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Biomedical subjects

H Turndorf

Publications and source records attributed to H Turndorf.

At least 55 records · Page 3Linked to original sources
PubMed1992

A two-dose epidural morphine regimen for cesarean section patients: therapeutic efficacy.

A single dose of epidural morphine (EM) usually produces 24 h of post-cesarean section (CS) analgesia and patients require supplemental analgesics beyond this period. This study assesses if a second dose of EM administered 24 h after the first one offers superior therapeutic efficacy compared to conventional analgesics. Patients (n = 100) were randomized to receive one or two doses of epidural morphine. In all patients, EM 5 mg was administered after delivery. After 24 h patients received epidurally either normal saline (n = 50, Group 1) or morphine 5 mg (n = 50, Group 2). An independent observer used a visual analogue scale to assess nausea, itching, and analgesia 24 h after each injection. Results were expressed as mean +/- 1 s.e. mean and analyzed using nonparametric methods. The second dose of EM produced a significantly lower incidence and severity of nausea and itching than did the first dose (P < 0.01) in Group 2 with no difference in analgesia. The second day postoperative pain score in Group 1 was significantly greater than the first day score in the same group, and significantly greater than the severity score in Group 2. Only 36% of patients receiving two doses of EM required supplemental analgesics beyond 48 h compared to 76% of those receiving one dose (P < 0.01). No serious complications were noted. In summary, the use of a second dose of EM for post-CS analgesia produces better analgesia and reduces the need for oral analgesics. The second dose produced fewer side-effects, probably due to acute tolerance to morphine.

Adult↗
PubMed1992

Uptake and distribution of bupivacaine and morphine after intrathecal administration in parturients: effects of epinephrine.

This study examines the plasma pharmacokinetics of bupivacaine and morphine and the urinary excretion of morphine administered for spinal anesthesia for cesarean section. Patients received 12 mg of hyperbaric bupivacaine and 0.6 mg of morphine with either 0.2 mL of normal saline (plain, n = 15) or 0.2 mg of epinephrine (n = 15). Venous blood and urine were collected at 0, 0.25, 0.5, 1, 2, 3, 6, 12, and 24 h. Total and unconjugated morphine (UCM) in plasma and urine were measured using radioimmunoassay, and plasma bupivacaine was measured by gas chromatography. Results were expressed as mean +/- SE and analyzed using Student's t-test at P less than 0.05. In the epinephrine group, plasma bupivacaine peaked at 15 min and remained approximately 30% higher (P less than 0.05) at 0.25, 0.5, and 1 h than in the plain group, which peaked at 30 min. Although UCM peaked at 3 h in both groups, the plasma levels remained approximately 66% lower in the epinephrine group. In the epinephrine group, bupivacaine had a smaller volume of distribution at steady state, and morphine had a more rapid clearance, shorter t1/2 beta, and smaller area under the curve compared with the plain group (P less than 0.05). Only 45% +/- 5% and 31% +/- 3% of morphine was recovered in the urine in the plain and epinephrine group, respectively (P less than 0.05). In conclusion, epinephrine added to a bupivacaine-morphine mixture increases the initial systemic uptake of bupivacaine and decreases the absorption and urinary excretion of morphine from the intrathecal space.

Adult↗
PubMed1992

A rat sciatic nerve model for independent assessment of sensory and motor block induced by local anesthetics.

The purpose of this study was to develop a reliable model to independently quantify motor and sensory block produced by local anesthetics. The sciatic nerve was blocked in 52 rats by injecting 0.2 mL of 0.125%, 0.25%, 0.5%, or 0.75% bupivacaine (n = 13 for each concentration). Accurate needle placement was achieved using a nerve stimulator at 0.2 mA and 1 Hz. Ten control rats received 0.9% saline (n = 5) or sham nerve stimulation (n = 5). Motor block was assessed by measuring hindpaw grip strength with a dynamometer. Sensory block was determined by measuring hindpaw withdrawal latency from radiant heat. The intensity of both motor and sensory block measured at 30-min intervals was plotted against time until full recovery to obtain the area under the curve. Intergroup comparisons using analysis of variance showed increasing area under the curve with increasing concentrations of bupivacaine for motor blocks (P < 0.05 for all intergroup comparisons except 0.5% vs 0.75%) and sensory blocks (P < 0.05 for all intergroup comparisons). Normal saline or sham nerve stimulation did not result in any motor or sensory block.

Animals↗
PubMed1992

Prolongation of epidural anesthesia using a lipid drug carrier with procaine, lidocaine, and tetracaine.

This study evaluated the effect of a lipid drug carrier (iophendylate) on epidural anesthesia. The intensity and duration of motor blockade produced by aqueous and lipid preparations of local anesthetics were assessed in rabbits with long-term indwelling catheters in the epidural space. Motor blockades produced by procaine (1%, 2%, and 4%), lidocaine (1%, 2%, and 4%), and tetracaine (0.5%, 1%, and 2%) in normal saline solution were compared with the effects produced by equimolar amounts of the drug solutions in iophendylate. Procaine (4%) in aqueous solution produced motor blockade lasting 30 +/- 3.54 min (mean +/- SD) versus 84 +/- 4.18 min in lipid solution. Lidocaine (2% and 4%) in aqueous solution produced motor blockade lasting 41 +/- 4.18 and 65 +/- 6.12 min versus 39 +/- 4.18 and 118 +/- 10.1 min, respectively, in lipid solution. Aqueous tetracaine (0.5%, 1%, and 2%) produced motor blockade of 106 +/- 9.62, 189 +/- 6.52, and 273 +/- 26.8 min versus 284 +/- 14.7, 335 +/- 15.8, and 365 +/- 26.9 min, respectively, in their lipid counterparts. A control group of animals that received normal saline solution or iophendylate alone did not exhibit motor blockade. These results may be attributed to sustained release of local anesthetics from the lipid vehicle. Hence, lipid drug carriers may be effective in prolonging epidural anesthesia.

Anesthesia, Epidural↗
PubMed1992

Intraoperative monitoring of the dorsal sacral roots: minimizing the risk of iatrogenic micturition disorders.

In 31 children (age, 2-17 years) and 1 adult, individual dorsal root action potentials (DRAPs) from the S1-S3 roots were recorded intraoperatively after electrical stimulation of the dorsal penile or clitoral nerves, in preparation for surgery within the cauda equina. In most patients, pudendal afferent activity was present in S2 and S3 bilaterally; in some, the afferent activity was confined to a single root bilaterally, and in one, to a single root on one side. Dorsal root action potentials of small amplitude were recorded from S1 in 15 patients, although in no patient was S1 the primary carrier of these afferents. No lesion of the roots or rootlets carrying significant afferent activity was created during the rhizotomy, and no dysfunction in micturition resulted. We propose that the neurophysiological identification of roots and rootlets carrying afferent activity from the penile or clitoral nerves allows for rhizotomy of the S2 roots with the least possible risk of postoperative micturition and sexual dysfunction.

Adolescent↗
PubMed1991

Antagonism of acute cocaine toxicity by buprenorphine.

The effect of buprenorphine pretreatment on the acute cocaine toxicity was assessed in male Swiss Webster mice. Buprenorphine pretreatment (0.15 or 0.30 mg/kg ip, 30 mins before) significantly attenuated the lethal effects of cocaine (60-140 mg/kg ip). The dose of cocaine which resulted in 50% mortality (LD50) in saline pretreated group was 100.61 mg/kg while the LD50 of cocaine in buprenorphine (0.15 and 0.3 mg/kg) pretreated groups were 113.57 and 118.16 mg/kg respectively. There was no significant change in the ratio of brain/plasma levels of cocaine in buprenorphine pretreated group when compared to the ratio from saline treated controls. Furthermore, neither naloxone (10 mg/kg ip, 15 mins before) nor naltrexone (3 mg/kg ip, 15 mins before) pretreatment affected the LD50 of cocaine. When tested 0.5, 1, 2, 4, 8 and 24 hrs after cocaine administration, sublethal dose of cocaine (80 mg/kg ip) injection resulted in significant increase in the plasma lactate dehydrogenase (LDH) levels. Buprenorphine pretreatment significantly attenuated cocaine-induced release of LDH. These results suggest that buprenorphine could be of potential advantage over naloxone in the management of cocaine and heroin ("speed ball") toxicity and in studies on the pharmacotherapy of cocaine-induced toxicity, LDH levels may be used as a biochemical marker to assess the protective effects of drugs.

Analysis of Variance↗
PubMed1991

Kappa-opioid receptor-mediated thermonociceptive mechanisms in streptozotocin diabetes.

The effects of the benzomorphan kappa-opiate antagonist MR 2266 and its dextro enantiomer MR 2267 were assessed on thermonociception in male Swiss Webster mice. Experimental diabetes was induced by injecting streptozotocin (200 mg/kg IP, 7-8 days before). Animals with dextrose treatment (5 g/kg, IP, at the time of opiate injection) were used as acute hyperglycemic controls. Nociception was assessed by supraspinal nociceptive reflex (licking and jumping in hot plate test) indicative of higher cognitive process as well as a predominantly lower spinal monosynaptic reflex (tail immersion test). In normoglycemic, acute hyperglycemic and diabetic mice, MR 2266 decreased, while MR 2267 increased, the reaction latencies. The results indicate tonic stereospecific kappa-opiate receptor-mediated spinal and supraspinal thermonociceptive reactions are not modulated by experimental diabetes and thus are distinct from those of naloxone-sensitive mu-opiate receptor sites.

Animals↗
PubMed1991

Lumbar subarachnoid catheterization in rats.

An animal model was developed for the study of subarachnoid (spinal) anesthesia and analgesia under unanesthetized, unsedated and unrestrained conditions. Sprague-Dawley rats were anesthetized with intraperitoneal ketamine (75-100 mg.kg-1). A PE10 catheter was inserted under direct vision into the lumbar subarachnoid space, through partial laminectomy of L1 or L2 with or without removal of adjacent intervertebral ligament. One week after surgery, correct position of the catheter was verified by subarachnoid injection of 0.03-0.05 ml of 1.5% lidocaine, which produced temporary hind limb paralysis in all but one animal in 28 consecutive operations. There was neither mortality nor major complication, intraoperatively or postoperatively. Only 2 animals developed minor subcutaneous would infections which responded to incision, drainage and debridement.

Animals↗
PubMed1991

Morphine-ethanol interaction on body temperature.

1. The interaction between ethanol and morphine on core temperature was investigated in Swiss Webster mice. 2. Morphine (2.5-30 mg/kg) and ethanol (0.5-3.0 mg/g) administered individually resulted in a dose dependent decrease in body temperature. 3. When both drugs were injected simultaneously, body temperature decreased less than it would be expected to if the effects were additive. 4. Naloxone antagonized the hypothermic effect of morphine, but the hypothermic effect of ethanol and that of the combination of morphine plus ethanol was only reversed with high doses of naloxone (10 mg/kg). 5. Individual morphine and ethanol plasma levels were not significantly altered by their concomitant administration. 6. Binding of tritiated naloxone to opiate receptors in mouse brain membrane preparations was unchanged by pretreatment with ethanol (0.5 and 2 mg/g). 7. The interaction between morphine and ethanol was found to be less than additive and not related to pharmacokinetic changes of either drug.

Animals↗
PubMed1991

Intracerebroventricular administration of kappa-agonists induces convulsions in mice.

Intracerebroventricular (ICV) administration of kappa-agonists (PD 117302, U-50488H and U-69593) induced convulsions in a dose-related manner in mice. The dose at which 50% of animals convulsed (CD50) was in nmol ranges for all opioids. Among the opioids used, PD 117302 was the most potent convulsant. ICV administration of either vehicle alone or U-53445E, a non-kappa-opioid (+) enantiomer of U-50488H did not induce convulsions. The convulsive response of kappa-agonists was differentially susceptible for antagonism by naloxone and/or MR 2266. Collectively, these findings support the view that convulsions induced by kappa-agonists in mice involve stereospecific opioid receptor mechanisms. Furthermore, the convulsant effect of kappa-agonists could not be modified by pretreatment with MK-801, ketamine, muscimol or baclofen. It is concluded that kappa-opioid but not NMDA or GABA receptor mechanisms are involved in convulsions induced by kappa-agonists. These results are the first experimental evidence implicating stereospecific kappa-receptor mechanisms in opioid-induced convulsions in mice.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1991

Kappa-opiate agonist-induced inhibition of gastrointestinal transit in different strains of mice.

The effects of kappa-opiate agonists on gastrointestinal motility was assessed in Swiss Webster, C57BL/6, BALB/c and DBA/2 strains of mice. The kappa-agonists, PD 117302, U-69593 and U-50488H (3 mg kg-1), were injected subcutaneously and the distance travelled by a charcoal meal in the gastrointestinal tract was measured. All kappa-agonists induced significant inhibition of charcoal meal transit; however, there were significant strain differences in the antitransit effect. It is concluded that kappa-receptors are involved in the inhibition of gastrointestinal transit and that the negative data reported in the literature may be due to a genotype-dependent effect of kappa-agonists.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1990

Effects of the benzomorphan kappa-opiate, MR 2266 and its (+) enantiomer MR 2267, on thermonociceptive reactions in different strains of mice.

The effects of the benzomorphan kappa opiate MR 2266 and its dextro enantiomer MR 2267 were assessed on thermonociception in Swiss Webster, C57BL/6, BALB/c and DBA/2 strains of mice. In the hot plate (60 +/- 0.5 degrees C, cut-off time 120 s and tail immersion tests, MR 2266 (10 mg/kg, s.c., 15 min before) decreased, while MR 2267 (10 mg/kg s.c., 15 min before) increased the reaction latencies. In the hot plate test, the sensitivities for the effects of MR 2266 and MR 2267 on jump latency in different strains of mice were as follows: MR 2266; BALB greater than Swiss greater than C57BL greater than DBA and MR 2267; DBA greater than BALB = Swiss greater than C57BL. In the immersion test, for the hyperalgesic response of MR 2266, the rank order of strains was; BALB greater than C57BL and DBA greater than or equal to Swiss while the rank order for the analgesic effect of MR 2267 was; Swiss greater than DBA and BALB. The results indicate the presence of tonic kappa-receptor-mediated regulation of the spinal and supra-spinal thermonociceptive reactions which is stereospecific and strain dependent.

Animals↗
PubMed1990

Synergistic interaction of morphine and halothane in the guinea pig ileum: effects of pertussis toxin.

The effects of pertussis toxin on the actions of morphine and halothane in the guinea pig ileum are described. Both morphine and halothane produce a dose-related inhibition of electrically induced muscle contraction. The IC50 of morphine was unchanged by the toxin (2.1 and 2.2 X 10(-7) M in control and toxin-pretreated animals). However, the IC50 of halothane was increased from 2.1 to an extrapolated value of 9.1 vol/vol% by pertussis toxin. At high levels of inhibition the interaction between morphine and halothane was synergistic and was converted to additive in the presence of the toxin. These results demonstrate that in the myenteric longitudinal muscle preparation the effects of halothane, but not those of morphine, are mediated by the substrate for pertussis toxin, possibly a Gi membrane protein. The present study provides significant evidence that the effects of halothane on neuronal tissue are dependent upon an interaction with a specific membrane protein.

Animals↗
PubMed1990

Effects of azepexole on opioid receptors and endogenous opioid release in the guinea pig ileum.

The interactions of the opioid and adrenergic systems were investigated in the guinea pig myenteric plexus longitudinal muscle preparation. Morphine and azepexole (a highly selective alpha 2-adrenergic agonist) inhibit the electrically induced contractions with ED50 of 1.9 X 10(-7) M and 3.1 X 10(-6) M, respectively. The effect of morphine but not that of azepexole was competitively antagonized by naloxone. Stimulation of the preparation at 10 Hz was used to induce endogenous opioid release that was unaffected by azepexole. The authors' findings indicate that the effects of morphine and azepexole are additive, but that there is no direct interaction between the opioid and adrenergic receptors in the ileum. These observations provide some additional insight into the ability of alpha 2-agonists to enhance the effects of opioids and inhalation anesthetics.

Adrenergic alpha-Agonists↗
PubMed1990

The maternal hemodynamic effects of bupivacaine-epinephrine mixture used for obstetrical anesthesia.

The maternal hemodynamic effects of bupivacaine (0.5%)-epinephrine (5 micrograms/ml) mixture used for lumbar epidural anesthesia were studied with an impedance cardiograph and an automated blood pressure device in term gravidas undergoing elective cesarean section. Following i.v. hydration with 2000 ml Ringer's lactate solution, 16 patients received bupivacaine-epinephrine mixture and 16 patients plain bupivacaine in 5-ml increments to a T4 level. Measurements were made before anesthesia, at T10 and at T4 sensory levels. Results were analyzed using analysis of variance (ANOVA) and the least significant difference method at P less than 0.05. In the epinephrine group, at T10 level, the diastolic (D) and mean (M) pressures decreased significantly 11 +/- 3, and 10 +/- 1% (mean +/- s.e. mean) respectively with no significant change in the S pressure. No significant changes were seen in the plain group. At T4, the S, D and M pressures decreased significantly 8 +/- 2, 18 +/- 4 and 16 +/- 2% in the epinephrine group. In the plain group the decrease in each one of these pressures was less than 5% and was not significant. In the epinephrine group, S, D and M pressures decreased significantly more than they did in the plain group at T10 and T4. Systemic vascular resistance decreased significantly from control values by 19 +/- 6% at T4 in the epinephrine group with no significant changes in the plain group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Streptozotocin-diabetes attenuates alpha 2-adrenoceptor agonist-induced delay in small intestinal transit in mice.

1. The effect of alpha 2-adrenoceptor agonists on gastrointestinal motility was assessed in normoglycaemic and streptozotocin-diabetic mice. 2. The alpha 2-adrenoceptor agonists used were: clonidine (0.1, 0.3 and 1 mg kg-1, azepexole (10, 20 and 40 mg kg-1), tizanidine (1, 3 and 10 mg kg-1) and ST-91 (10, 20 and 30 mg kg-1). 3. Acute hyperglycaemia was induced by D-(+)-glucose (5 g kg-1) and chronic hyperglycaemia by streptozotocin (200 mg kg-1) injection. 4. The gut motility was quantitated using the charcoal meal test. 5. The results indicate that in normoglycaemic and acutely hyperglycaemic mice, all of the alpha 2-adrenoceptor agonists used produced significant inhibition of meal transit. 6. However, in streptozotocin-diabetic mice, the anti-transit effect of alpha 2-adrenoceptor agonists was attenuated. 7. Since streptozotocin-induced diabetes but not acute hyperglycaemia was associated with the attenuation of anti-transit effect, elevated blood sugar is not the mechanism for the observed effect. 8. As with groups treated with clonidine, azepexole or tizanidine, the anti-transit effect of a peripherally acting alpha 2-adrenoceptor agonist, ST-91, was attenuated in streptozotocin-diabetic mice. This suggests the involvement of peripheral mechanism(s) in attenuating the anti-transit effect of alpha 2-adrenoceptor agonists. 9. These results identify the need for critical evaluation of the role and efficacy of alpha 2-adrenoceptor agonists in the therapeutic management of diabetic diarrhoea.

Adrenergic alpha-Agonists↗