Fentanyl Augments the Blockade of the Sympathetic Response to Incision (MAC-BAR) Produced by Desflurane and Isoflurane 

1998 ◽  
Vol 88 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Malcolm Daniel ◽  
Richard B. Weiskopf ◽  
Mariam Noorani ◽  
Edmond I. Eger
Keyword(s):  
Nitrous Oxide ◽  
Cardiovascular Response ◽  
Dependent Manner ◽  
Surgical Incision ◽  
Arterial Blood ◽  
Adrenergic Response ◽  
The Mean ◽  
End Tidal ◽  
Inhaled Anesthetic ◽  
Dose Dependent

Background Heart rate (HR) or mean arterial blood pressure (MAP) may increase in response to incision despite the absence of a motor response. The authors hypothesized that the MAC-BAR (minimum alveolar concentration of an anesthetic that blocks adrenergic response to incision) for isoflurane would exceed that for desflurane, and that fentanyl would decrease the MAC-BAR for each anesthetic in a dose-dependent manner. Methods Seventy-one patients were randomly allocated to one of six groups: desflurane or isoflurane without fentanyl or with 1.5 or 3 microg/kg fentanyl given intravenously 5 min before surgical incision. Anesthesia was induced with 2 mg/kg propofol given intravenously, and tracheal intubation facilitated with 0.1 mg/kg given intravenously. The first patient in each group received 1 MAC (end-tidal) of the inhaled anesthetic in 60% nitrous oxide (0.55 MAC), balance oxygen, maintained for at least 10 min before incision. The response was considered positive if the HR or MAP increased 15% or more. If the response was positive, the end-tidal concentration given to the next patient was 0.3 MAC greater; if the response was negative, the end-tidal concentration was 0.3 MAC less. The MAC-BAR level was calculated as the mean of four independent cross-over responses in each group. Results Desflurane and isoflurane anesthesia with 60% nitrous oxide did not change HR (P > 0.05) and decreased MAP (P < 0.05) before incision. Plasma epinephrine and norepinephrine concentrations after anesthesia and before incision were normal in all groups. The MAC-BAR level, without fentanyl, did not differ (P > 0.05) between desflurane (1.30 +/- 0.34 MAC [mean +/- SD]) and isoflurane (1.30 +/- 0.18 MAC). Fentanyl given at 1.5 microg/kg intravenously equivalently (P > 0.05) reduced the MAC-BAR for desflurane (to 0.40 +/- 0.18 MAC; P < 0.05) and isoflurane (to 0.55 +/- 0.00 MAC; P < 0.05), but a further increase in fentanyl to 3 microg/kg caused no greater decrease in the MAC-BAR for desflurane (0.48 +/- 0.16 MAC) and isoflurane (0.40 +/- 0.30 MAC). Conclusions Clinically attainable doses of desflurane and isoflurane, in 60% nitrous oxide (0.55 MAC), block the cardiovascular response to surgical incision at 1.3 MAC. Fentanyl given at 1.5 microg/kg decreases the MAC-BAR for each agent with no further decrease produced by 3 microg/kg fentanyl.

Effect of endothelin-1 on pulmonary resistance in rats

1990 ◽  
Vol 68 (6) ◽  
pp. 2391-2393 ◽  
Author(s):  
T. Matsuse ◽  
Y. Fukuchi ◽  
T. Suruda ◽  
T. Nagase ◽  
Y. Ouchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Bolus Administration ◽  
Dependent Manner ◽  
Pulmonary Resistance ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
The Mean ◽  
Dose Dependent

We examined the effect of endothelin-1 (ET-1), a novel 21-residue vasoconstrictor peptide, on pulmonary resistance (RL) in Wistar rats. The lung volume, tracheal flow, and transpulmonary pressure of tracheotomized and paralyzed rats were measured with a fluid-filled esophageal catheter and a pressure-sensitive body plethysmograph. RL was calculated by the method of von Neergaard. The femoral artery was cannulated to measure the mean arterial blood pressure. Intravenous bolus administration of synthetic ET-1 provoked a dose-dependent increase in RL in rats. The bronchoconstricting effect reached maximum at 500 pmol/kg. This bronchoconstriction was observed in less than 5 min, increased up to 15 min, and was sustained for 60 min. ET-1 increased the mean arterial blood pressure in a dose-dependent manner. We conclude that ET-1 is a hitherto unknown potent bronchoconstrictor that has a sustained effect in vivo. The potential physiological and pathophysiological role of this new peptide in the development of respiratory disease warrants further investigation.

Effects of Two Target-controlled Concentrations (1 and 3 ng/ml) of Remifentanil on MACBARof Sevoflurane

2004 ◽  
Vol 100 (2) ◽  
pp. 255-259 ◽  
Author(s):  
Andrea Albertin ◽  
Andrea Casati ◽  
Piercarlo Bergonzi ◽  
Greta Fano ◽  
Giorgio Torri
Keyword(s):  
Nitrous Oxide ◽  
Skin Incision ◽  
Double Blind Study ◽  
Double Blind ◽  
Surgical Incision ◽  
Arterial Blood ◽  
Sequential Allocation ◽  
Sympathetic Responses ◽  
American Society ◽  
End Tidal

Background The aim of this prospective, randomized, double-blind study was to determine the effects of two different target-controlled concentrations of remifentanil (1 and 3 ng/ml) on the sevoflurane requirement for blunting sympathetic responses after surgical incision (MACBAR). Methods Seventy-four patients aged 20-50 yr, with American Society of Anesthesiologists physical status I, were anesthetized with propofol, cisatracurium, and sevoflurane with a mixture of 60% nitrous oxide in oxygen. Then, patients were randomly allocated to receive no remifentanil infusion (n = 27) or a target-controlled plasma concentration of 1 ng/ml (n = 27) or 3 ng/ml remifentanil (n = 20). Sympathetic responses to surgical incision (presence or absence of an increase in either heart rate or mean arterial blood pressure of 15% or more above the mean of the values measured during the 2 min before skin incision) were determined after a 20-min period of stable end-tidal sevoflurane and target-controlled remifentanil concentrations. Predetermined end-tidal sevoflurane concentrations and the MACBAR for each group were determined using an up-and-down sequential-allocation technique. Results The MACBAR of sevoflurane was higher in the group receiving no remifentanil (2.8% [95% confidence interval: 2.5-3.0%]) as compared with patients of the groups receiving 1 ng/ml (1.1% [0.9-1.3%]; P = 0.012) and 3 ng/ml remifentanil (0.2% [0.1-0.3%]; P = 0.006). When considering a minimum anesthetic concentration (MAC) value in this age population and the contribution of 60% nitrous oxide (0.55 MAC), the combined MACBAR values, expressed as multiples of the MAC, were 1.95 MAC, 1.1 MAC, and 0.68 MAC, in the three groups, respectively. Conclusion A target-controlled concentration of 1 ng/ml remifentanil results in a 60% decrease in the MACBAR of sevoflurane combined with 60% nitrous oxide. Increasing the target concentration of remifentanil to 3 ng/ml produces a further 30% decrease in the MACBAR values of sevoflurane.

Anesthetic Doses of Sevoflurane To Block Cardiovascular Responses to Incision when Administered with Xenon or Nitrous Oxide 

1999 ◽  
Vol 91 (2) ◽  
pp. 369-373 ◽  
Author(s):  
Yoshinori Nakata ◽  
Takahisa Goto ◽  
Yoshiki Ishiguro ◽  
Katsuo Terui ◽  
Yoshinari Niimi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nitrous Oxide ◽  
Mean Arterial Pressure ◽  
Minimum Alveolar Concentration ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Suppressive Effect ◽  
Skin Incision ◽  
The Mean ◽  
End Tidal

Background The authors' previous study demonstrated that xenon (Xe) and nitrous oxide (N2O) in combination with sevoflurane can attenuate cardiovascular responses to skin incision. To quantitatively evaluate their suppressive effects on cardiovascular responses, the authors compared the MAC-BAR (minimum alveolar concentration that blocks adrenergic or cardiovascular response to incision) values of sevoflurane when administered with Xe or N2O. Methods Forty-three patients received sevoflurane with one of three anesthetics; 1 MAC Xe, 0.7 MAC Xe and 0.7 MAC N2O. The MAC-BAR of sevoflurane was determined in each anesthetic using the "up and down" method. The response was considered positive if the heart rate or mean arterial pressure increased 15% or more. The end-tidal sevoflurane concentration given to the next patient was increased or decreased by 0.3 MAC if the response was positive or negative in the previous patient, respectively. The MAC-BAR was calculated as the mean of four independent cross-over responses. Results The MAC-BAR of sevoflurane, including the contribution of Xe or N2O, was 2.1+/-0.2 MAC and 2.7+/-0.2 MAC when administered with 1 MAC and 0.7 MAC Xe, respectively, and 2.6+/-0.4 MAC when administered with 0.7 MAC N2O (mean +/- SD). Conclusions Although 1 MAC Xe has a more potent suppressive effect on cardiovascular responses to incision than 0.7 MAC Xe or N2O, Xe and N2O have a similar suppressive effect at 0.7 MAC.

Effects of NO-Donors on Thrombus Formation and Microcirculation in Cerebral Vessels of the Rat

1996 ◽  
Vol 76 (01) ◽  
pp. 111-117 ◽  
Author(s):  
Yasuto Sasaki ◽  
Junji Seki ◽  
John C Giddings ◽  
Junichiro Yamamoto
Keyword(s):  
Blood Flow ◽  
Thrombus Formation ◽  
Dependent Manner ◽  
Red Cell ◽  
Cell Velocity ◽  
Red Cell Velocity ◽  
The Mean ◽  
Wall Shear ◽  
Dose Dependent

SummarySodium nitroprusside (SNP) and 3-morpholinosydnonimine (SIN-1), are known to liberate nitric oxide (NO). In this study the effects of SNP and SIN-1 on thrombus formation in rat cerebral arterioles and venules in vivo were assessed using a helium-neon (He-Ne) laser. SNP infused at doses from 10 Μg/kg/h significantly inhibited thrombus formation in a dose dependent manner. This inhibition of thrombus formation was suppressed by methylene blue. SIN-1 at a dose of 100 Μg/kg/h also demonstrated a significant antithrombotic effect. Moreover, treatment with SNP increased vessel diameter in a dose dependent manner and enhanced the mean red cell velocity measured with a fiber-optic laser-Doppler anemometer microscope (FLDAM). Blood flow, calculated from the mean red cell velocity and vessel diameters was increased significantly during infusion. In contrast, mean wall shear rates in the arterioles and venules were not changed by SNP infusion. The results indicated that SNP and SIN-1 possessed potent antithrombotic activities, whilst SNP increased cerebral blood flow without changing wall shear rate. The findings suggest that the NO released by SNP and SIN-1 may be beneficial for the treatment and protection of cerebral infarction

Prolactin stimulates food intake in a dose-dependent manner

1989 ◽  
Vol 256 (1) ◽  
pp. R276-R280 ◽  
Author(s):  
T. Gerardo-Gettens ◽  
B. J. Moore ◽  
J. S. Stern ◽  
B. A. Horwitz
Keyword(s):  
Food Intake ◽  
Female Rats ◽  
High Dose ◽  
Dependent Manner ◽  
Additional Control ◽  
The Mean ◽  
Ovine Prolactin ◽  
Dose Dependent ◽  
Medium Dose ◽  
Cumulative Food Intake

Lactation in the rat is marked by pronounced hyperphagia and suppression of brown fat (BAT) thermogenic capacity. We previously examined the possibility that elevated prolactin levels mediate these changes. The present study evaluated the effect of varying prolactin levels on food intake, BAT mitochondrial GDP binding, and carcass adiposity. Female rats were injected daily for 10 days with ovine prolactin at one of three doses: high = 3.0, medium = 1.0, or low = 0.3 micrograms/g body wt. Controls were injected with 0.9% NaCl. A group of uninjected rats served as an additional control. Cumulative food intake was significantly elevated in a dose-dependent manner in the prolactin-treated animals relative to the saline-injected and uninjected controls. Compared with the saline controls, the mean cumulative food intake was greatest at the high dose (20% increase), intermediate at the medium dose (17%), and smallest at the low dose (12%). Prolactin-treated rats gained significantly more weight during the experiment than did controls. Despite the hyperphagia in the prolactin-treated rats, no significant differences in BAT mitochondrial GDP binding were observed among the five groups. These data indicate that elevated prolactin levels stimulate food intake in a dose-dependent manner and that this hyperphagia is not accompanied by an increase in BAT mitochondrial GDP binding.

Phasic Genioglossus and Palatoglossus Muscle Activity during Recovery from Sevoflurane Anesthesia

2013 ◽  
Vol 119 (3) ◽  
pp. 562-568 ◽  
Author(s):  
Ilavajady Srinivasan ◽  
Samuel Strantzas ◽  
Mark W. Crawford
Keyword(s):  
Muscle Activity ◽  
Upper Airway ◽  
Dependent Manner ◽  
Sevoflurane Anesthesia ◽  
Phasic Activity ◽  
Similar Dose ◽  
Inhalational Anesthetic ◽  
Recovery From Anesthesia ◽  
End Tidal ◽  
Dose Dependent

Abstract Background: Inhalational anesthetic effects on upper airway muscle activity in children are largely unknown. The authors tested the hypothesis that phasic inspiratory genioglossus and palatoglossus activity increases during recovery from sevoflurane anesthesia in a dose-dependent manner in children. Methods: Sixteen children, aged 2.0 to 6.9 yr, scheduled for elective urological surgery were studied. Electromyogram recordings were acquired using intramuscular needle electrodes during spontaneous ventilation. After a 15-min period of equilibration, electromyogram activity was recorded over 30 s at each of three end-tidal concentrations, 1.5, 1.0, and 0.5 minimum alveolar concentration (MAC), administered in sequence. Results: Phasic genioglossus activity was noted in four children at 1.5 MAC, five at 1.0 MAC, and six children at 0.5 MAC sevoflurane. Phasic palatoglossus activity was noted in 4 children at 1.5 MAC, 6 at 1.0 MAC, and 10 children at 0.5 MAC sevoflurane. Both the proportion of children exhibiting phasic activity, and the magnitude of phasic activity increased during recovery from anesthesia. For the genioglossus, decreasing the depth of sevoflurane anesthesia from 1.5 to 1.0 MAC increased phasic activity by approximately 35% and a further decrease to 0.5 MAC more than doubled activity (median [range] at 1.5 and 0.5 MAC: 2.7 μV [0 to 4.0 μV] and 8.6 μV [3.2 to 17.6], respectively; P = 0.029). A similar dose-related increase was recorded at the palatoglossus (P = 0.0002). Conclusions: Genioglossus and palatoglossus activity increases during recovery from sevoflurane anesthesia in a dose-dependent manner over the clinical range of sevoflurane concentrations in children.

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

Arterial-alveolar CO2 equilibration in exercising dogs during prolonged rebreathing

1985 ◽  
Vol 58 (5) ◽  
pp. 1654-1658 ◽  
Author(s):  
J. A. Loeppky ◽  
P. Scotto ◽  
H. Rieke ◽  
M. Meyer ◽  
J. Piiper
Keyword(s):  
Steady State ◽  
Carotid Artery ◽  
Average Rate ◽  
Blood Gas ◽  
O2 Uptake ◽  
Full Agreement ◽  
Arterial Blood ◽  
Simultaneous Measurements ◽  
The Mean ◽  
End Tidal

Arterial-alveolar equilibration of CO2 during exercise was studied by normoxic CO2 rebreathing in six dogs prepared with a chronic tracheostomy and exteriorized carotid loop and trained to run on a treadmill. In 153 simultaneous measurements of PCO2 in arterial blood (PaCO2) and end-tidal gas (PE'CO2) obtained in 46 rebreathing periods at three levels of mild-to-moderate steady-state exercise, the mean PCO2 difference (PaCO2-PE'CO2) was -1.0 +/- 1.0 (SD) Torr and was not related to O2 uptake or to the level of PaCO2 (30–68 Torr). The small negative PaCO2-PE'CO2 is attributed to the lung-to-carotid artery transit time delay which must be taken into account when both PaCO2 and PE'CO2 are continuously rising during rebreathing (average rate 0.22 Torr/s). Assuming that blood-gas equilibrium for CO2 was complete, a lung-to-carotid artery circulation time of 4.6 s accounts for the observed uncorrected PaCO2-PE'CO2 of -1.0 Torr. The results are interpreted to indicate that in rebreathing equilibrium PCO2 in arterial blood and alveolar gas are essentially identical. This conclusion is at variance with previous studies in exercising humans during rebreathing but is in full agreement with our recent findings in resting dogs.

Effect of ethyl alcohol on motor function in canine stomach

1992 ◽  
Vol 262 (2) ◽  
pp. G223-G230
Author(s):  
L. C. Knight ◽  
A. H. Maurer ◽  
R. Wikander ◽  
B. Krevsky ◽  
L. S. Malmud ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Solid Food ◽  
Blood Levels ◽  
Lag Phase ◽  
Dependent Manner ◽  
Solid Meal ◽  
The Mean ◽  
High Doses ◽  
Mean Time ◽  
Dose Dependent

The aim of this study was to elucidate the effects of ethanol on gastric emptying and the trituration of solid food. With the use of a noninvasive physiological imaging technique, gastric processing of a radiolabeled solid meal was evaluated in unanesthetized dogs which ingested 6-8% ethanol solutions or received intravenous alcohol before the meal. Oral alcohol (resulting in blood levels up to 174 mg/dl) decreased the amplitude of antral contractions or completely abolished them. Alcohol did not significantly affect the fundamental frequency of contractions except at high doses, at which contractions were abolished. Alcohol lengthened the mean time to 50% of gastric emptying in a dose-dependent manner, from 132 +/- 3 min without alcohol to 160 +/- 10 min with oral alcohol at blood levels of 80-120 mg/dl (P less than 0.05). This was manifested by a lengthening of the lag phase, but there was no effect on the terminal slope of emptying (emptying rate) of the processed meal. At equal blood levels up to 120 mg/dl, orally administered alcohol had a more pronounced effect than intravenous alcohol. These data suggest that even low doses of dilute alcohol affect the ability of the antrum to process solid food and thereby contribute to impairment of gastric emptying.

Central effect of endothelin on blood pressure in conscious rats

1989 ◽  
Vol 256 (6) ◽  
pp. H1747-H1751 ◽  
Author(s):  
Y. Ouchi ◽  
S. Kim ◽  
A. C. Souza ◽  
S. Iijima ◽  
A. Hattori ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Artificial Cerebrospinal Fluid ◽  
Male Wistar Rats ◽  
The Mean ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Lateral Cerebral Ventricle

This study was conducted to investigate the effect of intracerebroventricular administration of endothelin (EDT), a novel potent vasoconstricting peptide, on blood pressure in conscious rats. The lateral cerebral ventricle of male Wistar rats was cannulated, and the femoral artery was also cannulated to measure the mean arterial blood pressure (MABP) and heart rate (HR). EDT dissolved in 10 microliters of artificial cerebrospinal fluid (ACSF) (8.25-66 pmol icv) provoked a dose-dependent increase in MABP. EDT also increased HR, although the effect of 66 pmol was variable. Intracerebroventricular ACSF did not provoke any effects on MABP and HR. Intracerebroventricular EDT also provoked contralateral rotational behavior. Pretreatment with 2 mg/kg iv phenoxybenzamine significantly suppressed the 16.5 pmol icv EDT-induced increase in MABP. Moreover, 16.5 pmol icv EDT markedly increased plasma epinephrine and norepinephrine concentration. These results indicate that EDT has a central pressor action, and the action might be mediated, at least in part, by catecholamine release to the periphery. EDT might play a role in the central control of blood pressure, although the physiological implications have not yet been determined.

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