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To assess the hemodynamic properties of the new inhalational anesthetic sevoflurane, 22 dogs were chronically instrumented for measurement of heart rate, aortic, left ventricular and left atrial pressures, cardiac output, and coronary blood flow. Dogs were randomly assigned to two groups, receiving either 1.2 and 2 MAC of sevoflurane (n = 11) or isoflurane (n = 11). At 1.2 and 2 MAC, sevoflurane produced an increase in heart rate (+60 +/- 12% and +54 +/- 9%, respectively), dose-dependent aortic hypotension (-22 +/- 4% and -38 +/- 4%, respectively), systemic vasodilation (-22 +/- 5% and -19 +/- 5%, respectively), dose-dependent decrease in stroke volume (-31 +/- 6% and -48 +/- 4%, respectively), and left ventricular dP/dt (-40 +/- 4% and -61 +/- 10%, respectively). Cardiac output decreased only at 2 MAC (-17 +/- 6%). Finally, coronary blood flow increased at 1.2 MAC of sevoflurane (+29 +/- 8%). Except for heart rate, sevoflurane and isoflurane produced similar effects. At 1.2 MAC, sevoflurane produced a greater increase in heart rate than isoflurane (+60 +/- 12% vs. +33 +/- 9%). The authors conclude that, except for heart rate, the effects of sevoflurane on cardiac function and coronary blood flow are almost identical to those induced by isoflurane in the chronically instrumented dog.
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PMID:Effects of sevoflurane and isoflurane on cardiac and coronary dynamics in chronically instrumented dogs. 232 83

To determine the cardiovascular actions of drugs commonly combined with inhalation anesthetics, we administered one drug from each of several classes of adjuvants to seven swine already anesthetized with equipotent concentrations (1.2 MAC) of desflurane, formerly I-653, a new inhaled anesthetic, or isoflurane. Succinylcholine (1 and 2 mg/kg), atracurium (0.6 mg/kg), and atropine (5 micrograms/kg) plus edrophonium (5 mg/kg) had no cardiovascular effects. Fentanyl was given in amounts that decreased MAC for the inhaled anesthetics by 25%-35%. A dose of 50 micrograms/kg IV had no cardiovascular effects during either anesthetic, whereas 100 micrograms/kg IV modestly increased systemic vascular resistance without changing other variables. Naloxone (100 micrograms/kg IV) during infusion of fentanyl decreased systemic vascular resistance and increased cardiac output during both desflurane and isoflurane anesthesia, increased heart rate during only isoflurane anesthesia, and did not affect mean arterial blood pressure during either anesthetic. Thiopental (2.5 and 5.0 mg/kg IV) decreased mean aortic blood pressure, cardiac output, stroke volume, and systemic vascular resistance during both anesthetics without altering heart rate or left- or right-sided cardiac filling pressures. The addition of 60% nitrous oxide caused no cardiovascular changes during desflurane anesthesia, but increased systemic vascular resistance and decreased cardiac output and stroke volume during isoflurane without altering heart rate or cardiac preload. We conclude that the usual clinical doses of adjuvants commonly administered during anesthesia have no untoward cardiovascular actions during 1.2 MAC desflurane or isoflurane anesthesia in swine.
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PMID:Cardiovascular actions of common anesthetic adjuvants during desflurane (I-653) and isoflurane anesthesia in swine. 237 16

Development of an index of myocardial contractility that is both load independent and easily quantified in vivo has been a difficult task. Recently, three measures of contractile state have been advocated that appear to fulfill these requirements: the end-systolic pressure-length relationship (ESPLR), the ESPLR area, and regional preload recruitable stroke work (PRSW). Because the effects of halothane and isoflurane on these indices of contractility have yet to be studied, the purpose of this investigation was to compare the effects of these volatile anesthetics on contractile function as evaluated via these techniques in chronically instrumented dogs. Because autonomic nervous system tone substantially influences systemic hemodynamics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Four groups comprised the 36 experiments that were performed with nine dogs. Following inhalational induction, the dogs were maintained on 1.5 MAC and 2 MAC of halothane or isoflurane. Pressure-length loops were generated after 1 h of equilibration using preload reduction via partial inferior vena caval occlusion or afterload augmentation by a phenylephrine infusion. The PRSW and ESPLR were then calculated, respectively. Slope and length intercept variables obtained from the ESPLR failed to significantly change from control with increasing levels of anesthetic depth despite substantial decreases in other indices of contractility. However, combination of slope and length intercept parameters into the ESPLR area model proved to be a sensitive and easily calculable measure of depressed myocardial function. Similarly, regional PRSW slope precisely reflected changes in contractile state when halothane (62 +/- 10 for control to 30 +/- 6 erg.cm-2.10(-3).mm-1 at 2 MAC) or isoflurane (83 +/- 14 for control to 55 +/- 8 erg.cm-2.10(-3).mm-1 at 2 MAC) were administered. The PRSW slope also demonstrated a significant difference in depressed contractility when equianesthetic concentrations of halothane and isoflurane were compared (63 +/- 7% of control with halothane versus 86 +/- 4% of control with isoflurane at 1.5 MAC; 50 +/- 5% of control with halothane versus 70 +/- 6% of control with isoflurane at 2 MAC). The ESPLR area also accurately demonstrated the differential depression in contractile function suggested by recent in vitro studies when equianesthetic doses of halothane and isoflurane were compared in vivo. Therefore, while ESPLR slope and length intercept variables fail as indices of myocardial contractility, ESPLR area and regional PRSW slope were shown to be useful indicators of contractile state in the conscious and anesthetized dog.
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PMID:Comparison of end-systolic pressure-length relations and preload recruitable stroke work as indices of myocardial contractility in the conscious and anesthetized, chronically instrumented dog. 201 75

In rats with incomplete cerebral ischemia the effects of 70% N2O alone, isoflurane alone (0.5 and 1 MAC), and the combination of N2O + isoflurane on neurologic outcome, neurohistopathology, and EEG were compared. Moderate and severe ischemia were produced by right carotid artery occlusion combined with hemorrhagic hypotension (moderate ischemia, MAP = 30 mmHg, FIO2 = 0.30; severe ischemia, MAP = 25 mmHg, FIO2 = 0.20). Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke), and neurohistopathology was evaluated using a 40-point scale from 0 = normal to 40 = total hemisphere infarct at the level of the caudate nucleus in coronal section. Compared with N2O alone, isoflurane (0.5 and 1 MAC) improved neurologic outcome following moderate ischemia (P less than 0.05). Isoflurane also decreased histopathologic damage following moderate ischemia (N2O control = 33 +/- 1 vs. 0.5 MAC isoflurane = 11 +/- 4 and 1 MAC isoflurane = 12 +/- 3, P less than 0.05), whereas only 0.5 MAC isoflurane decreased histopathologic damage following severe ischemia (N2O control = 38 +/- 1 vs. 0.5 MAC isoflurane = 25 +/- 5; P less than 0.05) Adding N2O to 0.5 MAC isoflurane attenuated the neurologic protective effect of isoflurane alone and increased histopathologic damage following both moderate and severe ischemia (moderate = 23 +/- 5, severe = 37 +/- 2; both P greater than 0.05 compared with N2O controls). The effect of adding 70% N2O to isoflurane on cerebral blood flow (CBF) and cerebral oxygen consumption(CMRO2) was also evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The interaction of nitrous oxide and isoflurane with incomplete cerebral ischemia in the rat. 271 9

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two-dimensional echocardiographic dimensions of the left ventricle and pulmonary artery blood flow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg.kg-1 IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in both groups, but decreases in EF (32 +/- 5 per cent vs 18 +/- 5 per cent) and increases in LVEDV (18 +/- 7 per cent vs 7 +/- 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 +/- 6 per cent), than during isoflurane anaesthesia (18 +/- 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 +/- 4 per cent) following atropine in both groups, and CO returned to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children. 272 Aug 67

Catecholamine and renin-angiotensin responses to enflurane- or isoflurane-hypotensive anesthesia were compared in a randomized study. Two groups of 10 patients undergoing total hip arthroplasty were premedicated with morphine hydrochloride (0.1 mg/kg). Anesthesia was induced with thiopental and the trachea intubated after pancuronium. Equal concentrations of each volatile agent (1.3 MAC) were administered until mean arterial blood pressure decreased to 50-60 mm Hg. Hemodynamic data and blood samples for measurements of plasma renin activity (PRA) and plasma epinephrine (E) and norepinephrine (NE) concentrations were collected 1) after induction and intubation but before the start of isoflurane or enflurane; 2) 15 min (T15) after the start of isoflurane or enflurane administration; and 3) 45 min (T45) after the start of isoflurane or enflurane administration. The desired level of hypotension was achieved at T15 with isoflurane and at T45 with both anesthetics. When hypotension was achieved, cardiac index and stroke index were significantly lower in the enflurane group while systemic vascular resistance index was lower in the isoflurane group. Increases in E and NE levels above baseline levels were significantly greater in the isoflurane group than in the enflurane group. Use of isoflurane to induce hypotension is associated with more rapid induction of hypotension, less depression of cardiac output, and better preservation of homeostatic responses than is use of enflurane.
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PMID:Hypotensive anesthesia with isoflurane and enflurane during total hip replacement: a comparative study of catecholamine and renin angiotensin responses. 231 93

This study, in open-chested dogs, sought to explore the relationship between whole-body oxygen delivery and oxygen consumption during anaesthesia, using increasing concentrations of halothane, enflurane and isoflurane. Results indicate that the cardiac index and oxygen delivery became critical at less than 1 MAC (minimal alveolar concentration of anaesthetic) for the three commonly used vapours. Halothane caused the least depression of contractility, but the stroke volume was reduced by the well-maintained afterload at 1 MAC. Enflurane and isoflurane were associated with more depression of contractility, but the cardiac output was maintained by an increase in heart rate in the case of isoflurane and reduced mean arterial pressure during the use of enflurane.
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PMID:The effect of halothane, enflurane and isoflurane on the circulation. 279 92

The haemodynamic effects of enflurane (1.7% and 3.4% expiratory concentrations) were investigated in sheep (n = 6) pretreated with an infusion of metoprolol (0.2 mg X kg-1 X h-1 for 5 days) and in control animals (n = 6). Chloralose was used as basal anaesthetic. A 90 s apnoea period was included in the experiment to evaluate further the possible side-effects of long-term metoprolol treatment in combination with enflurane anaesthesia. MAC 1.0 for enflurane in the sheep was found at 1.45% end-tidal concentration by separate measurements. Before enflurane administration, the only significant differences between the two groups of animals were a lower systemic vascular resistance and a higher stroke volume during metoprolol treatment. Enflurane abolished these discrepancies in a dose-dependent fashion and similar cardiovascular depression was observed in both groups of animals at 3.4% expiratory concentration of enflurane. Metoprolol did not significantly affect the hypertensive response to apnoea during chloralose anaesthesia alone. At enflurane 1.7% expiratory concentration the apnoea response was small and only the metoprolol-treated animals showed a significant increase in left ventricular end-diastolic pressure. We conclude that 5 days of pretreatment with metoprolol in the sheep model does not significantly impair cardiovascular performance during enflurane anaesthesia.
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PMID:Cardiovascular effects of enflurane and asphyxia during long-term beta 1-adrenoceptor blockade. 286 1

Two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular function in 31 unmedicated infants and small children. In 15 patients, the cardiovascular effects of equipotent levels of halothane were compared with and without N2O. In 16 patients, the cardiovascular effects of isoflurane with and without N2O were compared. Prior to anesthesia induction, cardiovascular measurements of heart rate (HR), mean blood pressure (MBP), and two-dimensional and pulsed Doppler echocardiography were recorded. The echocardiographic measurements were used to determine cardiac output (CO), stroke volume (SV), ejection fraction (EF), and left ventricular end-diastolic and end-systolic volume (LVEDV and LVESV). Twenty minutes after mask inhalation induction with halothane or isoflurane with N2O and O2 (3:2 liters/min), cardiovascular measurements were repeated with end-expired halothane or isoflurane maintained at 0.9 MAC. A third set of cardiovascular data was collected 10 minutes after the discontinuation of N2O, with inspired isoflurane or halothane levels in O2 (5 liters/min) increased to maintain 1.5 MAC end-expired levels. Ventilation was controlled throughout the study period and the study was completed before intubation and the start of elective surgery. Heart rate and MBP decreased to similar degrees below awake levels in both patient groups during N2O with halothane or isoflurane. When N2O was discontinued and end-expired levels of halothane or isoflurane increased, MBP remained at levels observed during N2O-O2 with halothane or isoflurane. Heart rate increased during isoflurane in O2. Cardiac output decreased significantly and similarly below awake levels during both halothane of isoflurane with and without N2O.
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PMID:Nitrous oxide: cardiovascular effects in infants and small children during halothane and isoflurane anesthesia. 318 95

To assess the dose-response effects of isoflurane and halothane anesthesia on hemodynamics and coronary artery reactivity, the authors studied myocardial hyperemic responses following brief single artery flow arrests in 21 open chest, isocapnic swine in which arterial blood pressures and cardiac outputs were recorded. A specially designed Doppler probe was used to measure the peak and time course of coronary blood flow velocity in the left anterior descending coronary artery (LAD) after 15-s LAD occlusions. The ratio of peak velocity of blood flow to resting velocity (coronary reserve), relative repayment of flow debt, and duration of hyperemic responses were studied. Surgery was performed at MAC end-tidal concentrations ([Et]isoflurane = 1.45%. [Et]halothane = 1.25%) of isoflurane (n = 7) or halothane (n = 7), and recordings were made after 15-min steady state [Et]agent at 0.5, 1, 1.25, 1.5, 1.75, 2 MAC, and further 0.5 MAC increments until the demise of each animal. To compare coronary reactivity at similar coronary pressures, an aortic snare was used to elevate arterial pressures in a third group of halothane anesthesized pigs (n = 7) to those in the previously studied isoflurane group at each MAC level. There were three major differences between halothane and isoflurane. First, cardiac depression (reduction in arterial pressure, cardiac output, and stroke volume) was less with isoflurane compared with halothane anesthesia. Second, with halothane anesthesia, there was a marked decrease in coronary reactivity independent of coronary perfusion pressures with marked, dose-dependent reductions in both coronary reserve and relative flow repayment. During isoflurane anesthesia, coronary reactivity and coronary reserve was well preserved within physiologic limits up to 1.75 MAC [Et]. Third, halothane anesthesized pigs died in cardiac collapse at much lower agent concentrations than with isoflurane (no animals survived 1.75 MAC halothane, whereas all animals survived 2.5 MAC isoflurane). Therefore, pigs anesthesized with isoflurane had greater coronary reserve, better preserved cardiac function, and greater tolerance to increasing agent concentration than pigs anesthesized with halothane.
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PMID:Comparative coronary vascular reactivity and hemodynamics during halothane and isoflurane anesthesia in swine. 334 77


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