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PubMedDate not supplied

Pulsus alternans during halothane anesthesia in a dog.

An adult dog with pyloric obstruction was anesthetized with thiamylal and halothane for surgical revision. When an ECG was attached, the QRS-complex rate was noted to differ dramatically from the peripheral pulse rate. A dorsal pedal arterial catheter was introduced, and direct arterial pressure measurements revealed a blood pressure waveform that alternated in amplitude. Blood pressure and ECG traces were recorded, and the condition was diagnosed as pulsus alternans. The inhalation anesthetic was changed to isoflurane, and the condition was resolved.

Anesthesia, Inhalation↗
PubMedDate not supplied

Butorphanol tartrate for partial reversal of oxymorphone-induced postoperative respiratory depression in the dog.

A randomized, blinded, crossover study was designed to evaluate the respiratory, cardiovascular, and behavioral effects of butorphanol given postoperatively to oxymorphone-premedicated and surgically stimulated dogs. Nine healthy adult dogs were premedicated intramuscularly with atropine (0.04 mg/kg), acepromazine (0.10 mg/kg), and oxymorphone (0.2 mg/kg). Anesthesia was induced with thiamylal (12 mg/kg) and maintained with halothane in oxygen. According to the protocol of a concurrent study, all dogs had percutaneous endoscopic gastrostomy (PEG) feeding tubes placed during the first anesthetic episode and removed during the second anesthetic episode. All dogs received postoperatively either butorphanol tartrate (0.2 mg/kg) or an isovolumetric dose of saline placebo, both given intravenously. Respiratory rate (RR), tidal volume (TV), minute ventilation (MV), end-tidal CO2 concentration (ETCO2), heart rate (HR), and indirect diastolic (DP), systolic (SP) and mean arterial (MAP) blood pressures were measured at times 0, 2, 5, 10, 20, 40, 80, and 120 minutes after injection. The time from injection of the test drug until extubation was recorded. RR, MV, HR, and DP were significantly (P < .05) increased, while ETCO2 was significantly decreased, for a minimum of 30 minutes in butorphanol-treated dogs compared with saline controls. TV, SP, and MAP were transiently (< or = 15 minutes) increased in butorphanol-treated dogs compared with saline controls. There was no significant difference between the times to extubation in the butorphanol-treated dogs versus the saline control dogs.

Anesthesia, Inhalation↗
PubMedDate not supplied

Blood gas values during intermittent positive pressure ventilation and spontaneous ventilation in 160 anesthetized horses positioned in lateral or dorsal recumbency.

One hundred sixty horses were anesthetized with xylazine, guaifenesin, thiamylal, and halothane for elective soft tissue and orthopedic procedures. Horses were randomly assigned to one of four groups. Group 1 (n = 40): Horses positioned in lateral (LRG1; n = 20) or dorsal (DRG1; n = 20) recumbency breathed spontaneously throughout anesthesia. Group 2 (n = 40): Intermittent positive pressure ventilation (IPPV) was instituted throughout anesthesia in horses positioned in lateral (LRG2; n = 20) or dorsal (DRG2; n = 20) recumbency. Group 3 (n = 40): Horses positioned in lateral (LRG3; n = 20) or dorsal (DRG3; n = 20) recumbency breathed spontaneously for the first half of anesthesia and intermittent positive pressure ventilation was instituted for the second half of anesthesia. Group 4 (n = 40): Intermittent positive pressure ventilation was instituted for the first half of anesthesia in horses positioned in lateral (LRG4; n = 20) or dorsal (DRG4; n = 20) recumbency. Spontaneous ventilation (SV) occured for the second half of anesthesia. The mean time of anesthesia was not significantly different within or between groups. The mean time of SV and IPPV was not significantly different in groups 3 and 4. Variables analyzed included pH, PaCO2, PaO2, and P(A-a)O2 (calculated). Spontaneous ventilation resulted in significantly higher PaCO2 and P(A-a)O2 values and significantly lower PaO2 values in LRG1 and DRG1 horses compared with LRG2 and DRG2 horses. Intermittent positive pressure ventilation resulted in normocarbia and significantly lower P(A-a)O2 values in LRG2 and DRG2 horses. In LRG2 the PaO2 values significantly increased from 20 minutes after induction to the end of anesthesia. The PaO2 and P(A-a)O2 values were not significantly different from the beginning of anesthesia after IPPV in DRG2 or DRG3. The PaO2 values significantly decreased and the P(A-a)O2 values significantly increased after return to SV in horses in LRG4 and DRG4. The PaO2 values were lowest and the P(A-a)O2 values were highest in all horses positioned in dorsal recumbency compared with lateral recumbency and in SV horses compared with IPPV horses. The pH changes paralleled the changes in PaCO2. Blood gas values during right versus left lateral recumbency in all groups were also evaluated. The PaO2 values were significantly lower and the P(A-a)O2 values were significantly higher during SV in horses positioned in left lateral (LRLG1) compared with right lateral (LRRG1) recumbency.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia, Intravenous↗
PubMed1989

High frequency jet ventilation in horses: an experimental study.

High frequency jet ventilation (HFJV) is a recently developed mode of ventilation that delivers small tidal volumes at frequencies greater than 60 cycles per min via an injection catheter to the animal's airway. The construction of a high frequency jet ventilator suitable for use in adult horses is described. The effectiveness of this ventilator in maintaining normal arterial blood-gas tension was evaluated in five healthy adult horses. The horses were anaesthetised with intravenous acetylpromazine, guaifenesin, and thiamylal, positioned in lateral recumbency and baseline measurements were made during spontaneous ventilation. The horses were then paralysed with succinylcholine and ventilated for at least 20 mins with HFJV. Air was delivered from the ventilator to the animal by a polyethylene tube. The tip of this tube remained within and approximately 30 cm from the cuffed end of a standard 30 mm internal diameter large animal orotracheal tube. Frequency of flow interruption was 3 Hz with a constant source pressure of 275 kPa and an inspiratory to expiratory ratio of approximately 1:2.6. Gas delivery to the horse, as estimated with a resonator system was approximately 2 litres/breath. During HFJV, arterial carbon dioxide tension was significantly reduced and arterial oxygen tension significantly increased above measurements made when the horses were spontaneously breathing air.

Animals↗
PubMed1990

Metabolic and hormonal changes associated with arthroscopic surgery in the horse.

The effect of general anaesthesia and arthroscopic surgery on blood glucose and lactate, plasma non-esterified fatty acids, insulin, beta-endorphin and cortisol was investigated in seven horses. Animals were premedicated with xylazine and anaesthesia was induced with guaifenesin and sodium thiamylal and maintained with halothane vaporised in oxygen. Blood samples were collected in the pre-, intra- and post operative period. Induction of anaesthesia was associated with a transient hyperglycaemia and a significant rise in plasma insulin levels. Plasma insulin values fell during surgery but showed a significant increase post operatively. Surgery stimulated a small but significant rise in plasma beta-endorphin and cortisol values but these had returned to baseline values in the early post operative period. No changes in blood lactate were recorded.

Anesthesia, General↗
PubMed1993

Cardiovascular effects of thoracic compression in horses subjected to euthanasia.

Six horses scheduled for euthanasia were instrumented for the measurement of blood flow by thermodilution, pulmonary arterial, right atrial and arterial blood pressures and collection of arterial blood for pH and blood gas analysis. The horses were anaesthetised with intravenous (iv) thiamylal sodium (10 mg/kg) and placed in right lateral recumbency. After euthanasia with an overdose of pentobarbitone sodium (100 mg/kg, iv) and loss of the electrocardiogram and arterial pulse pressure, thoracic compression at rates of 40, 60 and 80 compressions/min was instituted. Thoracic compression was accomplished by an investigator who delivered a blow to the chest wall with his knee while dropping from a standing or crouching position. Compression rates of 40, 60 and 80/min produced blood flows of 5.65 +/- 0.5, 6.33 +/- 1.11 and 8.28 +/- 2.16 litres/min, respectively. Compression rates of 80/min produced significantly (P < 0.05) greater blood flows and mean arterial blood pressures than did slower rates. The blood flows produced by 80 thoracic compressions/min were approximately 50% of those reported for deeply anaesthetised horses and while not sufficient to sustain life might be used to prolong life in order to facilitate distribution of resuscitative drugs to vital tissues.

Animals↗
PubMed1995

The haemodynamic effects of milrinone HCl in halothane anaesthetised horses.

The haemodynamic effects of milrinone hydrochloride were determined in halothane-anaesthetised horses. Six healthy adult horses were anaesthetised with guaifenesin and thiamylal and maintained with halothane in oxygen (end-tidal halothane concentration of 1.15%). Baseline haemodynamic data were recorded after a 45 min stabilisation period. All 6 horses received a single loading dose of milrinone HCl, 0.2 microgram/kg i.v., followed by progressively increasing infusions of 2.5, 5, 10 and 20 micrograms/kg bwt/min. Each infusion lasted for 15 min and produced dose related increases in heart rate, mean arterial blood pressure, cardiac output, maximum rate of increase and decrease of left ventricular pressure (+/- dP/dtmax) and ejection fraction in halothane anesthetised horses. Median artery blood flow increased following milrinone administration. Right atrial and pulmonary artery pressures, systemic vascular resistance and left ventricular end-diastolic and end-systolic volumes decreased. Most haemodynamic changes were sustained throughout the infusion period and for 30 min following the termination of milrinone infusion. Systemic vascular resistance was increased above baseline values at 30 min following the termination of milrinone infusion. No adverse side effects were observed during this study although a milrinone infusion rate of 20 micrograms/kg bwt/min increased heart rate to values greater than 50 beats/min. The results of this study suggest that milrinone produces beneficial haemodynamic effects in halothane anaesthetised horses and is potentially useful in the treatment of patients with a reduced cardiac output.

Anesthetics, Inhalation↗
PubMed1975

Corticofugal effects from sensorimotor area I and somatosensory area II on neurones of the pontine nuclei in the cat.

1. The objective of the present experiments was to study the cortical influence from sensorimotor area I (SM I) and from somatosensory area II (S II) on single neurones of the pontine nuclei (PN) in cats under N2--thiamylal anaesthesia. 2. Extracellular single unit recordings revealed a considerable convergence from S II and SM I. Out of ninety-one PN neurones (identified as ponto-cerebellas neurones by antidromic stimulation of the contralateral brachium pontis), fifty-seven neurones were influenced by stimulation of at least one cortical site. Slightly less than half of these neurones (twenty-five) had a convergent input from SM I and S II; twenty-three PN neurones were excited by SM I only and nine PN neurones by S II only. The proportion of PN neurones excited via collaterals of cortico-spinal neurones was small and restricted to those neurones which had an input from SM I. 3. Sixty per cent of the ponto-cerebellar neurones were reliably activated by natural stimulation such as tapping or passive manipulations of limbs of various joints. The vast majority (thirty-three out of thirty-six PN neurones) which had receptive fields were also influenced by electrical stimulation of one or both cortical areas. The long latency and low probability of discharge to peripheral nerve stimulation suggest a complex, probably transcortical, pathway from the periphery to the PN. 4. The distribution of latencies to both cortical and brachium pontis stimulation indicates that the PN are a relay for fast and slow cerebro-cerebellar connexions. 5. The convergence from cortical areas on PN indicates that the neurones influenced from somatic areas SM I and S II transmit integrated patterns of activity to the cerebellum.

Animals↗
PubMed2004

Inhibition of activator protein 1 by barbiturates is mediated by differential effects on mitogen-activated protein kinases and the small G proteins ras and rac-1.

Barbiturates are known to suppress protective immunity, and their therapeutic use is associated with nosocomial infections. Although barbiturates inhibit T cell proliferation, differentiation, and cytokine synthesis, only thiobarbiturates markedly reduce the activation of immune regulatory transcription factors such as nuclear factor-kappaB and nuclear factor of activated T cells. In this study, we investigated barbiturate-mediated effects on the regulation of the transcription factor activator protein 1 (AP-1) in primary T lymphocytes. We show that both thiobarbiturates and their oxy-analogs inhibit AP-1-dependent gene expression and AP-1 complex formation at clinically relevant doses. Furthermore, mitogen-activated protein (MAP) kinase activity, which transcriptionally and posttranslationally regulates AP-1 complex formation, is suppressed by most barbiturates. CD3/CD28- or phorbol 12-myristate 13-acetate (PMA)/ionomycin-induced p38 and extracellular signal-regulated kinase 1/2 phosphorylation or c-jun NH2-terminal kinase (JNK) 1/2 kinase activity was significantly diminished by pentobarbital, thiamylal, secobarbital, or methohexital treatment. These barbiturates also inhibited the initiators of the MAP kinase cascade, the small G proteins ras and rac-1, and prevented binding to their partners raf-1 and PAK, respectively. Thiopental, unlike the other barbiturates, only reduced ras and JNK activity upon direct CD3/CD28 receptor engagement. Contrarily, upon PMA/ionomycin stimulation, thiopental blocked AP-1-dependent gene expression independently of the small G protein ras and MAP kinases, thus suggesting an additional, unknown mechanism of AP-1 regulation. In conclusion, our results contribute to the explanation of a clinically manifested immune suppression in barbiturate-treated patients and support the idea of a MAP kinase-independent regulation of AP-1 by PKC and calcium in human T cells.

Barbiturates↗
PubMed2003

Effects of barbiturates on human platelet aggregation differ depending on their chemical structures.

The effects of barbiturates on human platelet function are not fully understood. Since we have already revealed the effects and mechanisms of thiopental, thiamylal, and pentobarbital in platelets, the present study attempted to elucidate (i) the effects of other barbiturates on human platelet aggregation, (ii) the underlying mechanisms, and (iii) the structure-function relationship of barbiturates in platelets. Barbiturates, including amobarbital, butalbital, secobarbital, barbital, phenobarbital, metharbital, and primidone, were examined. Human platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, and (+)-9,11-epithia-11,12-methano-thromboxane A2 (STA2), a thromboxane A2 analog, was measured using an 8-channel light-transmission aggregometer. The cytosolic free calcium concentration ([Ca2+]i) was measured by fluorometer using fura-2 loaded platelets. Inositol 1,4,5-trisphosphate (IP3) formation induced by STA2 was determined by a commercially available IP3 assay kit. Amobarbital, butalbital, and secobarbital suppressed ADP-, epinephrine- and STA2-induced platelet aggregation and the STA2-induced [Ca2+]i increase, even when Ca2+ influx was blocked by Ni2+. However, they did not affect STA2-induced IP3 formation. Barbital, phenobarbital, metharbital, and primidone (up to 1 mM) had no effect on ADP- and epinephrine-induced platelet aggregation. Thus, we conclude that amobarbital, butalbital, and secobarbital inhibit platelet aggregation by suppressing [Ca2+]i increase without affecting IP3 formation. However, these antiaggregatory effects may not have clinical importance, since the barbiturate concentrations used were higher than clinically relevant ones. The other tested barbiturates had no effects on platelet aggregation. The data indicate that the effects of barbiturates on platelet aggregation differ depending on their chemical structures.

Adult↗
PubMed1994

Barbiturate attenuation of agonist affinity in cerebral arteries correlates with anesthetic potency and lipid solubility.

Barbiturates are known to reduce agonist sensitivity (EC50) in vascular smooth muscle; we provide evidence that the reduced agonist sensitivity can be correlated with a reduction in agonist affinity for its receptor. The histamine receptor was chosen since this agonist caused a consistent and maximum contraction of the cerebral artery used in this study. Segments of the basilar artery of white New Zealand male rabbits were set up in a small-vessel myograph in physiological salt solution, kept at 37 degrees C, pH 7.4, and bubbled with a 95% oxygen and 5% carbon dioxide gas mixture. The equilibrium dissociation constant (KA) of histamine for its receptor was calculated according to Furchgott's method by making three concentration-response curves to histamine: control, in the presence of phenoxybenzamine (0.02 microM), and after addition of a barbiturate in concentrations between 0.1 and 1.0 mM. All barbiturates tested, i.e., thiamylal, thiopental, pentobarbital, and phenobarbital, significantly reduced both histamine sensitivity and affinity. There is a significant correlation between histamine sensitivity and receptor affinity for histamine in a series of arterial segments from different animals. The attenuation of both pharmacological properties was consistent with the known rank order of anesthetic potency and with lipophilicity (r = 0.98; p < 0.05). Receptor reserve did not correlate with sensitivity. Thus, most of the change in receptor sensitivity was due to a change in agonist affinity. We suggest that barbiturates alter agonist receptor affinity by causing a perturbation in the membrane lipid environment of the receptor, leading to a conformational change, although alterations in intracellular mechanisms cannot be excluded.

Animals↗
PubMed1978

Blood flow distribution in dogs during hypothermia and posthypothermia.

Blood flow distribution in tissues of mongrel dogs during hypothermia was studied with radionuclide-tagged microspheres. The animals were cooled at 21 degrees C and rewarmed under thiamylal sodiuni anesthesia. During hypothermia, cardiac output fell to 20% of the control; the highest rate of blood flow relative to normothermic values was observed in the subendocardium of the left ventricle, and the lowest in the hypophysis. Each tissue showed specific reactions to hypothermia. During hypothermia the myocardial and brain-stem blood flows were about 40% of the control; almost all of the digestive tract, striated muscle, adrenal gland, and hypophysis blood flows were maintained at 20% or less of the control. After rewarming, cardiac output recovered to values significantly lower than control. The myocardium, brain, renal cortex, and striated and smooth muscle recovered to control levels; however, blood flow to the digestive organs, bronchial artery flow to the lung, and flow to the endocrine organs did not completely recover by 2 after rewarming.

Animals↗
PubMed1988

Characteristics of tachyphylaxis to inhaled histamine in anesthetized dogs.

Three consecutive dose-response curves to aerosolized histamine were obtained in 11 anesthetized dogs. All dogs showed desensitization (i.e., tachyphylaxis) to high doses of histamine. Tachyphylaxis was highly reproducible. No tachyphylaxis occurred with inhaled acetylcholine or methacholine. Beta-Adrenergic blockade with propranolol or muscarinic blockade with atropine given intravenously had no effect on the histamine tachyphylaxis. Duration of thiamylal anesthesia did not alter the histamine responsiveness. Histamine tachyphylaxis was also seen with chloralose-urethan anesthesia. Since tachyphylaxis is not observed with acetylcholine, it cannot be attributed to a general decline in muscle contractility. We conclude that histamine tachyphylaxis in vivo is not explained by effects of cholinergic reflexes, catecholamine release, duration of anesthesia, or, probably, type of anesthetic agent.

Acetylcholine↗
PubMed1988

Histamine tachyphylaxis in canine airways despite prostaglandin synthesis inhibition.

Tachyphylaxis to aerosolized histamine was studied in dogs anesthetized with thiamylal after pretreatment with prostaglandin synthesis inhibitors. Three consecutive histamine dose-response curves were obtained in nine dogs pretreated with 5 mg/kg indomethacin; two of these nine were also pretreated with 10 mg/kg indomethacin. Seven of the nine dogs were pretreated with 4 mg/kg sodium meclofenamate; four of these seven were also pretreated with 12 mg/kg. All dogs had tachyphylaxis at high concentrations of histamine regardless of inhibitor used. Pretreatment with indomethacin while the dogs were under alpha-chloralose-urethan anesthesia gave similar results. Histamine tachyphylaxis was also studied both in the presence and in the absence of indomethacin in tracheal smooth muscle strips obtained from seven additional dogs. A decrease in the median effective dose to histamine was observed in the indomethacin-treated strips, but tachyphylaxis to histamine remained. We conclude that prostaglandin synthesis inhibition does not reverse histamine tachyphylaxis either in vivo or in vitro. Thus the mechanism of histamine tachyphylaxis remains unexplained.

Airway Resistance↗
PubMed1989

Measurement of lung fluid volumes and albumin exclusion in sheep.

A radioactive tracer technique was used to determine interstitial diethylenetriaminepentaacetic acid (DTPA) and albumin distribution volume in sheep lungs. 125I- and/or 131I-labeled albumin were injected intravenously and allowed to equilibrate for 24 h. 99mTc-labeled DTPA and 51Cr-labeled erythrocytes were injected and allowed to equilibrate (2 h and 15 min, respectively) before a lethal dose of thiamylal sodium. Two biopsies (1-3 g) were taken from each lung and the remaining tissue was homogenized for wet-to-dry lung weight and volume calculations. Estimates of distribution volumes from whole lung homogenized samples were statistically smaller than biopsy samples for extravascular water, interstitial 99mTc-DTPA, and interstitial albumin. The mean fraction of the interstitium (Fe), which excludes albumin, was 0.68 +/- 0.04 for whole lung samples compared with 0.62 +/- 0.03 for biopsy samples. Hematocrit may explain the consistent difference. To make the Fe for biopsy samples match that for homogenized samples, a mean hematocrit, which was 82% of large vessel hematocrit, was required. Excluded volume fraction for exogenous sheep albumin was compared with that of exogenous human albumin in two sheep, and no difference was found at 24 h.

Albumins↗
PubMed1976

Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs.

Vasodilator responses to acute intra-arterial infusions of K+ are attenuated in dogs with chronic one-kidney perinephritic hypertension in rats with chronic two-kidney Goldblatt hypertension, and in men with essential hypertension. There is evidence that K+ evokes vasodilation by stimulating vascular smooth muscle membrane Na+-K+-activated adenosine triphosphatase, thereby increasing activity of the cellular Na+-K+ electrogenic pump. We therefore proposed that there may be an underlying decrease in the operation of this pump in vascular smooth muscle of hypertensives. The operation of the cellular Na+-K+ pump may be estimated by measurement of rubidium uptake. Thus, so further investigate our hypothesis, we measured 86Rb uptake in small mesenteric arteries and splanchnic veins from 12 dogs with chronic uncomplicated one-kidney perinephritic hypertension and from 12 normotensive control dogs. Vessels were excised under thiamylal anesthesia and incubated in cold medium (plasma or Krebs-Henseleit solution) for sodium loading and then the velocity of 86Rb uptake was estimated in the absence of or in the presence of ouabain, a specific inhibitor of the Na+-K+ pump. In neither arteries nor veins was there evidence for differences between hypertensives and normotensives in the ouabain-insensitive uptake of 86Rb. In contrast, the ouabain-sensitive 86Rb uptake was depressed by 42% in arteries (P less than 0.05) and by 49% in veins (P less than 0.01) from hypertensive dogs, if incubated in the dog's own plasma. These results indicate that the activity of a ouabain-sensitive Na+-K+ pump may be depressed in vascular tissue from dogs with chronic one-kidney perinephritic hypertension. Because the Na+-K+ pump in vascular smooth muscle is probably electrogenic, such an abnormality, by partially depolarizing the muscle cell membrane, would help to account for the elevated vascular resistance found in these dogs.

Adenosine Triphosphatases↗
PubMed1982

Prolactin secretion after hypophysial stalk transection in pigs.

Hypothalamic regulation PRL secretion was investigated in 13 7-month-old Yorkshire gilts by comparing the effects of hypophysial stalk transection and sham operation. Ovariectomized gilts were fitted with an indwelling cannula in the anterior vena cava to determine sequential serum profiles of PRL secretion before, during, and 190 h after cranial surgery. A nylon disc was inserted between severed ends of the hypophysial stalk to prevent vascular and tissue regeneration; sham operations included all surgical procedures with exception of stalk transection and insertion of the disc. During a preoperative period of 120 min, PRL concentrations in peripheral serum remained consistently low [2.3 +/- 0.3 ng/ml (mean +/- SEM)] in all gilts. During 105 min of anesthesia (induced by thiamylal sodium and maintained by halothane and oxygen), PRL increased (8.2 +/- 1.9 ng/ml) in all gilts. Peak PRL values averaged 10.7 ng/ml at hypophysial stalk transection or sham operation and then declined steadily in both groups during the last 105 min of surgery. PRL remained elevated (P less than 0.002) in hypophysial stalk-transected gilts compared with sham-operated controls throughout a postoperative period from 6-190 h (3.7 +/- 0.4 vs. 1.9 +/- 0.2 ng/ml). These results indicate that basal secretion of PRL in the pig is inhibited by the hypothalamus.

Animals↗
PubMedDate not supplied

Effect of morphine-diazepam on signs of anesthesia, awareness, and dreams of patients under N2O for cesarean section.

Morphine (0.2 mg/kg) and diazepam (0.1 mg/kg) were injected IV after delivery of the fetus in 68 parturients undergoing cesarean section (CS). General anesthesia was with thiamylal-N2O-O2 (4:2) and muscle relaxant. Twenty-four to 36 hours postoperatively, 1 patient had recall, 1 had unpleasant dreams, and 2 had pleasant dreams. The incidence of recall and unpleasant dreams was 3.8 percent in elective CS and 0 percent in emergency cesareans. Morphine-diazepam combination caused anterograde and retrograde amnesia. During the cesarean, movement of patient, size of pupils, or changes in blood pressure were not indicative of awareness or dreams. During anesthesia, 33 percent O2 produced adequate oxygenation of mother and fetus.

Amnesia↗