Nystagmus following epidural morphine.
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Biomedical subjects
Publications and source records attributed to R A Stevens.
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To test the hypothesis that increasing levels of epidural analgesia will produce progressive decreases in circulating catecholamines, we sequentially produced three levels of analgesia, T8, T4, and C8, to pin prick in young, healthy volunteers. Three percent chloroprocaine (plain) was used as the local anesthetic. The epidural analgesia was allowed to dissipate following the T8 and T4 levels of block. After the C8 level the block was reinforced to study the effect of a "top-up" dose. Blood samples were drawn from a central venous catheter. Plasma concentrations of norepinephrine and epinephrine were determined by the single isotope radioenzymatic method. Despite extensive block, hemodynamic alterations were minimal, and no significant decrease in plasma epinephrine was observed as the level of analgesia was raised to the C8 dermatome. When the level of analgesia was raised above T8, there was a trend for norepinephrine to decrease, but this decrease did not become statistically significant until analgesia reached the C8 dermatome. Reinforcing the epidural block at the C8 level of analgesia resulted an insignificant decrease in epinephrine and norepinephrine NE. Under the conditions of the present study, epidural block with a sensory analgesia level as high as C8 did not significantly decrease the plasma concentration of epinephrine in unstressed volunteers. The plasma concentration of norepinephrine significantly decreased only when the level of sensory analgesia was approximately C8.
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The effect of a high epidural block on the catecholamine response to hypoventilation was studied in six unanesthetized dogs given intravenous sufentanil (15 micrograms.kg-1). Sufentanil alone resulted in a increase of norepinephrine (NE) concentration from 108 +/- 73 pg.ml-1 to 843 +/- 399 pg.ml-1 and epinephrine (E) from 279 +/- 80 pg.ml-1 to 2010 +/- 1416 pg.ml-1. At least one week later, an epidural block to T1 was achieved using 8-10 ml, two per cent lidocaine. Plasma NE and E decreased after EA to about 50 per cent of resting baseline measurements. The addition of sufentanil increased NE and E levels to reach approximately the resting base-line levels. In all dogs intravenous sufentanil resulted in bradypnoea, bradycardia, hypoxaemia, and hypercarbia. Intravenous lidocaine infusions had no significant effect on plasma catecholamine levels when plasma lidocaine levels ranged from 1.7 micrograms.ml-1 to 5.3 micrograms.ml-1. We conclude that a high two per cent lidocaine epidural block attenuates the catecholamine response to hypoventilation in dogs, but the persistence of baseline plasma levels of NE and E suggests that the efferent sympathetic block by high EA is incomplete.
The effect of pH-adjustment of three per cent 2-chloroprocaine (2-CP, Nesacaine MPF) on the onset, duration, and spread of epidural analgesia and anaesthesia was studied in patients undergoing lower extremity surgery. Forty ASA physical status I and II patients were randomized to two groups. In a double-blinded fashion, patients in both groups received an epidural injection of 15 ml of local anaesthetic (LA) solution via a Tuohy needle at the L3-4 interspace. Local anaesthesia for Group I was prepared by adding 3 mEq NaHCO3 to 27 ml three per cent 2-CP and for Group II was prepared by adding 3 ml 0.9 per cent NaCl to 27 ml three per cent 2-CP. Both solutions contained epinephrine (1:200,000). The pH of commercially prepared Nesacaine MPF was 3.19 +/- 0.02. The pH of the solutions used for Group I and Group II patients were 7.32 +/- 0.01 and 3.27 +/- 0.02, respectively. Times to analgesia and anaesthesia at the L2 dermatome were significantly decreased in Group I patients by 2.5 and 6.6 minutes, respectively. Likewise, pH-adjustment accelerated the attainment of maximum level of block by 2.8 min. No statistical differences were found between groups in the maximum level of epidural block, or in time to 2-segment regression. No precipitation of LA was observed in pH-adjusted solutions of 2-CP after 24 hours. We recommend the use of pH-adjusted three per cent 2-CP (Nesacaine MPF) to accelerate the onset of epidural block.
A case is presented of a 30-year-old female with a 4-month history of post-lumbar puncture headache (PLPHA) resulting from an accidental dural puncture during an attempted epidural anesthetic for cesarean section. Epidural blood patches were attempted at 4 days and 3 months post-lumbar puncture, but were unsuccessful. At 4 months post-lumbar puncture, a 24-h epidural saline infusion relieved the PLPHA for 48 h, but the headache returned. Finally, a second epidural saline infusion was done, followed by an epidural blood patch, which permanently cured the PLPHA. Follow-up to 4 months showed no return of the PLPHA. The rationale for epidural blood and saline patches is discussed.
We determined binding characteristics of the triiodothyronine (T3) analog tracer used in the Amerlex and Amerlex-M FT3 radioimmunoassay for the three endogenous binding proteins in serum: thyroxin-binding globulin (TBG), thyroxin binding prealbumin (PA), and albumin. Both T3 and its analog bind to the same sites on TBG and PA. However, the analog has significantly lower association constants (1.0% and 3.8%, respectively, of T3 binding affinity) and it binds to different sites on albumin. Analog binding is characterized by two (weak) specific binding sites [K = 0.46 (SD 0.03) X 10(5) L/mol]; T3 is bound at about 28 very weak, nonspecific sites [K = 0.41 (SD 0.03) X 10(4) L/mol]. Sera from healthy subjects with a wide range of concentrations of binding proteins showed no interference from analog binding in the FT3 assay. In contrast, in vitro studies of albumin binding revealed a weak dependence of both assays on albumin concentration (0.05 pmol of FT3 per gram of albumin per liter), an interference probably unimportant for most laboratory samples. Nonesterified fatty acids (NEFA) and the T3 analog apparently bind to different sites on albumin; thus the Amerlex FT3 assay is insensitive to moderately increased concentrations of NEFA in serum.
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An exocellular inducible alginase from a strain of Alginovibrio aquatilis was purified 61-fold by ammonium sulfate precipitation and column chromatography on Sephadex G-150 and diethylaminoethyl-cellulose. The purified enzyme was more resistant than the crude enzyme to elevated temperatures. The monovalent cations Cs+, Rb+, K+, Na+, and Li+, in order of decreasing enzyme activation, were required for activity. The pH optimum of the purified alginase was 8.0 and its molecular weight from exclusion chromatography on Sephadex G-150 was 110,000.
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A procedure for the preparation of crystalline UDP-glucose pyrophosphorylase is described. K(s) values for UDP-glucose and UTP were determined as 7 and 20 muM respectively, the latter being confirmed by three methods. By assuming an octameric structure, 1 mol of enzyme subunit bound 1 mol of substrate. The metal-ion activator, Mg2+, did not affect the equilibrium between nucleotide and enzyme. A substrate analogue, alphabeta-methylene-UTP, was synthesized and had the same K(s) value as UTP. In its presence, the K(s) for glucose 1-phosphate decreased by two orders of magnitude, thus confirming a compulsory binding order and excluding an uridylated enzyme intermediate. The results are discussed with respect to their implications in vivo.
This study contrasts the graduate training and subsequent careers of a cohort of United States-born foreign medical graduates (USFMGs) and foreign medical graduates (FMGs) who were in training positions in Connecticut in 1964 and who were located in 1971. The data suggest that although USFMGs were foreign-educated, they had certain advantages--both cultural and administrative--in hospital training positions which helped them to pursue different career alternatives than FMGs. However, the data further suggest that they retained characteristics of their foreign training which continued to differentiate them from United States medical graduates (USMGs).
Equations defining the reaction of microbial alginase on commercial sodium alginate are presented with respect to the viscometric assay of enzyme activity. The negative log of K was found to be linearly related to the concentration of algin, where K is defined as the change in the reciprocal of relative viscosity with time. The negative log of K was also found to be linearly related to the amount of enzyme in reaction mixtures when the substrate concentration was held constant.
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BACKGROUND AND OBJECTIVES: Loss of sensation to pinprick and cold are commonly used to test the extent of epidural anesthesia. To see what difference exists between the level of epidural block determined by various sensory modalities, we performed this study in ten volunteers using epidural anesthesia with plain 3% chloroprocaine hydrochloride. METHODS: Four injections of chloroprocaine were made via an epidural catheter inserted at L2-3 with increasing larger volumes. Sensory modalities tested were (1) absence of sensation when tested by pinprick (anesthesia), (2) loss of a sharp sensation compared to an unblocked dermatome when tested by pinprick (analgesia), and (3) loss of cold sensation when tested with an alcohol swab compared to an unblocked dermatome. RESULTS: At 20 minutes after each injection the level of anesthesia was found to be most caudad and the level of analgesia most cephalad. The zone of differential block was greater than four dermatomes at the highest level of block tested. The level of loss of cold sensation was found between the other two levels. Differences between the levels of analgesia and cold sensation tended to be greater with more extensive block. Differences between levels of anesthesia and cold sensation did not significantly change as the extent of epidural anesthesia was increased. CONCLUSIONS: This study establishes the existence of a differential epidural anesthesia during high thoracic block with chloroprocaine and suggests that the intensity of block diminishes as distance from site of injection increases.
The incidence, character and treatment of backache associated with epidural anesthesia (EA) using 3% chloroprocaine (2-CP, Nesacaine-MPF) were observed in ten volunteers undergoing a study of the effects of EA upon plasma catecholamines. Three levels of epidural analgesia were sequentially sought, T10, T4 and C8, in ascending order. Each block was allowed to fully dissipate prior to the next injection. For the first, second and third injections, 15-20 ml, 25-35 ml and 52-60 ml, respectively, of 3% 2-CP were injected via an epidural catheter. Mean total volume of 2-CP injected was 103 ml (range, 92-115 ml) over seven hours. Back pain was first reported after as little as 15 ml (mean +/- SEM, 24.0 +/- 3.9 ml; range, 15-45 ml). The pain was described as a dull ache deep in the lumbar back, ranging in severity from mild to severe. No profound spasm of the erector spinae muscles was observed. Mean verbal analog scale pain scores after regression of the first, second and third blocks were 2.2, 4.3 and 6.5, respectively. Epidural fentanyl (100-200 micrograms) was effective in providing rapid relief of the pain. Large doses or possibly repeated injections of epidural Nesacaine-MPF are associated with an increased incidence and severity of postanesthesia lumbar back pain.
Dural puncture during lumbar sympathetic block (LSB) is a recognized but apparently uncommon complication. Interestingly, post dural puncture headache (PDPH) has not been reported as a complication of LSB. The authors report two cases of PDPH after LSB. In the first case an attempt to treat the PDPH with an epidural blood patch failed. In the second case the patient developed PDPH and a subdural block during separate LSBs. Possible anatomic explanations for these complications are discussed.