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

The studies were undertaken to determine whether isoflurance inhalation is associated with a degree of beta-adrenergic action that is potentially important in clinical situations, and to compare the circulatory tolerance to isoflurane and halothane in dogs following beta blockade. We measured arterial and pulmonary artery pressure, left and right ventricular filling pressure, heart rate and cardiac output, and derived stroke volume and systemic and pulmonary vascular resistances in 13 mongrel dogs. The haemodynamic response to 1 MAC and 2 MAC isoflurane was studied in seven dogs and was similar before and after propranolol 0.1mg/kg i.v. In six dogs, propranolol 0.5mg/kg caused no significant changes in the circulatory response to 1 MAC and 2 MAC isoflurane or 1 MAC halothane. However, in three dogs, administration of 2 MAC halothane after propranolol 0.5mg/kg resulted in such profound circulatory depression as to preclude further study. These data suggest that (a) isoflurane possesses no clinically important beta-adrenergic stimulating activity; (b) there is no adverse drug interaction upon the circulation with the combination of isoflurane and propranolol; (c) in the presence of moderated profound beta-adrenergic blockade, 2 MAC isoflurane may be tolerated better than 2 MAC halothane.
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PMID:Lack of beta-adrenergic activity of isoflurane in the dog: a comparison of circulatory effects of halothane and isoflurane after propranolol administration. 1 56

The cardiocirculatory responses to equianaesthetic concentrations (MAC 0.5 and MAC 1.0 plus 67% N2O) of halothane, methoxyflurane, enflurane and isoflurane were studied in a total of 35 closed-chest dogs during ventilation controlled to produce normocapnia. Each anaesthetic produced a dose-related decrease in mean arterial pressure and in values reflecting cardiac function. These included cardiac output, stroke volume, left ventricular max dp/dt and ejection fraction. Isoflurane seemed slightly less depressant to the heart than the other 3 anaesthetics. Total peripheral resistance remained nearly unaffected during halothane and methoxyflurane anaesthesia but decreased significantly with MAC 1.0 enflurane and isoflurane. There was no change in heart rate at low anaesthetic concentrations. The deeper levels of anaesthesia were associated with moderate increases in heart rate. In spite of the obvious depression of myocardial contractility there was a fall in pulmonary artery and left ventricular end-diastolic pressures and in left ventricular end-diastolic volumes with each of the agents. We take this as an expression of decreased ventricular filling resulted from pooling of blood in peripheral capacitive vessels. With the exception of isoflurane, each of the other three anaesthetics reduced coronary blood flow. Coronary vascular resistance was not substantially influenced by halothane and methoxyflurane, but decreased with MAC 1.0 enflurane and isoflurane. Myocardial oxygen availability was always found to be adequate. Isoflurane even produced a significant rise in coronary venous oxygen saturation indicating coronary vasodilation. Parallel with the depression in cardiac performance and blood pressure as two of the main predictors of energy demand, myocardial oxygen consumption was found to be significantly reduced by each of the anaesthetics. The ratio of the external work of the left ventricle to its oxygen consumption indicated that myocardial efficiency deterioated. The clinical implications are discussed.
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PMID:[Influence of modern inhalation anaesthetics on haemodynamics, myocardial contractility, left ventricular volumes and myocardial oxygen supply (author's transl)]. 87 90

Acupuncture by electrocautery, moxibustion, at Jen Chung (Go-26) acupoint produces a sympathomimetic effect on the cardiovascular system of dogs under halothane anaesthesia (MAC I). This effect is manifest by significant increase in cardiac output, stroke volume, heart rate, mean arterial pressure and pulse pressure while total peripheral resistance is significantly decreased during a two-hour period of observation. Pretreatment with the beta blocker, propranolol, caused a significant decrease in cardiac output, heart rate, mean arterial pressure and pulse pressure while total peripheral resistance is significantly increased. Similar responses were observed when propranolol was administered without moxibustion at Jen Chung (Go-26).
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PMID:Inhibition of the cardiovascular effects of acupuncture (moxibustion) by propranolol in dogs during halothane anaesthesia. 93 68

Serial invasive and noninvasive (systolic time interval) measurements of left ventricular performance were obtained in six healthy volunteers during general anesthesia employing the following sequence: thiopental induction, succinylcholine (prior to endotracheal intubation), and halothane--100 per cent oxygen at 1.25 and 1.75 MAC. Heart rate (HR), mean pulmonary arterial "wedge" pressure (PAW) and mean systemic arterial pressure (MAP) were measured continuously; cardiac index and systolic time intervals (STI's) were measured during each intervention. At both levels of halothane, MAP and stroke work index decreased (both P less than 0.02), while HR and systemic vascular resistance did not change. At 1.25 MAC halothane PAW was unchanged, but at 1.75 MAC PAW increased from 8 +/- 4 (SD) to 11 +/- 5 torr (P less than 0.02). Preload was altered at 1.25 MAC by administration of 600-1,000 ml lactated Ringer's solution; PAW increased from 9 +/- 4 to 17 +/- 3 torr (P less than 0.01). At 1.75 MAC halothane, volume expansion increased PAW in a similar manner, but the resultant ventricular function curve was depressed compared with 1.25 MAC halothane. In additon, at each level of halothane anesthesia, the ventricular function curve was depressed compared with results obtained in awake normal subjects. Afterload was altered at 1.25 MAC halothane by infusion of phenylephrine sufficient to raise MAP by 30 per cent. This intervention resulted in a greater depression of cardiac performance than that observed at 1.75 MAC halothane alone. Although alterations in STI's were directionally similar to changes observed in invasive hemodynamic measurements, STI's were sensitive to acute alternations in loading conditions. It is concluded that the levels of halothane commonly employed for general anesthesia significantly depress left ventricular performance in normal subjects, as evidenced by abnormal responses to alterations in preload and afterload, and that STI's should not be employed for routine measurement of left ventricular performance during anesthesia unless both the afterload and the preload on the myocardium are known.
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PMID:Alterations of normal left ventricular performance by general anesthesia. 98 77

The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.
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PMID:Circulatory effects of halothane and halothane-nitrous oxide anesthesia in the dog: spontaneous ventilation. 111 85

The hemodynamic response to the combination of isoflurane (1 MAC) and propranolol (0.5 mg/kg) was studied in 12 intact ventilated dogs following basal anesthesia with chloralose-urethane. When propranolol was administered during isoflurane anesthesia, stroke volume was maintained with a higher pulmonary capillary wedge pressure (3.2 plus or minus 0.7 mm Hg to 6.3 plus or minus 1.4 mm Hg), while systemic vascular resistance remained unchanged. When isoflurane was administered to the previously beta-adrenergically blocked dog, there were declines in systemic pressure and cardiac output (P smaller than 0.01) and in pulmonary arterial pressure and stroke volume (P smaller then 0.05), without change in systemic vascular resistance. When isoflurane was subsequently discontinued, these changes were reversed, and in addition, systemic vascular resistance increased (P smaller than 0.05). These data indicate that isoflurane has pharmacologic properties compatible with a peripheral beta-adrenergic stimulating action.
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PMID:Hemodynamic consequences of the combination of isoflurane anesthesia (1 MAC) and beta-adrenergic blockade in the dog. 113 Jul 22

The effects of isoflurane(I), halothane(H) and enflurane(E) on hemodynamics of 36 patients (12, 11 and 13, respectively) were studied during the inhalation of 1.5 MAC of each anesthetics before the surgery. Mean arterial pressure(MAP), heart rate(HR), cardiac index(CI), systemic vascular resistance index(SVRI), and stroke volume index (SVI) were measured noninvasively using the automatic blood pressure manometer and the ultrasonic Doppler method (Accucom). MAP decreased with I, E and H, but a larger decrement was observed with E than with H. CI and SVI with H were less than with E. SVRI decreased with I and E but a significant difference was observed between E and H. Each value with I was between those with H and E. These results indicate that isoflurane causes the depression of blood pressure mostly by its effect to decrease afterload during the induction of anesthesia, although its depressing effect is less than that of enflurane.
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PMID:[Effect of isoflurane, enflurane and halothane on hemodynamics during the induction of anesthesia]. 143 45

This study compared systemic hemodynamic and organ blood flow responses to equipotent concentrations of halothane and sevoflurane during spontaneous ventilation in the rat. The MAC values for halothane and sevoflurane were determined. Cardiac output and organ blood flows were measured using radiolabeled microspheres. Measurements were obtained in awake rats (control values) and at 1.0 MAC halothane or sevoflurane. The MAC values (mean +/- SEM) for halothane and sevoflurane were 1.10% +/- 0.05% and 2.40% +/- 0.05%, respectively. The PaCO2 increased to a similar extent in both groups compared with control values. During halothane anesthesia, heart rate decreased by 12% (P < 0.01), cardiac index by 26% (P < 0.01), and mean arterial blood pressure by 18% (P < 0.01) compared with control values. Stroke volume index and systemic vascular resistance did not change. During sevoflurane anesthesia, hemodynamic variables remained unchanged compared with control values. Coronary blood flow decreased by 21% (P < 0.01) and renal blood flow by 18% (P < 0.01) at 1.0 MAC halothane, whereas both remained unchanged at 1.0 MAC sevoflurane. Cerebral blood flow increased to a greater extent with halothane (63%; P < 0.01) than with sevoflurane (35%; P < 0.05). During halothane anesthesia, hepatic arterial blood flow increased by 48% (P < 0.01), whereas portal tributary blood flow decreased by 28% (P < 0.01). During sevoflurane anesthesia, hepatic arterial blood flow increased by 70% (P < 0.01) without a concomitant reduction in portal tributary blood flow. Total liver blood flow decreased only with halothane (16%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation. 144 79

The purpose of this study was to measure and compare the relationship of cardiovascular depression and dose during equal potent levels of halothane and isoflurane anesthesia in neonates (n = 19) (16.7 +/- 6.9 days) and infants (n = 54) (6.1 +/- 3.1 mo). Seventy-three children had heart rate, arterial blood pressure, and pulsed Doppler pulmonary blood flow velocity as well as two-dimensional echocardiographic assessments of left ventricular area and length recorded just before anesthesia induction. Anesthesia was induced by inhalation of increasing inspired concentrations of halothane or isoflurane in oxygen using a pediatric circle system and mask. During controlled ventilation, halothane and isoflurane concentrations were adjusted to maintain 1.0 MAC and then 1.5 MAC (corrected for age), and echocardiographic and hemodynamic measurements were repeated. A final cardiovascular measurement was recorded after intravenous administration of 0.02 mg/kg of atropine. All measurements were completed before tracheal intubation and the start of elective surgery. In neonates, 1.0 MAC concentrations of halothane and isoflurane decreased cardiac output (74% +/- 16%), stroke volume (75% +/- 15%), and ejection fraction (76% +/- 15%) similarly from awake levels. Decreases in cardiac output, stroke volume, and ejection fraction with halothane and isoflurane were significantly larger at 1.5 MAC (approximately 35% decreases from awake values) than at 1.0 MAC. Heart rate decreased significantly during 1.5 MAC halothane anesthesia (94% +/- 4%) but remained unchanged during isoflurane anesthesia. In infants, 1.0 MAC halothane and isoflurane decreased cardiac output (83% +/- 12%), stroke volume (78% +/- 12%), and ejection fraction (74% +/- 12%) when compared with awake measures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative hemodynamic depression of halothane versus isoflurane in neonates and infants: an echocardiographic study. 153 10

Hemodynamic effects of hypotension induced by ketanserin were investigated in 18 mongrel dogs under 0.87% halothane in oxygen (1 MAC). They were randomly allocated to one of two groups. Group C (n = 9) received no vasodilator therapy and served as a control and group K (n = 9) received 0.1% ketanserin solution. Mean arterial pressure decreased and was maintained at 60 mmHg for 60 minutes in group K. No change was noted in hemodynamic variables measured in group C throughout the experiment. During and after induced hypotension in group K, stroke volume index increased significantly compared with the control value. On the other hand, systemic vascular resistance was significantly reduced, reaching 50% of the control value at the end of the hypotensive period. Left ventricular maximum dp/dt showed a significant reduction during hypotension but then increased gradually to the control value. In addition, heart rate decreased significantly during and after induced hypotension, therefore these vasodilator effects were not accompanied by reflex tachycardia. Cardiac index remained unchanged throughout the experiment. Further, no changes in central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure and pulmonary vascular resistance were observed. In conclusion, the data indicate that ketanserin is a potent systemic vasodilator producing stable hemodynamics. It also reduces systemic vascular resistance without reflex tachycardia and this is a favorable effect of ketanserin.
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PMID:[Hemodynamic effects of induced hypotension by ketanserin in anesthetized dogs]. 157 17


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