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M D Sokoll

Publications and source records attributed to M D Sokoll.

18 recordsLinked to original sources
PubMed1991

Effect of (+/-)-DOI on neuromuscular transmission: a microelectrode study.

DOI (1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane) significantly depressed end plate current (EPC) amplitude. It decreased quantum content, increased the extent of neurally evoked EPC rundown during the train, produced a nonlinear current-voltage relationship, shortened time constant of decay, and depressed iontophoretically evoked EPC. The depressant response of DOI on EPC amplitude was antagonized by 5-HT1-like receptor antagonists, but was resistant to 5-HT2 and 5-HT3 receptor antagonists. This suggests that inhibitory 5-HT receptors roughly correspond to 5-HT1-like receptors.

Amphetamines↗
PubMed1991

Apology.

Explore the source record for details and available documents.

Publishing↗
PubMed1990

Neuromuscular and cardiovascular effects of mivacurium chloride (BW B1090U) during nitrous oxide-fentanyl-thiopentone and nitrous oxide-halothane anaesthesia.

Seventy-two adult surgical patients were studied to compare neuromuscular and cardiovascular effects of mivacurium chloride during nitrous oxide-fentanyl-thiopentone (BAL group) or nitrous oxide-halothane (HAL group) anaesthesia. Eighteen patients in the BAL group received an initial bolus of mivacurium, either the ED25 (n = 9) or the ED50 (n = 9) (0.03 and 0.05 mg kg-1). These doses were based on the assumption that the slope of the dose-response curve during nitrous oxide-opioid anaesthesia would be approximately the same as the slope of the neuromuscular response from the first human studies with mivacurium. Twenty-seven additional patients were allocated to subgroups of nine patients to receive mivacurium 0.04, 0.08 or 0.15 mg kg-1. Twenty-seven patients in the HAL group were allocated also to subgroups of nine patients to receive mivacurium 0.03, 0.04 or 0.15 mg kg-1. During stable anaesthesia, mean endtidal halothane concentrations were maintained at 0.49 +/- 0.01%. The estimated ED50, ED75 and ED95 for BAL and HAL groups were 0.039, 0.05 and 0.073 mg kg-1 and 0.040, 0.053 and 0.081 mg kg-1, respectively. Halothane did not potentiate maximum block or time to maximum block. Halothane did affect spontaneous recovery. With the 0.15-mg kg-1 dose, time to 95% recovery was prolonged significantly in the HAL group (30.0 (SEM 1.4) min) compared with the BAL group (24.1 (1.5) min). Recovery index from 25% to 75% recovery was also prolonged significantly in the HAL group (7.0 (0.4) min) compared with the BAL group (5.4 (0.4) min). There were no significant haemodynamic changes in groups given mivacurium doses up to and including 2 x ED95 by bolus i.v. administration.

Adolescent↗
PubMed1990

Anesthesia for craniotomy: a double-blind comparison of alfentanil, fentanyl, and sufentanil.

Using a prospective, randomized, and double-blind study design, alfentanil (n = 15), fentanyl (n = 14), or sufentanil (n = 16), in combination with N2O, were administered to patients undergoing craniotomy for supratentorial tumor resection. Physicians were given two syringes, one of which was labeled as "load" for the initial loading dose and the other as "maintenance" for continuous infusion. The concentration of drug in each syringe was adjusted to permit administration on a milliliter per kilogram basis. The target loading doses for alfentanil, fentanyl, and sufentanil were 75, 10, and 1 microgram/kg, respectively, and initial infusion rates were 33.5, 2.0, and 0.3 microgram.kg-1.h-1, respectively. Additional supplementary boluses and changes in maintenance infusion rate were made according to predetermined guidelines. Isoflurane, in increasing 0.2% inspired increments, was used only when the maximum allowed opioid dose had been given (i.e., supplementary bolus doses equal to 75% of the calculated loading dose or supplementary bolus doses equal to 50% of the calculated loading dose combined with a 50% increase in the maintenance infusion rate). Opioid infusions were stopped at the time of bone flap replacement. Antihypertensive medications and naloxone were subsequently given at the discretion of the anesthesiologist. Group demographics were not different. Total volumes of drug were similar among groups indicating equipotent preparations. Administration of isoflurane, antihypertensive medications, and naloxone were not different among groups. Although decreases in blood pressure seen with induction were similar among groups, alfentanil-treated patients received ephedrine more frequently before intubation. Thirty minutes after entry into the postanesthesia recovery area, respiratory rate and pH were lowest in sufentanil-treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Neuromuscular and cardiovascular effects of mivacurium chloride (BW B109OU) during nitrous oxide-narcotic, nitrous oxide-halothane and nitrous oxide-isoflurane anesthesia in surgical patients.

One hundred seventeen adult surgical patients were studied to compare neuromuscular and cardiovascular effects of mivacurium chloride during nitrous oxide-narcotic (BAL, n = 45) nitrous oxide-halothane (HAL, n = 27) and nitrous oxide-isoflurane (ISF, n = 45) anesthesia. Anesthesia was maintained with nitrous oxide (60%-70%) and oxygen (30%-40%) with end-tidal concentrations of halothane or isoflurane to yield a total MAC of approximately 1.25, or with supplemental fentanyl and thiopental as clinically indicated. Twitch response of the adductor pollicis muscle was elicited by supramaximal square wave pulses of 0.2 msec duration at a frequency of 0.15 Hz (Grass S44 stimulator) to the ulnar nerve and quantitated by a Grass FT10 transducer. Nine patients in each of the HAL and ISF groups received one of four doses of mivacurium (0.03, 0.05, 0.10 or 0.15 mg/kg). Ninety patients in the balanced anesthesia group received one of seven doses of mivacurium (0.03, 0.04, 0.05, 0.08, 0.15, 0.20, 0.25 mg/kg). The ED50, ED75 and ED95 of mivacurium in each group were estimated from linear regression plots of log dose versus probit of maximum percentage depression of twitch height. The ED50, ED75 and ED95 for halothane and isoflurane are 0.040, 0.053 and 0.081 and 0.037, 0.043 and 0.053, respectively. The ED50, ED75, and ED95 for the balanced group are 0.039, 0.050, and 0.073 mg/kg respectively. There was no significant difference between the slopes of the HAL and BAL inhalation anesthetic dose-response curves. The slope of the ISF group was significantly than the slope of the BAL group. Intercepts of the HAL and BAL curves were not different. The isoflurane curve's intercept was significantly less than the other groups' intercepts, lying above the halothane curve, but below the BAL curve. For the 0.05 mg/kg dose, maximum block was greater in the ISF group (89.1 +/- 2.7%, n = 9) than in the HAL (70.3 +/- 7.6%, n = 9) or BAL (67.7 +/- 6.4%, n = 9) groups. At higher doses of mivacurium, isoflurane produces a greater potentiation of neuromuscular block than halothane or balanced anesthesia. There were no significant cardiovascular changes seen in any group following mivacurium doses up to 0.15 mg/kg (approximately 2xED95).

Adult↗
PubMed1979

Malignant hyperthermia.

A short review of the history, incidence, and present-day concept of the etiology of malignant hyperthermia is presented. Protocols for diagnosis, treatment of the unexpected occurrence, and management of known malignant hyperthermic patients is presented. The exact etiology of the syndrome is still unknown.

Anesthesia, Inhalation↗
PubMed1977

Effect of sodium nitroprusside and trimetaphan on neuromuscular transmission in the frog.

In summary, it appears from this and other studies that trimetaphan has the potential for producing neuromuscular blockade when used in large doses or when combined with other muscle relaxants. The mode of action appears to be principally that of non-depolarizing neuromuscular blockade. Sodium nitroprusside, on the other hand, even in doses beyond these accepted clinically, does not affect neuromuscular transmission and unless otherwise contraindicated is safe to use with muscle relaxants.

Acetylcholine↗
PubMed1975

Studies of the neuromuscular blocking effects of BW 403C65 in frog and cat muscle.

BW 403C65, an isoquinolinium bisquaternary compound, was investigated for its neuromuscular blocking properties. In vitro in from preparations, low concentrations induced an increase in miniature endplate potentials (m.e.p.p.) frequency without altering their amplitude. With increasing concentrations m.e.p.p. frequency returned to control value and amplitude started to decrease concomitantly with the decreased sensitivity of the endplate to iontophoretically applied acetylcholine and depression of the twitch tension. Acetylcholine released at the neuromuscular junction was also decreased. In vivo in the cat preparation the intra-arterial injection of low doses of the drug produced an increase in the strength of the muscle twitch, and the development of contracture, as well as the appearance of post-drug repetition at the ventral roots. Greater doses produced a progressive decline in post-tetanic potentiation with prolonged return to control.

Acetylcholine↗
PubMed1975

Actions of a new muscle relaxant (AH8165) on neuromuscular transmission.

The effects of a new muscle relaxant, AH8165, on miniature endplate potential (MEPP) amplitude and frequency, endplate sensitivity to acetylcholine, and muscle twitch tension were studied in vitro in the frog sartorius muscle. Nerve terminal effects were studied in vivo in the cat soleus muscle and its ventral root fibers. AH8165 stimulates the nerve terminal, as evidenced by increased MEPP frequency and the appearance of post-drug repetitive activity. In the same concentration range at which MEPP frequency is increased, MEPP amplitude, endplate sensitivity to acetylcholine, and twitch tension are decreased. This suggests that AH8165 produces muscle relaxation by blocking postsynaptic cholinergic receptors. (Key works: Neuromuscular relaxants, AH8165.).

Acetylcholine↗
PubMed1975

Intracranial pressure during hypotension and subsequent vasopressor therapy in anesthetized cats.

The effects of vasopressor therapy on intracranial pressure (ICP) during hypotension were evaluated in 45 adult cats anesthetized with pentobarbital and hyperventilated via an endotracheal tube with nitrous oxide, 70 per cent, and oxygen, 30 per cent, to maintain Paco2 25 plus or minus 5 torr. Hypotension was induced by intravenous administration of trimethaphan camsylate or sodium nitroferricyanide and by hemorrhage. Vasopressor (norepinephrine, ephedrine, or isoproterenol) administration in the absence of hypotension caused slight transient increases in ICP. Trimethaphan produced increases in ICP averaging 4.3 mm Hg, while sodium nitroferricyanide caused no change and hemorrhage decreased ICP by 3.9 mm Hg. After hypotension was established, vasopressors caused increases in ICP of 1-21 mm Hg. The greatest increase was seen with norepinephrine administration during sodium nitroferricyanide-induced hypotension. Increases in ICP were pronounced in absolute magnitude and rapidity of rise but were of short duration (2 to 5 minutes). The elevation of pressure might be of clinical significance in patients who have pre-existing intracranial hypertension or space-occupying lesions.

Anesthesia, Inhalation↗
PubMedDate not supplied

Dibutyryl cyclic adenosine monophosphate effects in the ischemic-hypoxic cat.

The effects of dibutyryl cyclic adenosine monophosphate (dB-cAMP) were studied in fifty cats, twenty anesthetized with pentobarbital and thirty with halothane. Nasopharyngeal temperature and Paco2 were maintained at normal values. Somatosensory evoked response was monitored and used as an indicator of cerebral cortical function. Ischemic hypoxic injury was produced by an orthopedic tourniquet snugly applied around the animal's neck and inflated for a period of fifteen minutes. This method produces a reliable and reproducible injury. Times for recovery of the evoked response to 10% of control value, as well as immediate and long-term animal survival, were noted. The dBcAMP was administered at the end of the hypoxic insult. Treated animals recovered the evoked response earlier than the untreated controls and had better immediate and long-term survival rates.

Anesthesia, General↗
PubMedDate not supplied

Vascular spasm in cat cerebral cortex following ischemia.

The reaction of brain parenchymal vessels in areas of no-reflow following ischemia in cats was evaluated. A method was devised by which brain biopsies following ischemia were quickly frozen at -170 degrees C, sections were cut and stained and vessel internal and external diameter measured. Vessels in the no-reflow areas had smaller internal and external diameters and thicker walls when compared to adjacent reflow areas as well as to normal control animals. By utilizing a 2-way analysis of variance in which reflow versus no-reflow vessel diameters were compared by region the differences were found to be statistically significant (p less than 0.05). The data raise the possibility that there may exist normal regional differences in the size of cerebral vessels.

Animals↗
PubMedDate not supplied

Anesthesia and subarachnoid intracranial pressure.

Intracranial pressure (ICP) was continuously monitored by the Richmond technic of Vries and Becker in 17 patients undergoing elective craniotomy. This method entails the placement, underlocal anesthesia, of a hollow screw through the cranium into the subarachnoid space. The screw was connected to a Statham P23Db pressure transducer with heavy vinyl tubing and with pressures recorded on a Beckman Dynograph. The effects of 3 anesthetic technice-halothane, enflurane, and nitrous oxide-narcotic-relaxant-on ICP during induction and maintenance were compared with preinduction control pressures. Control ICP in awake, lightly premedicated patients was 15 plus or minus 10 torr. Mask inductions with halothane and enflurane consistently caused significant increases in ICP from preinduction levels in the absence of excitement or airway obstruction. Induction with nitrous oxide-narcotic-relaxant did not increase ICP. Decreases in ICP following barbiturate administration were noted. Addition of halothane and enflurane to the inspired mixture of patients controlled and hyperventilated with nitrous oxide and oxygen caused consistent increases in ICP. With control hyperventilation (Paco2 25 plus or minus 5 torr), the ICP did not return toward preinduction values within 5 minutes with enflurane and halothane.

Anesthesia, Inhalation↗
PubMedDate not supplied

The effects of heparin on recovery from ischemic brain injuries in cats.

Since ischemic anoxia in experimental animals has been reported to produce areas of cerebral postocclusive nonperfusion, the authors studied the effect of heparin on recovery from tourniquet-produced cerebrovascular injury in 41 barbiturate-anesthetized, ventilated cats (PaCO2 30 +/- 2.5 torr). Twenty-four control animals were subjected to 2-to-12-minute ischemic injuries without further treatment. Seven experimental animals were given heparin (1000 u/kg) 1 minute before 4-to-7-minute ischemic injuries, while 10 animals received heparin (1000 u/kg) immediately after 4-to-7-minute injuries. All animals were monitored with continuous arterial and intracranial pressure (ICP) recordings, EEG, and evoked cortical responses. Ischemia and evoked-response recovery times were linearly related in all groups (r = 0.998 control, r = 0.936 heparin preinjury, r = 0.951 heparin postinjury). Regression-line slope comparison indicated shorter evoked response and EEG recovery times in the heparin-treated groups than in the control group. Heparin administration did not effect elevations of ICP seen 6 and 12 hours postinjury in control versus experimental groups. In cats with injuries lasting 5 minutes or more, all control animals were decerebrate and apneic, while 5/12 heparin-treated animals had lesser neurologic deficits.

Animals↗
PubMedDate not supplied

Comparative neuromuscular effects of lincomycin and clindamycin.

The effects of lincomycin and clindamycin on neuromuscular transmission in vitro were studied. Standard microelectrode technics were used to measure miniature endplate potential (MEPP) amplitude and frequency, and endplate sensitivity to acetycholine on the frog sartorius muscle. Twitch tension and nerve terminal acetycholine release were also studied. In the drug concentration range where twitch tension changes occurred, both drugs caused marked decreases in MEPP amplitude and decreases in endplate sensitivity to iontophoretically applied acetylcholine. Lincomycin did not alter MEPP frequency but decreased acetylcholine release. Clindamycin increased MEPP frequency and increased acetylcholine release. The study shows that both lincomycin and clindamycin cause blockade of neuromuscular transmission through a postsynaptic action. However, at high concentrations, lincomycin has a nerve-terminal depressant effect, while clindamycin has a marked presynaptic stimulatory effect.

Acetylcholine↗
PubMedDate not supplied

Management of suspected malignant hyperpyrexia in an infant.

A case of possible malignant hyperthermia in a 6-month-old child is presented. Malignant hyperthermia was manifested in this patient by persistent metabolic acidosis in the intraoperative and postoperative periods, by a rapid rise in temperature with concomitant unresponsiveness in the postoperative period, and by a positive caffeine-halothane stimulation test. The malignant hyperthermia occurring in the postoperative period resolved promptly following administration of dantrolene sodium. An unusual aspect of this case is that both of the child's parents had normal CPK values and negative caffeine-halothane stimulation tests.

Caffeine↗
PubMedDate not supplied

Mechanism for antagonism of paraoxon by hemicholinium-3 analogues.

In a newly synthesized series of DMAE analogues (bis-diethyl analogue of hemicholinium-3), selected chemicals (TL-402 = NAM-242 greater than JGC-VII-110) showed significant protection of mouse lethality after acute toxic doses of paraoxon (in vivo). DMAE and NAM-250 (like hemicholinium-3) showed minimal or no antagonism against paraoxon-induced toxicity in mice. Studies with DMAE analogues demonstrate weak anticholinesterase activity. The pattern for the neuromuscular inhibition of TL-402, NAM-242 and JGC-VII-110 is different from that of hemicholinium-3. LD50 studies identified compounds with less inherent toxicity (TL-402, NAM-242 and JGC-VII-110) and showed significant antagonism in contrast to DMAE and NAM-250. These chemicals (DMAE and NAM-250) are as toxic as the parent compound hemicholinium-3. All compounds in this series showed potent antinicotinic activity in different nicotinic-receptor preparations. The antinicotinic activity correlates with their action on the acetylcholine receptor-ion channel complex at frog neuromuscular junctions (in vitro). Electrophysiological studies demonstrate that the antinicotinic agents significantly depressed both the end plate current (EPC) amplitude and the time constant of decay (tau EPC) at the end plate of frog. In presence of paraoxon, voltage- and concentration-dependent shortening of tau EPC is observed which is more prominent than the decrease of the amplitude of EPC. The antinicotinic agents which showed significant antagonism of paraoxon both in vivo and in vitro (TL-402, NAM-242 and JGC-VII-110) also produced profound tetanic rundown after neurally or ionophoretically evoked EPC. These effects are voltage-dependent. The marked shortening of tau EPC, linear relationship between 1/tau vs DMAE analogue concentrations and potential-dependent tetanic rundown suggest that these analogues produce antagonism of paraoxon primarily by reducing end plate permeability by blocking nicotinic ACh-R associated ion channels in their open form. The antinicotinic activity of these agents is related to acetal or corresponding ether substitution.

Animals↗