90 min. The measures of cardiac filling (central venous pressure and left ventricular end-diastolic cross-sectional area) did not differ between the early and late periods of anesthesia. Systemic vascular resistance decreased further during the late period, but systolic wall stress did not differ between the two time periods. During the seventh hour of desflurane anesthesia, heart rate and cardiac index were higher at both anesthetic concentrations than during the first 90 min of anesthesia. Left ventricular ejection fraction and velocity of fiber shortening did not change with duration of desflurane anesthesia. Oxygen consumption, oxygen transport, the ratio of the two, mixed venous PO2, and mixed venous oxyhemoglobin saturation (SO2) increased late in the anesthetic in comparison with the first 90 min.
...
PMID:Cardiovascular actions of desflurane in normocarbic volunteers. 185 29

We determined the cardiovascular effects of 0.91, 1.34, and 1.74 MAC of desflurane/nitrous oxide anesthesia (60% inspired nitrous oxide contributed 0.5 MAC at each level) in 12 healthy, normocapnic male volunteers. Desflurane/nitrous oxide anesthesia decreased systemic blood pressures, cardiac index, stroke volume index, systemic vascular resistance, and left ventricular stroke work index, and increased pulmonary arterial pressures and central venous pressure in a dose-dependent fashion, while heart rate was 10%-12% and mixed venous oxygen tension was 2-4 mm Hg higher at all MAC levels than at baseline (awake). Desflurane/nitrous oxide anesthesia modestly increased left ventricular end-diastolic cross-sectional area (preload) and decreased velocity of left ventricular circumferential fiber shortening, systolic wall stress (afterload), and area ejection fraction; this combination of changes indicates myocardial depression. At approximately comparable MAC levels, heart rate was lower and systemic blood pressures, central venous pressure, left ventricular stroke work index, and systemic vascular resistance usually were significantly higher during anesthesia with desflurane and nitrous oxide than during desflurane anesthesia alone (same volunteers, data collected in crossover design). After 7 h of anesthesia, regardless of the background gas, somewhat less cardiovascular depression and/or modest stimulation was apparent: cardiac index, area ejection fraction, and velocity of left ventricular circumferential fiber shortening recovered to or toward awake values, whereas heart rate was further increased. Evidence of circulatory insufficiency did not develop in any volunteers during the study. Segmental left ventricular function was normal at baseline, and no segmental wall-motion abnormalities, ST-segment change, or dysrhythmias developed.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Hemodynamic effects of desflurane/nitrous oxide anesthesia in volunteers. 185 30

We investigated the cardiovascular actions of desflurane (formerly I-653) during spontaneous ventilation. We gave 0.8-0.9, 1.2-1.3, and 1.6-1.7 MAC desflurane in oxygen (n = 6) and in 60% nitrous oxide, balance oxygen (n = 6) to unmedicated healthy male volunteers. Both anesthetic regimens decreased ventilation, increased partial pressure of arterial carbon dioxide, and produced similar cardiovascular changes. In comparison with values obtained when the volunteers were conscious, desflurane anesthesia with spontaneous ventilation decreased systemic vascular resistance and mean arterial blood pressure. Cardiac index, heart rate, stroke volume index, and central venous blood pressure increased. Left ventricular ejection fraction increased at 0.83 MAC desflurane in oxygen, and otherwise did not differ from the conscious value. The velocity of ventricular circumferential fiber shortening, estimated by echocardiography, increased with desflurane in oxygen but did not change with desflurane in nitrous oxide. Oxygen consumption increased during desflurane and oxygen anesthesia, but not when nitrous oxide plus oxygen was the background gas. Desflurane increased oxygen transport, the ratio of oxygen transport to oxygen consumption, mixed venous partial pressure of oxygen, and oxyhemoglobin saturation. The cardiovascular changes with desflurane during spontaneous ventilation differ from those during controlled ventilation. With both background gases, spontaneous ventilation, in comparison with controlled ventilation, increased cardiac index, stroke volume, central venous pressure, left ventricular ejection fraction, velocity of circumferential fiber shortening, oxygen transport, and the ratio of oxygen transport to oxygen consumption but did not change mean arterial blood pressure except at 1.66 MAC desflurane in oxygen (when it was higher with spontaneous than with controlled ventilation).
...
PMID:Cardiovascular actions of desflurane with and without nitrous oxide during spontaneous ventilation in humans. 185 31

The purpose of this study was to compare the cardiovascular effects of halothane when used alone at increasing doses (1.2, 1.45 and 1.7 minimum alveolar concentration, MAC) to those produced with equipotent doses of halothane after potentiation of the anesthetic effect with acepromazine (ACP) sedation (45% reduction of halothane MAC). Six healthy mature dogs were used on three occasions. The treatments were halothane and intramuscular (IM) saline (1.0 mL), halothane and ACP (0.04 mg/kg IM), or halothane and ACP (0.2 mg/kg IM). Anesthesia was induced and maintained with halothane in oxygen and the dogs were prepared for the collection of arterial and mixed venous blood and for the determination of heart rate, systolic, diastolic and mean arterial pressure, mean pulmonary arterial pressure (PAP), central venous pressure and cardiac output. Following animal preparation the saline or ACP was administered and positive pressure ventilation instituted. Twenty-five minutes later the dogs were exposed to the first of three anesthetic levels, with random assignment of the sequence of administration. At each anesthetic level, measurements were obtained at 20 and 35 min. Calculated values included cardiac index, stroke index, left ventricular work, systemic vascular resistance, arterial oxygen content, mixed venous oxygen content, oxygen delivery and oxygen consumption. Heart rate was significantly higher with halothane alone than with both halothane-ACP combinations and was significantly higher with high dose ACP compared to low dose ACP. Systolic and mean blood pressures were lowest with halothane alone and highest with 0.2 mg/kg ACP, the differences being significant for each treatment. Oxygen uptake and PAP were significantly lower in dogs treated with ACP. It was concluded that ACP does not potentiate the cardiovascular depression that accompanies halothane anesthesia when the resultant lower dose requirements of halothane are taken into consideration.
...
PMID:Comparative hemodynamic effects of halothane and halothane-acepromazine at equipotent doses in dogs. 188 90

In anesthesiology and intensive care medicine it is often necessary to treat disorders involving cardiac failure or low-output syndrome. However, in patients who are endangered by ischemic heart disease, any pharmacologic therapy with positive inotropic agents should improve cardiac output without increasing myocardial oxygen demand significantly: the heart should perform its task as efficiently as possible. In the present study a mathematical model of myocardial efficiency was developed. The implications of this theoretical concept of myocardial efficiency were evaluated in animal experiments. THEORETICAL MODEL. Cardiac efficiency is predominantly dependent on preload, afterload, and inotropic state. Quantitatively, it can be calculated from end-diastolic volume, left ventricular systolic pressure (Psyst), stroke volume (SV), and ejection time. The implications of the theoretical analysis are: (1) the inotropic state, which leads to optimal myocardial efficiency, is specifically determined by preload and afterload: for each preload and afterload one matched inotropic state is necessary to achieve optimal efficiency; (2) an increase in blood pressure leads to a decrease in myocardial efficiency even if the inotropic state is optimally matched to preload and afterload; and (3) an increase in end-diastolic volume improves the efficiency of myocardial pump work. ANIMAL EXPERIMENTS. The validity of the theoretical model was studied in animal experiments with emphasis on the following items: (1) is theoretically optimal efficiency of myocardial pump work achieved by physiologic regulation of myocardial performance? (2) how does sympathetic stimulation influence myocardial efficiency? and (3) how do cardiodepressive agents such as beta-blockers or volatile anesthetics influence myocardial efficiency? METHODS. Experiments were performed on nine mongrel dogs after induction of piritramide--nitrous oxide anesthesia. Standard hemodynamics: heart rate, Psyst, maximum left ventricular pressure rise (dP/dtmax), and SV (thermodilution) as well as coronary blood flow (pressure difference catheter) and myocardial oxygen consumption (Fick principle) were measured. In order to create a broad range of different hemodynamic settings, blood withdrawal and retransfusion of blood and/or colloid osmotic solutions were used to modify intravascular volume. Additionally, the inotropic state was varied by infusion of catecholamines (isoproterenol 0.4-0.8 microgram.kg-1.min-1 or norepinephrine 1-2 micrograms.kg-1.min-1). Experimental myocardial failure was induced by adding halothane (0.8-1.5 MAC) to the basic anesthesia, beta-blockade with propranolol (125-250 micrograms.kg-1), and combination of beta-blockade with a pressure load imposed on the myocardium (propranolol 125-250 micrograms.kg-1 + norepinephrine 1-2 micrograms.kg-1.min-1). RESULTS. During variation of the intravascular blood volume by normo-, hypo-, and hypervolemia, the myocardial efficiency very closely matched the theoretically predicted values of optimal efficiency: the average observed efficiency was 98.8% of predicted optimal efficiency. Increasing afterload with norepinephrine did not alter this close relationship, although absolute values of efficiency decreased as predicted by the theoretical model. Application of isoproterenol resulted in SVs that exceeded optimal values by 41.5%. In contrast, during experimental myocardial failure SVs were too small to achieve the necessary values for optimal pump work; observed myocardial efficiency was therefore significantly lower than optimal efficiency. CONCLUSIONS. For pharmacological interventions, it can be concluded that maximal efficiency of cardiac pump work requires maximal end-diastolic filling in combination with minimal afterload. (ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:[The energetics and economics of the cardiac pump function]. 195 41

Seven mongrel dogs were chronically instrumented for the measurement of aortic and left ventricular blood pressures, cardiac output, left ventricular wall thickening, left ventricular dP/dt, and circumflex coronary, renal, hepatic and portal blood flows under the influence of desflurane (D) and isoflurane (I). Administration of the two anesthetics, was randomized, as was the order of the concentrations administered. Each dog was studied awake and at 1.2, 1.4, 1.75, and 2.0 MAC of each anesthetic on different days. Both anesthetics decreased mean arterial pressure, stroke volume, systemic vascular resistance, left ventricular dP/dt, and wall thickness. The decreases were dose-dependent for mean arterial pressure (percent of awake values: D 78, I 85 at 1.2 MAC, and D 67, I 69 at 2.0 MAC); stroke volume (D 66, I 72 at 1.2 MAC, and D 52, I 57 at 2.0 MAC); dP/dt (D 61, I 64 at 1.2 MAC, and D 46, I 49 at 2.0 MAC); and WT (D 68, I 70 at 1.2 MAC, and D 47, I 60 at 2.0 MAC). Systemic vascular resistance decreased approximately the same at 1.2 MAC (D 71, I 87%) as at 2.0 MAC (D 71, I 79%). Heart rate increased but also not in a dose-dependent fashion (percent of awake values: D 177, I 145 at 1.2 MAC, and D 176, I 155 at 2.0 MAC). Coronary blood flow was increased by both anesthetics at all concentrations (percent of awake values: I 136 at 1.2 MAC and 161 at 2.0 MAC of awake, and D 131 at 1.2 MAC and 138 at 2.0 MAC.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Comparison of the effects of isoflurane and desflurane on cardiovascular dynamics and regional blood flow in the chronically instrumented dog. 200 Oct 36

The direct effects of desflurane on myocardial contractility in vivo have not been characterized. Therefore, the purpose of this investigation was to systematically examine the effects of desflurane on myocardial contractile function and compare these actions to equianesthetic concentrations of isoflurane in chronically instrumented dogs. Contractility was evaluated using an established index of inotropic state, the preload recruitable stroke work (PRSW) versus end-diastolic segment length (EDL) relationship. Since autonomic nervous system tone may influence the hemodynamic effects of the volatile anesthetics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Two groups of experiments were performed with seven dogs instrumented for measurement of aortic and left ventricular pressure, the maximum rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. After autonomic nervous system blockade, ventricular pressure-segment length loops were generated using preload reduction via partial inferior vena caval occlusion. The PRSW versus EDL relation was calculated from the pressure-length loops. Dogs were then anesthetized with 1.0 or 1.5 MAC desflurane or isoflurane in a random fashion, and measurements were repeated after 30 min of equilibration at each anesthetic concentration. The PRSW versus EDL slope reflected similar changes in contractile state when desflurane or isoflurane was administered (53 +/- 4 during control to 26 +/- 4 erg.cm-2 x 10(-3).mm-1 at 1.5 MAC desflurane, and 57 +/- 5 during control to 31 +/- 3 erg.cm-2 x 10(-2).mm-1 at 1.5 MAC isoflurane). In conclusion, desflurane and isoflurane produced equivalent direct decreases in myocardial contractility.
...
PMID:Influence of volatile anesthetics on myocardial contractility in vivo: desflurane versus isoflurane. 202 Dec 8

The effects of four commonly used anesthetic agents, halothane, isoflurane, alfentanil, and ketamine, on cardiovascular function and oxygen balance were studied in a dog model of septic shock. After initial pentobarbital administration, the dogs were given Escherichia coli endotoxin (3 mg/kg) and, after 30 min, fluids to restore cardiac filling pressures to baseline levels. This resulted in a low resistance shock in all animals. Dogs were then given for 2 h either halothane (n = 9, 0.5 MAC), isoflurane (n = 9, 0.5 MAC), or alfentanil (n = 9, 150 micrograms/kg IV plus 2 micrograms.kg-1.min-1) or ketamine (n = 9, 2 mg/kg IV plus 0.2 mg.kg-1.min-1) or no anesthetic (control: n = 9). Mean arterial pressure increased in the control group (+11 +/- 18 mm Hg) and with ketamine (+10 +/- 20 mm Hg), remained unchanged with isoflurane (-2 +/- 11 mm Hg), and decreased with halothane (-22 +/- 23 mm Hg) and alfentanil (-9 +/- 23 mm Hg). Heart rate tended to increase in the control group but decreased with the four anesthetic agents, especially with alfentanil and halothane. Cardiac index and left ventricular stroke work index increased in the control group and in each anesthetic group except the halothane group. Systemic vascular resistance decreased in all groups except in the ketamine group. In the control group, the increase in cardiac index was associated with significant increases in oxygen delivery and consumption, and with a significant decrease in blood lactate levels. There was a dramatic decrease in oxygen consumption in all anesthetic groups, whereas oxygen delivery failed to increase only with halothane. Blood lactate increased significantly with halothane (5.0 +/- 1.5 to 6.3 +/- 1.4 mM/L) and isoflurane (4.8 +/- 1.1 to 5.3 +/- 1.2 mM/L), remained unchanged with alfentanil (4.5 +/- 1.5 and 4.6 +/- 0.8 mM/L), and tended to decrease with ketamine (4.9 +/- 1.4 to 4.5 +/- 1.4 mM/L). In conclusion, among the four anesthetic agents tested, halothane had the least desirable effects. Ketamine best preserved cardiovascular function and appeared to have the least deleterious effects on the hypoxic tissues. Thus, ketamine could be the anesthetic agent of choice in septic shock.
...
PMID:Comparison of halothane, isoflurane, alfentanil, and ketamine in experimental septic shock. 218 26

Using a rat model of incomplete cerebral ischemia the effects of isoflurane (iso) and methohexital (metho) were compared with those of 70% nitrous oxide controls (N2O). Two levels of incomplete cerebral ischemia were produced by right carotid occlusion plus hypotension for 30 min: moderate = 30 mmHg, FIO2 = 0.30; severe = 25 mmHg, FIO2 = 0.20. The iso doses (1 and 2 MAC) and metho doses (0.01 and 0.1 mg.kg-1.min-1) were tested at each ischemic level. These iso and metho doses were selected because without ischemia they produced similar decreases in cerebral oxygen consumption (CMRO2) compared with that produced in N2O controls. In the absence of ischemia, the electroencephalogram (EEG) was suppressed by 0.01 mg.kg-1.min-1 metho and 1 MAC iso and showed burst-suppression with 0.1 mg.kg-1.min-1 metho and 2 MAC iso. The EEG was further depressed by ischemia under all anesthetic conditions. Neurologic outcome was evaluated for 3 days following incomplete cerebral ischemia by using a graded deficit score (0 = normal, 5 = death associated with stroke). Following moderate ischemia all four anesthetic treatments improved outcome compared with N2O controls, but after severe ischemia only 2 MAC iso significantly improved outcome. Neurohistopathology was evaluated on a scale of 0 to 40, 24 h after ischemia. The neurohistopathology score was significantly improved by all four anesthetic treatments compared with N2O following moderate ischemia and was better with 2 MAC iso compared with 0.1 mg.kg-1.min-1 metho after both moderate and severe ischemia. These results show that both iso and metho improve outcome from cerebral ischemia compared with that associated with N2O, but only 2 MAC iso resulted in an improved outcome following severe ischemia. This difference in outcome between the two anesthetics may be related to greater neuronal depression with iso, which may occur with little difference in cerebral metabolic depression.
...
PMID:Comparison of methohexital and isoflurane on neurologic outcome and histopathology following incomplete ischemia in rats. 229 37

<< Previous 1 2 3 4 5 6 7 Next >>