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Experimental studies carried out in unselected dogs often face the problem of instabilit of various parameters both in terms of haemodynamics as well as acid-base balance. It is possible, with the injection of a single dose of Fentanyl of 0.35 mg.kg-1 given over a period of ten minutes to obtain, from the 30th minute after the injection, satisfactory cardiovascular stability (confirmed during 120 minutes in 9 dogs and 360 minutes in 2 of them). This haemodynamic state at T + 30 is obtained with a fall in mean blood pressure of -40 per cent, and an increase in peripheral resistance of +38 per cent and stroke volume of +11 per cent. This stability, obtained at the price of a stable normacapnia, correction of any possible metabolic acidosis and maintenance of body temperature, makes it possible to study the cardiovascular effects of certain types of treatment or of induced pathology.
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PMID:[Cardiovascular effects of a single injection of fentanyl in dogs under acute experimental conditions]. 4 Apr 90

The cardiovascular effects of three doses of intravenous fentanyl (50, 100, and 200 microgram) were determined in 42 adult patients undergoing intraabdominal surgical procedures with enflurane (2--3%) and nitrous oxide (50%) in oxygen. Fentanyl was administered a minimum of 40 minutes after induction of anesthesia and 30 minutes after initiation of the surgical procedure. Stroke volume, heart rate, cardiac output, mean arterial and central venous blood pressures, and peripheral arterial resistance were determined by computer analysis of the central aortic pulse-pressure curve according to the method of Warner. Measurements were made before and 2, 4, 6, 8, and 10 minutes after fentanyl. Fentanyl (50 microgram) produced increases in stroke volume and cardiac output as well as a decrease in peripheral arterial resistance but did not alter heart rate or mean arterial blood pressure. Fentanyl (100 microgram) did not significantly change any variable at any time. Fentanyl (1l (200 microgram) produced sustained decreases in stroke volume, cardiac output and mean arterial blood pressure and increased central venous pressure but did not alter heart rate or peripheral arterial resistance. The data indicate that fentanyl (50--100 microgram) stimulates or has no effect on cardiovascular dynamics during enflurane-nitrous oxide anesthesia but fentanyl (200 microgram) produces significant cardiovascular depression. Our findings suggest that small doses of intravenous fentanyl may be of benefit during enflurane-nitrous oxide but larger doses should probably be avoided.
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PMID:Cardiovascular effects of fentanyl during enflurane anesthesia in man. 57 55

A combination of fentanyl-droperidol was administered intravenously alone or with atropine sulfate (2 doses--0.04 or 0.02 mg/kg of body weight) to determine if stable neuroleptanalgesia could be produced in the dog. Cardiovascular responses were recorded at 5, 15, and 30 minutes. Fentanyl-droperidol given alone caused a significant increase of peripheral resistance and mean arterial pressure at 5 minutes and then a decrease of these values over a postinjection period of 30 minutes. Left ventricular dP/dt increased significantly at postinjection minutes 15 and 30. In dogs given atropine concurrently with fentanyl-droperidol, there was significant increase in heart rate and decrease in stroke volume. Also, there were significant initial increases in diastolic and mean arterial blood pressures, ventricular contractility, and coronary blood flow. The dose of 0.02 mg of atropine/kg seemed optimal for intravenous administration with fentanyl-droperidol in the dog; when the atropine dose was 0.04 mg/kg, large inotropic and chronotropic effects were produced.
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PMID:Cardiovascular response to fentanyl-droperidol and atropine in the dog. 85 Dec 80

The effects of large doses of fentanyl (0.05 to 2 mg/kg) and fentanyl plus N2O on cardiovascular dynamics were determined in 10 unpremedicated dogs breathing 100% O2. Using computer analysis of the central aortic pulsepressure curve, stroke volume (SV), cardiac output, heart rate (HR), peripheral vascular resistance (PVR), and systolic, diastolic, and mean arterial blood pressures (BP) were determined while fentanyl was being given at a rate of 0.3 to 0.44 mg/min. Fentanyl caused a dose-related decrease in HR, which was significant at 0.05 mg/kg. Cardiac output, PVR, and systolic, diastolic, and mean arterial BP were also decreased and SV increased. The latter changes became significant at 0.1 mg/kg for diastolic BP; 0.15 mg/kg for cardiac output and mean BP; 0.25 mg/kg for sv and systolic BP; and at 1.25 mg/kg for peripheral vascular resistance. Addition of N2O after fentanyl did not significantly change any parameter, although SV, cardiac output, and HR were usually increased and PVR decreased. These data demonstrate that, while large doses of fentanyl or fentanyl plus N2O do alter cardiovascular dynamics in dogs, the changes appear to be less profound than those produced by equianalgesic doses of morphine. Our findings suggest that large doses of fentanyl-O2 may be an attractive alternative to morphine-O2 anethesia in critically ill patients.
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PMID:Cardiovascular dynamics after large doses of fentanyl and fentanyl plus N2O in the dog. 94 74

The cardiovascular effects of diazepam 0.5 and 1.0 mg/kg and diazepam with pancuronium 0.1 mg/kg after fentanyl 0.5 mg/kg were determined in thirteen dogs premedicated with atropine. Fentanyl produced significant reductions in heart rate, cardiac ouptut and arterial blood pressure. Administration of 0.5 mg/kg of diazepam after fentanyl did not significantly alter stroke volume, arterial blood pressure or peripheral vascular resistance but did increase heart rate and cardiac output. Additional diazepam did not further change the heart rate, but did reduce stroke volume, cardiac output, arterial blood pressure and peripheral vascular resistance. Administration of pancuronium after fentanyl and diazepam produced marked elevations in heart rate, cardiac output and arterial blood pressure. There was no difference in mean heart rate and cardiac output when values prior to fentanyl and those obtained three minutes following pancuronium were compared. These data demonstrate that large doses of fentanyl decrease heart rate, cardiac these changes can be partially reversed with diazepam 0.5 mg/kg and completely antagonized with pancuronium 0.1 mg/kg.
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PMID:The cardiovascular effects of diazepam and of diazepam and pancuronium during fentanyl and oxygen anaesthesia. 94 1

Fentanyl (10 mug/kh) or fentanyl (10 mug/kg) plus droperidol (100 mug/kg) administered intravenously during 20 minutes to adult patients with acquired valvular heart disease produced minimal circulatory changes. The trend during drug infusion was for mean arterial pressure and systemic vascular resistance to decrease, and for cardiac index and stroke volume index to increase without change in heart rate. Central venous pressure increased during drug infusion (P less than 0.05) but decreased to awake levels following controlled ventilation and skeletal-muscle paralysis, probably reflecting thoracoabdominal-muscle rigidity rather than a circulatory response. Hypoventilation during drug infusion necessitated assisted or controlled ventilation, with or without skeletal muscle paralysis, in 14 of 16 patients. Addition of 60 per cent nitrous oxide following fentanyl or fentanyl-droperidol infusion significantly decreased mean arterial pressure, heart rate, and cardiac index. All circulatory changes were similar in direction and extent to those previously found during morphine-nitrous oxide anesthesia. (Key words: Anesthetics, intravenous, fentanyl; Anesthetics, gases, nitrous oxide; Heart, effect of fentanyl, dorperidol, and nitrous oxide.).
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PMID:Hemodynamic and ventilatory responses to fentanyl, fentanyl-droperidol, and nitrous oxide in patients with acquired valvular heart disease. 111 86

The acute effect of Fentanyl and Althesin upon haemodynamics, inotropism of the heart and myocardial oxygen consumption has not been studied in man so far. Healthy premedicated pateints (n = 16) were lightly anaesthetized with nitrous oxide-oxygen (ratio 2:1), 0.3 Vol.-% forane and 0.3 Vol.-% halothane respectively. In order to avoid any interference with respiratory depression all subjects were normoventilated via an orotracheal tube. In a circulatory steady state a single dose of 0.01 mg/kg Fentanyl (n = 7) and 0.075 mg/kg Althesin (n = 9) respectively was injected intravenously within 20 sec. After the application of Fentanyl there was a delayed (5th min) fall in blood pressure by 23%, which was due to a reduction in total peripheral resistance (12%) and in cardiac output (thermodilution technique) by 13%. The decrease in cardiac output was the result of a bradycardia (18%). Considering heart rate, pre- and afterload simultaneously, the fall in max dp/dt (catheter-tip manometer) by 20% could not be explained as a decrease in myocardial contractility. The altered haemodynamics led to a decrease of the myocardial oxygen consumption (control 6.4 ml O2/min x 100 g) by 31%. The energy demand of the heart was quantitatively calculated using the formula of the complex haemodynamic parameter developed by Bretschneider. Immediately after the administration of Althesin the cardiac output rose on account of tachycardia slightly, while stroke volume (19%), total peripheral resistance (32%) and mean arterial pressure (24%) reacted reversely. Since heart rate increased (11%), preload remainded unchanged and afterload decreased, the fall in dp/dt max (20%) has to be understood as a moderate reduction in myocardial inotropism. The energy demand of the heart decreased only initially by 15%. The clinical implications of the results were discussed.
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PMID:[The effect of Fentanyl and Althesin on haemodynamics, inotropism of the heart and myocardial oxygen consumption in man (author's transl)]. 125 26

The energetic role of inosine (INO) remains controversial. The aim of the present study was first to test whether endogenous INO consumption/production correlates with regional myocardial contractile performance and second to test whether locally increased levels of INO influence contractility and blood flow in severely ischemic myocardium. Fentanyl-anesthetized dogs with implanted sonomicrometry crystals and independently perfused left anterior descending coronary arteries were studied. Two relatively load-independent indexes of regional myocardial contractility derived from left ventricular pressure-segment length loops were used: the regional stroke work-end-diastolic segment length relationship (Wr/L(ed)) and the end-systolic pressure-segment length relationship (Plv/L(es)). Very good correlations between myocardial contractile performance (as measured by the slope of the regional Wr/L(ed) relationship) and endogenous INO consumption/production under both nonischemic and ischemic conditions were found. Ischemia severely depressed contractility, significantly shifting rightward the Wr/L(ed) and Plv/L(es) relationships. INO infused into the left anterior descending bypass, in a concentration of 600 to 800 mumol/L, partially restored contractile performance as evidenced by a significant leftward displacement of both relationships. Wr, measured at a common maximum L(ed), increased significantly by 61 +/- 5%. Border-zone collateral flow (microspheres) increased by 35 +/- 7% within the endocardial segments and by 34 +/- 9% in the epicardial segments, but no increase in flow in the ischemic region was measureable. With the current emphasis on recanalization with thrombolytic therapy and considering the apparent safety of INO, this naturally occurring nucleoside might prove to be a useful adjunctive agent in the treatment of acute myocardial ischemia.
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PMID:Inosine--a natural modulator of contractility and myocardial blood flow in the ischemic heart? 146 98

We have studied the effects of dopexamine and dopamine on systemic and renal haemodynamics in 20 male patients undergoing elective coronary artery bypass surgery. Patients were allocated randomly to two groups (n = 10) who were treated with incremental doses of either dopexamine 1, 2 and 4 micrograms kg-1 min-1, or dopamine 2.5 and 5 micrograms kg-1 min-1, each dose being maintained for 15 min. Measurements were performed before administration of the drug and at the end of the infusion period at each dose. Fentanyl and midazolam were used as anaesthetic agents. Renal blood flow was measured with the argon washin technique. Dopexamine 4 micrograms kg-1 min-1 produced an increase in cardiac index of 117% caused by a 65% reduction in afterload and an increase in heart rate by 61%. Dopamine 5 micrograms kg-1 min-1 caused a 40% increase in cardiac index as a result of an increase in stroke volume. Renal vascular resistance decreased more than systemic vascular resistance with dopamine. With dopexamine, the increase in renal blood flow (66%) was less than the increase in cardiac index, while renal vascular resistance and systemic vascular resistance declined to almost the same extent. The results show that dopexamine exerts systemic and renal effects mainly via stimulation of beta 2-receptors. An action of dopexamine at renal DA1-receptors could not be demonstrated in this study.
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PMID:Cardiovascular and renal haemodynamic effects of dopexamine: comparison with dopamine. 202 87

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


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