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Biomedical subjects

H Turndorf

Publications and source records attributed to H Turndorf.

At least 19 recordsLinked to original sources
PubMed1992

Effect of nitric oxide on mitogenesis and proliferation of cerebellar glial cells.

In the brain, nitric oxide (NO) has been identified as a messenger molecule and a mediator of excitatory amino acid-induced neurotoxicity. In this study, the effects of NO on serum-induced mitogenesis and cell proliferation of the cerebellar glial cells were assessed. NO-generating agent, S-nitroso-N-acetylpenicillamine (SNAP) increased intracellular cyclic guanosine monophosphate (cGMP) levels. Furthermore, 2 chemically dissimilar NO-generating agents, SNAP and sodium nitroprusside (SNP) inhibited serum-induced thymidine incorporation and cell proliferation. The antimitogenic effect of NO was mimicked by 8-bromo-cGMP and blocked by hemoglobin, a known inhibitor of NO. The effect of NO was not cytotoxic, since the cells were not stained with Trypan blue and did not show increased release of lactate dehydrogenase in the culture supernatants. However, NO-treated cells showed decreased conversion of tetrazolium to blue formazan suggesting that NO inhibited mitochondrial activity in the glial cells. These results demonstrate that NO inhibits serum-induced mitogenesis and cell proliferation of cultured rat cerebellar glial cells.

Animals↗
PubMed1992

Halothane anesthesia causes state-dependent retrieval failure in mice.

Effects of exposure to halothane on memory processing was studied using single-trial inhibitory avoidance learning to measure retention. Mice were anesthetized with halothane either before training, immediately after training, or both before training and before testing. Results showed that memory was not impaired by posttraining halothane exposure, indicating that the anesthetic does not cause retrograde amnesia. Mice trained after recovery from halothane showed a robust memory loss 24 h later. This deficit could be alleviated by reexposure to the anesthetic before the retention test. Mice given multiple training trials following recovery from the anesthetic showed a normal rate of learning when compared with controls, but deficient retention. This indicates that the performance deficit was the result of impaired retention (anterograde amnesia) rather than disrupted acquisition. Anterograde amnesia occurred when training was delayed up to 2 h after recovery from anesthesia. These findings indicate that the memory impairment following halothane anesthesia is the result of a state-dependent retrieval failure.

Amnesia, Retrograde↗
PubMed1992

On the mechanism of the interaction of ketamine and halothane in vitro.

1. Electrically induced contraction of guinea pig ileum myenteric plexus-longitudinal muscle was inhibited by ketamine and halothane with IC50s of 2.1 x 10(-4) M and 1.8 v/v% respectively. 2. The inhibitory action of ketamine was partially antagonized by naloxone and the selective kappa antagonist nor-binaltorphimine. 3. The actions of ketamine and halothane were synergistic at high levels of response (above 30% inhibition). 4. The actions of ketamine and halothane became antagonistic after treatment with pertussis toxin. 5. The interaction of ketamine and halothane was similar to the interaction of morphine and halothane.

Animals↗
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

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↗
PubMed1979

The pattern of memory loss resulting from intravenously administered diazepam.

A word recognition task was designed to determine the stage in memory affected by a single 10-mg intravenous injection of diazepam and the duration of the effect. Injection in three experimental subjects produced an anterograde amnesia for the 14 to 24-minute period immediately after injection. Memory loss resulted from impaired storage, the stage during which information is entered into memory. Retention and retrieval stages of memory were unaffected. This temporary amnesia may result from increased inhibition in the hippocampal system produced by diazepam, which shares many properties with the inhibitory neurotransmitter gamma-aminobutyric acid.

Amnesia↗
PubMed1979

Hand-held toy squeaker during carotid endarterectomy in the awake patient.

A toy squeaker held by the patient in the contralateral hand is used to monitor cerebral circulation during carotid endarterectomy. Regional anesthesia--cervical plexus block--allowed the patient to cooperate and give useful information, especially during the crucial period of test clamping. In a series of 300 cases, during a period of five years, it was instrumental in avoiding brain damage in 6% of the cases.

Anesthesia, Conduction↗
PubMed1979

Humidity and the anesthetized patient.

Damage to the ciliated cells of the tracheobronchial tree and incidence of postoperative pulmonary complications were measured by point-scoring systems in 202 patients who breathed dry and humidified anesthetic gases for 225 +/- 78 min. The incidence of postoperative pulmonary complications decreased as the humidity of administered anesthetic gases increased from 0 to 32.5 mg H2O/l. A similar relationship was found between the amount of inhaled moisture and the damage to the ciliated epithelium of the tracheobronchial tree. These results appear to indicate that a high inspired humidity is beneficial for operations on normothermic patients, and that cellular damage caused by dryness is a possible contributory factor in the production of the pulmonary atelectasis that follows stoppage of the mucociliary transport system in the immmediate postoperative period.

Adolescent↗
PubMed1979

Impact of cardiopulmonary resuscitation training on resuscitation.

Restoration of adequate spontaneous circulation after "arrest" and cardiopulmonary resuscitation (CPR) of 546 patients before and 460 patients after initiation of a CPR training course in a 500-bed city hospital is reported. Between January 1972 and June 1976, adequate circulation after CPR was present in 38.6% of patients before and 50.4% after training ICU nurses and house physicians in modern resuscitation techniques. Factors crucial to resumption of adequate circulation are: (1) CPR training of all hospital personnel so that effective CPR can be started immediately after recognition of an arrest situation, (2) production of a palpable pulse with closed chest cardiac massage, and (3) prompt effective therapy so that the time interval between arrest and resumption of adequate spontaneous circulation is short.

Blood Circulation↗
PubMed1979

An improved program to calculate intrapulmonary shunting.

A computer program was developed to calculate intrapulmonary venous admixture on a Texas Instruments TI 59 programmable calculator. The program incorporates the following characteristics: 1) a correction for saturated water vapor pressure which varies with body temperature; 2) a mathematical model of the standard oxyhemoglobin dissociation curve; and 3) correction factors for shifts of the dissociation curve due to variations in pH and carbon dioxide tension. It also corrects oxygen tensions obtained at electrode temperature to those at patient temperature, and calculates variations of the Bunsen solubility coefficient of oxygen in blood with body temperature.

Bionics↗
PubMed1978

Prevention of nitroprusside-induced cyanide toxicity with hydroxocobalamin.

To investigate hydroxocobalamin's role in preventing cyanide intoxication from sodium nitroprusside, we studied two groups of patients. One group received nitroprusside alone, and the other received nitroprusside and hydroxocobalamin. Red-cell and plasma cyanide levels were 83.44 +/- 23.12 and 3.51 +/- 1.01 microgram per 100 ml after nitroprusside alone and were 33.18 +/- 17.29 and 2.18 +/- 0.65 microgram per 100 ml after nitroprusside plus hydroxocobalamin. Acidosis developed in patients with red-cell cyanide levels higher than 75 microgram per 100 ml. When hydroxocobalamin infusion was stopped before sodium nitroprusside infusion was discontinued, blood cyanide levels and base deficit increased in a manner similar to that in the untreated group. The dose of nitroprusside used in each group did not differ statistically. These data show that hydroxocobalamin prevents cyanide transfer from red cells and plasma to tissue after nitroprusside metabolism, and thereby prevents cyanide toxicity from large intravenous doses of the drug.

Adult↗