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Biomedical subjects

H Turndorf

Publications and source records attributed to H Turndorf.

At least 73 records · Page 4Linked to original sources
PubMed1990

Effects of kappa- and mu-selective opiate agonists on colonic temperature in normoglycaemic and streptozotocin-treated hyperglycaemic mice.

The thermic responses of highly selective k-(U-69593 and U-50488H) and mu-(sufentanil and fentanyl) agonists were assessed in normoglycaemic and hyperglycaemic mice. Hyperglycaemia was induced by streptozotocin injection. The opiates were injected subcutaneously and colonic temperatures monitored for 90 min. after injection. In normoglycaemic animals the k-agonists induced a significant hypothermic response and hyperglycaemia did not modify this effect. In normoglycaemic mice, low doses of mu-selective agonists predominantly produced hypothermia, while in high doses resulted in hyperthermia. In chronic hyperglycaemic mice, hyperthermia was the predominant effect of mu-opiates. The present results characterize the time course and dose response of some of the currently available highly selective kappa- and mu-opiate agonists for the first time in mice and suggest that hyperglycaemia differentially affects the opiate receptor subtypes that mediate thermoregulatory events.

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

Effect of pertussis toxin on the interaction of azepexole and halothane.

The effect of pertussis toxin on the interaction of azepexole and halothane was determined on the guinea pig ileum. Both azepexole and halothane inhibited electrically induced contractions with IC50 values of 3.3 X 10(-6) M and 1.5 V/V%, respectively. The two drugs interacted synergistically at concentrations producing inhibition greater than 50%. Pretreatment with pertussis toxin reduced the potency of each agent individually and abolished the synergistic interaction. The results demonstrate that the effects of halothane and azepexole involve a pertussis-sensitive G protein, thus suggesting that the effects of volatile anesthetics are mediated in part by this group of membrane associated proteins.

Adrenergic alpha-Agonists↗
PubMed1990

Anesthesia for angioembolization of brain arteriovenous malformations: a retrospective assessment.

We reviewed the anesthetic management of 55 patients under 18 years of age during angioembolization of arteriovenous malformations. Patients were grouped according to age: less than 1 month (A), 1-11 months (B), 1-5 years (C) and 7-13 years (D). All had general endotracheal anesthesia. In groups A and B, approximately 43% received pure narcotic and 43% balanced while only 14% had pure inhalational anesthesia. In groups C and D, 41 and 52% received pure inhalation and balanced anesthesia, respectively, while only 7% had pure narcotics. Hypotension was induced in 50% (C and D) and in 20% (A and B) of the patients. Intraoperative lasix or phlebotomy was used in 28, 16, 13 and 0% of groups A, B, C and D, respectively. Two arrests occurred immediately after the injection of the embolizing material. From our review, no single type of anesthesia can be advocated over all others. The use of invasive monitoring (arterial and central venous lines), precise fluid management and the avoidance of nitrous oxide will help to decrease the incidence of intraoperative complications during anesthesia.

Anesthesia, General↗
PubMed1989

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice.

In mice with streptozotocin-induced hyperglycemia, nociception was tested after naloxone administration in hot plate and tail immersion tests. The choice of these two tests was to include a supra-spinal nociceptive reflex indicative of higher cognitive process (hot-plate test) as well as a reflex which predominantly represents lower spinal motor mechanisms (tail immersion test). Naloxone-induced hyperalgesia was attenuated in both tests in mice with streptozotocin-induced diabetes. In mice with hyperglycemia induced by intraperitoneal dextrose administration, naloxone hyperalgesia was significantly enhanced in the hot plate test. The basal nociceptive threshold in streptozotocin-treated animals was decreased in the immersion but not in the hot plate test. These results indicate that hyperglycemia per se does not adequately explain the changes in naloxone hyperalgesia in experimental models of diabetes. They also suggest that acute hyperglycemia may modify the interaction of endogenous opioid peptides with their receptors only at supra-spinal sites. However, chronic hyperglycemia appears to affect endogenous opioid peptides both at spinal and supra-spinal levels and their interaction with the opiate receptors.

Animals↗
PubMed1989

Effect of yohimbine on nociceptive threshold in normoglycemic and streptozotocin-treated hyperglycemic mice.

The effects of yohimbine (0.1, 1, 3 and 10 mg/kg SC) on nociceptive threshold were tested in mice using the tail-immersion and hot-plate tests. The tail-flick (withdrawal) latency, a monosynaptic spinal nociceptive response, was significantly lowered by yohimbine. This hyperalgesic response was at its peak 0.5 hr after yohimbine injection. The tail-flick latencies expressed as % of basal latencies were, 95 +/- 8, 100 +/- 10, 62 +/- 10, 33 +/- 7 and 28 +/- 4 in vehicle and 0.1, 1, 3 and 10 mg/kg in yohimbine-treated groups respectively. Yohimbine-induced hyperalgesia was observed when stimulus temperature was either 50 degrees C or 45 degrees C; however, the opiate antagonist naloxone (3 mg/kg SC) induced a hyperalgesic response at 50 degrees C and an analgesic response at 45 degrees C stimulus temperature. Streptozotocin-induced hyperglycemia did not influence the hyperalgesic response of yohimbine. In the hot-plate (60 degrees C) test, which involves higher centers and a polysynaptic nociceptive reflex, yohimbine did not modify the jump latency. The data provide evidence for the presence of a tonic spinal noradrenergic inhibitory control of nociceptive mechanism(s) which does not appear to be readily altered by hyperglycemia.

Animals↗
PubMed1989

Tail immersion test for the evaluation of a nociceptive reaction in mice. Methodological considerations.

The effect of two commonly used methods to immobilize the animals, viz. tube restrainer and wrapping in a diaper (chux) on the tail flick latency in immersion test, was evaluated in mice using a stimulus temperature of 50 degrees C. The animals were immobilized either in the tube or chux briefly (25-30 sec) during the tail flick measurements. The basal tail flick latency was 2.8 +/- 0.2 in the tube restrained and 5.5 +/- 0.3 sec in chux restrained groups (p less than 0.001). The analgesic effect of morphine (1, 3, 4, 7, and 10 mg/kg) was significantly higher in the chux-restrained animals as indicated by the dose ratio of 2.16 for the 50% analgesic response in the chux versus tube restrained mice. The tail flick latency, 15 min after naloxone injection (1 and 3 mg/kg), expressed as % of predrug latency was significantly reduced in the chux- but not the tube-restrained group. The hyperalgesic effect of naloxone could not be detected in chux-restrained animals, when the water temperature was increased to 55 degrees C. The results demonstrate that the restraining procedure will influence the analgesic effects of test drugs in tail immersion test. Furthermore, the stimulus temperature appears to be an important variant that could influence the results in this test. The present results demonstrate the hyperalgesic effect of naloxone after systemic administration in the tail immersion test and supports the concept that tail flick response is tonically inhibited by endogenous opioid systems.

Animals↗
PubMed1989

Antinociceptive effects of azepexole (BHT 933) in mice.

Subcutaneous (s.c.) administration of azepexole (BHT 933) at doses between 4 and 40 mg/kg produced dose-dependent antinociceptive effects in mice as assessed by tail-immersion, tail-pinch and acetic acid writhing tests. The ED16s were 5.6 +/- 0.4, 6.7 +/- 1.2 and 2.96 +/- 0.2 mg/kg respectively. Similarly, morphine produced analgesia in the same tests with ED16s of 0.87 +/- 0.03, 0.47 +/- 0.1 and 0.45 +/- 0.01 mg/kg respectively. In all instances naloxone (0.1 mg/kg s.c.) shifted the dose-response curves to morphine to the right in a parallel manner. Naloxone (0.1 and 1 mg/kg s.c.) partially antagonized the effect of azepexole in the tail-immersion and tail-pinch tests but significantly decreased the slope of the dose-response curve suggesting that a competitive interaction at the level of the opioid receptors did not occur. Naloxone had no effect on the antinociceptive action of azepexole in the acetic acid writhing test.

Analgesics↗
PubMed1989

Beta-endorphin and ACTH levels in the perioperative period.

1. The purpose of this study was to determine the plasma levels of beta-endorphin (beta-END) and ACTH in the perioperative period, define correlations of hormonal plasma levels with clinical parameters and establish the effect of droperidol premedication on hormonal levels and clinical parameters. 2. Twenty two were assigned to one of two groups: (1) Control (no premedication) and (2) droperidol (7.5 mg im) premedication. 3. Venous blood samples and clinical evaluations were done the day prior to surgery, just prior to induction of anesthesia and 1-1.5 hr postoperatively. 4. The results indicate that (1) expectancy of surgery on arrival to the operating room increases beta-END but not ACTH plasma levels, (2) this increase in beta-END is not affected by droperidol administration and (3) postsurgical stress increases beta-END and ACTH above operating room levels. 5. These results indicate that although beta-END and ACTH are both produced by the pituitary and derived from a common precursor, the type of stimuli (pre- versus postsurgical stress) seems to differentially affect their plasma levels.

Adrenocorticotropic Hormone↗
PubMed1989

Hyperglycemia does not modify the pupillary effects of mu and kappa opiate agonists in mice.

The effects of mu and kappa opiate agonists were assessed on the pupillary size in normoglycemic and hyperglycemic conditions in mice. The mu agonists used were, morphine (10, 30 and 100 mg/kg), fentanyl (50, 100 and 150 micrograms/kg) and sufentanil (5, 10 and 20 micrograms/kg). The highly selective kappa opiate agonists used were, U-50488H and U-69593 (30 mg/kg). Chronic hyperglycemia was induced by streptozotocin injection (200 mg/kg i.p) 7-8 days before the experiment. Acute hyperglycemia was induced by intraperitoneal glucose (5 g/kg i.p) injection at the time of subcutaneous injection of opiates. In the normoglycemic mice, the mu agonists produced significant mydriasis (P less than 0.05), while kappa agonists had no effect on the pupil. However, both acute and chronic hyperglycemic condition did not affect the mydriatic ratio of the mu opiate agonists. These results indicate that mu opiate receptors induce mydriasis in mice and suggest that the hyperglycemia is not the mechanism involved in the opiate induced mydriasis in mice. With the dose of kappa agonists used, the involvement of kappa receptors in the pupillary effects in mice were not clear. These results support the hypothesis that hyperglycemia is not the primary mechanism for the altered sensitivity of opiates in the animal models of diabetes.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1989

Distribution of 3H-morphine following lumbar subarachnoid injection in unanesthetized rabbits.

Morphine sulfate (40-100 micrograms) and 3H-morphine (125-200 pmol) were injected into the lumbar subarachnoid space of 18 unanesthetized rabbits through a surgically implanted catheter. Radioactivity remaining in the spinal cord 2, 4, 6, and 12 h later revealed recovery (mean +/- SEM) of 45 +/- 5.6% (n = 3), 30.5 +/- 14.1% (n = 4), 11.23 +/- 4.4% (n = 3), and 3.7 +/- 1.1% (n = 3), respectively, of the injected radioactivity. Tritiated morphine was found to be predominantly centered around the injection site, with limited rostral and caudal spread in the cord. No significant radioactivity was detected in plasma or cerebrospinal fluid (CSF) samples from the cisterna magna taken at 5, 15, 30, min and 1, 2, 4, 6, 12, and 24 h after receiving radioactive labeled drug (with the exception of that in one rabbit). Of the injected radioactivity, 75% was recovered in the urine in 12 h. These results suggest that the persistence of morphine in the spinal cord could account for its prolonged analgesic effect following intrathecal administration.

Animals↗
PubMed1989

Subarachnoid injection--a potential complication of retrobulbar block.

This study was undertaken to illustrate the potential for subarachnoid injection during retrobulbar block as a cause of respiratory arrest. Cadaver orbits were used to document the connection between the optic nerve sheath and the subarachnoid space. Following dissections of the orbits on one side of 24 cadavers, the optic nerve sheaths were identified and injected with 0.5 ml of water for measurement of pressure generated during injection. This was followed by intrasheath injection of equal volume of methylene blue for demonstrating the subarachnoid space surrounding the optic nerves. All injections were performed with a 1-ml syringe with a one-and-one-half-inch 22-G needle over a period of 10 s. The blue dye was found to track along the subarachnoid space of the optic nerve sheath to the chiasmatic cistern in the middle cranial fossa. Retrobulbar injections were performed on the contralateral undissected orbits and intrascleral injections were performed on undissected eyes. The size of the syringes, the gauge of the needles, and the speed of injection were uniform for all injections. The pressure generated by injection into the optic nerve sheath or intrascleral injection (approximately 138 mmHg) was three- to fourfold that produced by injection into the retrobulbar adipose tissue (approximately 35 mmHg) (P less than 0.05). The authors conclude that any resistance encountered during retrobulbar block should serve as a warning signal, mandating redirection of the needle, in order to prevent subarachnoid injection.

Anesthetics, Local↗
PubMed1989

The effects of local anesthetics on maternal and neonatal platelet function.

The effects of bupivacaine (B), lidocaine (L) and 2-chloroprocaine (C) on maternal (M) and neonatal (N) platelet function were studied using in vitro beta-thromboglobulin (beta-tg) release (radioimmunoassay), and in vitro platelet aggregation. Aggregation produced by adenosine diphosphate (ADP), epinephrine and collagen was measured in the presence of 1, 10, 100, 500 or 1000 micrograms/ml concentrations of B, L or C. In addition, spontaneous in vivo beta-tg release was measured in M and N blood. In vivo beta-tg level in M and N blood was approximately double that in non-pregnant subjects (p less than 0.025). In vitro beta-tg release in M and N samples was inhibited only at concentrations exceeding 1000 micrograms/ml, and the inhibition was less in M and N samples than in non-pregnant subjects. None of the anesthetics inhibited aggregation of M or N platelets at 1 and 10 micrograms/ml. Only concentrations of 500 micrograms/ml or greater consistently inhibited platelet aggregation produced by the three aggregants in M and N samples, and L was the least effective of the three agents. Neonatal platelet aggregation was affected more by local anesthetics than was maternal aggregation. It is concluded that plasma local anesthetic concentrations achieved during normal maternal epidural anesthesia do not affect M or N platelet aggregation or beta-tg release.

Anesthesia, Epidural↗
PubMed1989

Hypothermia enhances the effects of morphine on hormonal and histamine release.

1. The effects of intravenous (i.v.) morphine on adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-END), total catecholamines (CA) and histamine (HIS) plasma concentrations, were determined in anaesthetized dogs at 30 degrees C and 37 degrees C. 2. Hypothermia initially increased CA levels by 29%, but the values returned to baseline after 2 h. Morphine (1 mg/kg, i.v.) produced a significant decrease in CA both at 37 degrees C and 30 degrees C (34% and 54%, respectively). Subsequent administration of naloxone (1 mg/kg, i.v.) significantly increased CA levels in both groups. 3. Hypothermia per se had no effect on ACTH, beta-END, and HIS concentrations. Morphine produced a significant increase in pituitary hormones and HIS, in hypothermic but not in normothermic animals. Morphine concentrations were significantly higher at 30 degrees C during the first 45 min. 4. The results suggest that the effects of morphine on hormonal and histamine release observed at 30 degrees C are concentration-dependent and related to changes in morphine pharmacokinetics.

Adrenocorticotropic Hormone↗
PubMed1989

Hyperglycaemia as a factor affecting kappa-opiate agonist-induced inhibition of the gastrointestinal transit in mice.

The effects of highly selective kappa-opiate agonists were assessed on the gastrointestinal motility in normoglycaemic and hyperglycaemic conditions in mice. Chronic hyperglycaemia was induced by streptozocin injection (200 mg kg-1 i.p.), 7-8 days before the experiment. Acute hyperglycaemia was induced by glucose injection (5 g kg-1 i.p.) at the time of opiate administration. The kappa-opiate agonists, U-50488H and U-69593 (1, 3 and 10 mg kg-1) were injected (i.p.) just before the charcoal meal. The animals were killed 45 min later and the distance travelled by the test meal was measured. In the normoglycaemic mice, both kappa-agonists significantly (P less than 0.05) inhibited the meal transit and this effect was significantly (P less than 0.05) augmented in acute hyperglycaemic animals. However, in chronic hyperglycaemic animals U-50488H failed to inhibit the charcoal meal transit, while U-69593 produced anti-transit effect comparable to that observed in normoglycaemic mice. These results demonstrate that kappa-opiate agonists produce anti-transit effects in mice that these effects are enhanced during acute hyperglycaemia. The disparity of anti-transit effects of kappa-opiate agonists in acute vs chronic hyperglycaemia supports the hypothesis that elevated glucose levels are not the primary mechanism for the altered response to opiates observed in the experimental models of diabetes.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1989

Plasma beta-endorphin levels in the umbilical cord blood of preterm human neonates.

Maternal venous (MV) and neonatal umbilical venous (UV) and umbilical arterial (UA) plasma beta-endorphin concentrations were measured at birth in two groups of patients undergoing cesarean section (CS). Patients in group 1 carried a term gestation (n = 12, birth weight 3,640 +/- 150 g, 1 SEM). Patients in group 2 (n = 12) carried a preterm gestation (birth weight 1,956 +/- 150 g). In the term neonate the UV and UA plasma beta-endorphin were 11.5 +/- 4 and 13.5 +/- 4 picomoles/liter, respectively. In the preterm neonate the UV and UA values were 23.6 +/- 4 and 23.5 +/- 5 picomoles/liter, respectively. Both values in the preterm neonate were significantly greater than the corresponding value in the term neonate (p less than 0.05). The MV plasma beta-endorphin did not significantly differ among the two groups. Data suggest that in preterm neonates increased plasma beta-endorphin levels occur at the time of birth.

Cesarean Section↗