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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Melanophores and xanthophores are pigment cell derivatives of the NC. In amphibian embryos they migrate from their original position on the neural tube dorsally (into the dorsal fin) as well as laterally (between somites and epidermis) and arrange themselves into typical pigment patterns of the skin. We investigated pigment pattern formation in two species of tailed amphibians, Triturus alpestris (alpine newt) and Ambystoma mexicanum (Mexican axolotl). In larvae of T. alpestris alternating longitudinal stripes or bands of melanophores and xanthophores develop, whereas in larvae of A. mexicanum a barred pattern with alternating transverse bands of melanophores and xanthophores is formed. Iridophores, a third type of pigment cell, are present later in both species and therefore play no role during early larval pigment pattern development. Visibly differentiated melanophores and xanthophores can be distinguished from each other under the light microscope by their contents of black melanins and yellow pterins respectively. With the dopa reaction (indicates tyrosinase in melanophores), and ammonia treatment (stimulates pterin fluorescence in xanthophores), the pigment cell phenotypes can be visualized even before their normal visible differentiation. In the TEM, melanophores and xanthophores can be distinguished from each other by their morphologically distinct pigment organelles and in the SEM by their different surface structure. 2. Because of the NC origin of melanophores and xanthophores and the ease with which these cells can be demonstrated even before they are visible from outside, their different arrangements in Triturus and axolotl embryos offer suitable model systems for studying the migration, interaction and localization of NC derivatives in relation to specific environmental influences. The environment of NC cells are the neural tube, epidermis, somites and lateral plate mesoderm, and the subepidermal ECM, a network of collagen fibrils associated with glycosaminoglycans, proteoglycans and glycoproteins. 3. Development of the pigment pattern in T. alpestris: Melanophores and xanthophores start to leave the NC at stage 28, melanophores slightly earlier than xanthophores. Both cell types become scattered in the dorsolateral trunk. In contrast to melanophores in the axolotl, melanophores in T. alpestris cannot be demonstrated with the dopa reaction before they become visibly black. From stage 29+ onwards, melanophores start to accumulate in zones alongside the dorsal and lateral somite edges, where they form compact stripes later. Xanthophores can be demonstrated from stage 28+ onwards only with the SEM (by means of their specific surface structures) or with the fluorescence microscope (by means of their fluorescing pterins). At state 34, xanthophores become visible externally as yellow cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The development of the larval pigment patterns in Triturus alpestris and Ambystoma mexicanum. 236 40

Forty-four patients, ASA physical status I or II, undergoing thiamylal, fentanyl, N2O/O2 anaesthesia were studied to determine the dose-response to succinylcholine (Sch) without prior defasciculation (24 pt - Group 1), or three minutes following d-tubocurarine (dTC), 0.043 mg.kg-1 (20 pt - Group 2). The individual log dose-logit response curve for each patient was determined using a cumulative dose plus infusion technique and integrated EMG monitoring of the first dorsal interosseous muscle. The mean (+/- SEM) ED50, ED90 and ED95 values for Sch in Group 1 were 0.13 +/- 0.01, 0.19 +/- 0.01 and 0.22 +- 0.01 mg.kg-1, and in Group 2 were 0.16 +/- 0.01, 0.25 +/- 0.01 and 0.29 +/- 0.02 mg.kg-1, respectively. The mean ED values in Group 2 were significantly greater than the equivalent values in Group 1 (P less than 0.05). Compared with values in Group 1, ED values in Group 2 represented mean increases of 23, 32, and 32 per cent, respectively. These pharmacodynamic data indicate that the dose of Sch needs to be increased by 32 per cent following a defasciculating dose of dTC 3 mg.70 kg-1 (0.043 mg.kg-1).
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PMID:A defasciculating dose of d-tubocurarine causes resistance to succinylcholine. 237 57

The effects of sodium thiopental on postganglionic muscle sympathetic nerve activity (MSNA) and the reflex augmentation in MSNA produced by hypotension were examined in seven ASA physical status I and II patients, 34-65 yr old. Direct recordings of MSNA were obtained from a 5-micron-tipped, epoxy-coated needle percutaneously placed into the common peroneal nerve. Induction of anesthesia with sodium thiopental (4 mg/kg) significantly decreased R-R interval duration an average of 157 +/- 44 ms (mean +/- SEM) decreased systolic pressure (radial artery) an average of 11 +/- 4 mm Hg, and reduced tonic MSNA from 38 +/- 11 to 18 +/- 5 bursts/100 cardiac cycles (P less than 0.01). Baroreceptor reflex regulation of cardiac intervals and MSNA were determined by sequential boluses of nipride (100 micrograms) and phenylephrine (150 micrograms). Awake baroreceptor slopes relating R-R interval to systolic pressure were 9.5 +/- 2.9 ms/mm Hg and decreased 61% to 2.4 +/- 0.5 ms/mm Hg (P less than 0.01) during sodium thiopental infusions (0.25 mg.kg-1.min-1). Moreover baroreceptor slopes relating MSNA to diastolic pressure in awake patients were -4.0 +/- 0.9 bursts/mm Hg and were reduced by 95% to -0.3 +/- 0.18 bursts/mm Hg (P less than 0.01). Despite the fact that hypotension did not elicit increases in MSNA in anesthetized patients, laryngoscopy and tracheal intubation produced profound augmentations in MSNA. Thus, sodium thiopental reduces tonic levels of MSNA and markedly attenuates baroreceptor reflex control mechanisms. However, profound augmentations in sympathetic activity occurred in response to laryngoscopy and tracheal intubation during thiopental anesthesia.
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PMID:Inhibition of sympathetic neural outflow during thiopental anesthesia in humans. 240 Jan 14

This study was performed to determine the effects of various doses of succinylcholine on resting tension and evoked twitch height at the masseter and adductor pollicis muscles in children. Twenty patients, aged 3-10 yr, ASA physical status I or II, were randomly assigned to receive succinylcholine 0.15, 0.25, 0.50 or 1.00 mg.kg-1, during halothane-nitrous oxide anaesthesia. Supramaximal train-of-four stimulation was applied simultaneously to the ulnar nerve and the nerve to the masseter. Transducers recorded force at the jaw and the thumb. Maximum blockade of the first twitch (T1) and maximum resting tension change were measured. Potency of succinylcholine at the two muscles was estimated by linear regression of the logit transformation of T1 versus log dose. The relationship between resting tension change and log dose was established by linear regression. The masseter muscle was more sensitive to succinylcholine than the adductor pollicis with an ED95 of 0.28 +/- 0.02 (mean +/- SEM) vs 0.44 +/- 0.05 mg.kg-1 (P less than 0.05). Onset of neuromuscular blockade was faster at the masseter, and recovery occurred simultaneously in both muscles. A dose-related increase in resting tension was observed in both muscles, but its magnitude was five times greater at the masseter. With succinylcholine, 1 mg.kg-1, this increase was 51.6 +/- 16.8 g at the masseter and 9.1 +/- 2.3 g at the adductor pollicis. Tension returned to baseline within 1-2 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dose-related effects of succinylcholine on the adductor pollicis and masseter muscles in children. 229 9

Recovery from inhalation anesthesia is often marked by the occurrence of postoperative tremor that resembles shivering, which is known to be associated with an increase in oxygen uptake (VO2), CO2 output (VCO2), and minute ventilation (VE). This study determined the time course of the ventilatory changes observed during the first hour of recovery from isoflurane anesthesia. Ten patients (ASA PS 1) scheduled for minor orthopedic surgery (knee arthroscopy) were included in this study. Anesthesia was induced with thiopental (5 mg/kg) and maintained with 70% N2O and isoflurane (1-2%) in oxygen, allowing spontaneous ventilation. In the recovery room, after N2O had been discontinued, patients were connected to a Beckman Metabolic measurement cart, which allowed a continuous monitoring of VE, VO2, VCO2, and PETCO2. Postoperative tremor was observed in all patients within 7.1 +/- 1.2 min (mean +/- SEM) after isoflurane discontinuation and was associated with a marked increase in the following: VO2, from 173 +/- 26 ml/min at the end of anesthesia to 457 +/- 88 ml/min; VCO2, from 149 +/- 18 ml/min at the end of anesthesia to 573 +/- 98 ml/min; and VE, from 6.8 +/- 0.7 l/min at the end of anesthesia to 16.6 +/- 2.8 l/min (values obtained 20 min after isoflurane discontinuation). In three patients during intense shivering, VO2, VCO2, and VE reached peak values higher than 800 ml/min, 1,300 ml/min and 30 l/min, respectively. This study shows that postoperative tremor following isoflurane anesthesia may be associated with prolonged and large increases in oxygen uptake, CO2 output, and minute ventilation.
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PMID:Changes in ventilation, oxygen uptake, and carbon dioxide output during recovery from isoflurane anesthesia. 249 61

We evaluated the clinical effectiveness of esmolol, an ultra-short-acting, cardioselective beta-adrenergic receptor blocker, in controlling sinus tachycardia and increased systolic blood pressure occurring perioperatively in 30 ASA physical status II or III patients having elective, non-cardiac surgery. Esmolol 80 mg I.V. bolus (N = 15) or placebo (N = 15) followed by 12 mg/min or placebo were infused in 30 isoflurane-anesthetized patients using a randomized double-blind study design. The bolus plus infusions were given when surgical stimuli caused heart rate to exceed 95 bpm or systolic blood pressure 140 mm Hg. Esmolol significantly decreased heart rate (107 +/- 4, mean +/- SEM to 99 +/- 4, mean +/- SEM bpm) within 45 sec after starting the bolus plus infusion; the placebo had no effect, heart rate being 105 +/- 4 before and 106 +/- 3 bpm after the bolus plus infusion. Patients given esmolol continued to have heart rates significantly lower than patients given placebo injections throughout a six min infusion (Ex., at 5 min 81 +/- 3 vs 91 +/- 4 bpm). The study demonstrated no apparent effect of esmolol on blood pressure but that esmolol is effective in treating perioperative sinus tachycardia.
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PMID:Use of esmolol during anesthesia to treat tachycardia and hypertension. 167 91

To determine the potencies of edrophonium and neostigmine as antagonists of nondepolarizing neuromuscular blockade produced by atracurium and vecuronium, dose-response curves were constructed for both antagonists when given at 10% spontaneous recovery of first twitch height. Ninety ASA physical status 1 and 2 adults were given either 0.4 mg/kg atracurium or 0.08 mg/kg vecuronium during thiopental-nitrous oxide-enflurane anesthesia. Train-of-four stimulation was applied to the ulnar nerve every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When spontaneous recovery of first twitch height reached 10% of its initial control value, edrophonium (0.1, 0.2, 0.4, or 1 mg/kg) or neostigmine (0.005, 0.01, 0.02, or 0.05 mg/kg) was administered by random allocation. Neuromuscular function in another ten subjects was allowed to recover spontaneously. Assisted recovery was defined as actual recovery minus mean spontaneous recovery observed in patients who were not given antagonists. First twitch recovery was initially more rapid when vecuronium was antagonized compared with atracurium, but no difference was detected after 10 min. At 10 min the neostigmine ED80 was 0.022 +/- 0.003 (SEM) mg/kg after atracurium and 0.024 +/- 0.003 mg/kg after vecuronium. The edrophonium ED80 was 0.44 +/- 0.11 mg/kg with atracurium and 0.46 +/- 0.12 mg/kg with vecuronium, giving a neostigmine:edrophonium potency ratio of 20. Atracurium train-of-four fade could be antagonized more easily with edrophonium, whereas that of vecuronium was more easily antagonized by neostigmine. It is concluded that edrophonium and neostigmine are not equally effective against atracurium and vecuronium.
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PMID:Dose-response relationships for edrophonium and neostigmine as antagonists of atracurium and vecuronium neuromuscular blockade. 256 67

The effect of arachidonic acid and its metabolites on the histamine-stimulated acid production in human isolated parietal cells provenient from endoscopic biopsies was examined. 14C-aminopyrine (14C-AP) accumulation in the parietal cells was used for evaluation of acid production. Histamine dose-dependently increased AP uptake. Histamine stimulation (taken as 100% at 10(-5) M) was significantly inhibited by prostaglandin (PG) E2 to 66 +/- 7% at 10(-8) M, 42 +/- 8% at 10(-6) M, and 13 +/- 10% at 10(-4) M (mean +/- SEM, n = 10). PGF2 alpha, PGD2, and PGI2 showed significant inhibitory effects only at very high concentrations (10(-5)-10(-4) M). Leukotriene (LT) B4 and LTC4 were without effect. The basal acid production (taken as 0%) was lowered significantly by 10(-6) M arachidonic acid to -20 +/- 7.4% (p less than 0.02, n = 10), and the histamine-stimulated (10(-6) M) acid production from 100% to 64 +/- 7.2% (p less than 0.001, n = 10). Aspirin (10(-3) M) increased basal (45 +/- 9.6%, p less than 0.001, n = 10) and histamine-stimulated (10(-6) M) acid production (164 +/- 16.3%, p less than 0.001). It is concluded that PGE2, the major product from arachidonic acid metabolism in the human gastric mucosa, is a significant inhibitor of the histamine-stimulated human parietal cell and may, in humans, play a role as a local physiologic inhibitor of acid secretion.
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PMID:The effect of arachidonic acid and its metabolites on acid production in isolated human parietal cells. 260 6

Propofol, a phenol compound with a short elimination half-life, was compared with thiopental and isoflurane for induction and maintenance of general anesthesia in 60 consenting ASA I, II, and III patients. The study was randomized and open label in design. Hemodynamically, the propofol patients showed a mean +/- SEM decrease in systolic blood pressure in comparison with the thiopental/isoflurane group at 2 (115.1 +/- 4.9 vs. 136.6 +/- 6.0 mmHg), 3 (125.7 +/- 5.1 vs. 149.4 +/- 5.6 mmHg), and 5 min (126.6 +/- 3.8 vs. 144.4 +/- 6.1 mmHg) postinduction and at intubation (135.2 +/- 4.7 vs. 157.8 +/- 6.0 mmHg) (p less than 0.05). The heart rate was lower in the propofol group throughout the induction period (p less than 0.05). Patients who received propofol were ready for discharge from the recovery room sooner (67.9 +/- 4.0 vs. 80.0 +/- 3.6 min) than the thiopental/isoflurane-treated patients (p less than 0.05). Propofol is as safe and effective for induction and maintenance of general anesthesia as thiopental and isoflurane.
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PMID:Comparison of propofol with thiopental and isoflurane for induction and maintenance of general anesthesia. 269 40

Favorable changes in lipoproteins, inhibition of platelet aggregation, reduction of serum thromboxane (TX), altered plasma-membrane fluidity, and reduced production of growth factors (mitogens) have all been implicated as possibly being involved in the inhibition of arteriosclerosis by fish oil (FO), which is rich in omega 3 fatty acids; however, causal relations are mostly lacking. Several putative mechanisms responsible for the salutary effects of FO were investigated in a canine model of accelerated vein-graft arteriosclerosis. Venoarterial autografts (N = 192) were implanted in 48 hypercholesterolemic dogs divided into six groups: group A, control; B, FO (as MaxEPA, 200 mg/kg/day eicosapentaenoic acid); C, aspirin (ASA, 50 mg/kg/day); D, TX synthetase inhibitor (TXSI [CGS-12970], 10 mg/kg/day); E, FO + ASA; and F, FO + TXSI. At sacrifice 3 months later, there was no significant difference in plasma lipoproteins, hepatic low density lipoprotein-receptor concentration, red blood cell fragility, bleeding time, or platelet count compared with controls; the decrease in platelet aggregation (30 +/- 5% [mean +/- SEM]) was similar in all treatment groups. Arterialized vein-graft intimal thickening was significantly inhibited by FO (with or without ASA), while ASA alone was ineffective. Conversely, serum TX was significantly lower only in the ASA and FO + ASA groups. Serum mitogenic activity was higher at 3 months in the control group versus all treatment groups. Compared with baseline values, serum mitogenic activity rose significantly over time in the control and the TXSI groups, and an increase or rising trend was present in all other treatment groups except for the FO-treated animals. Thus, the salutary biologic effect of FO in this hypercholesterolemic model of arterialized vein grafts may have been more related to in vivo inhibition of platelet-mitogen growth factor release than to changes in lipoproteins, low density lipoprotein receptors, platelet function, or eicosanoid metabolism. These observations underscore the need for further studies to clarify the interactions between FO (omega 3 fatty acids) and paracrine cellular mitogenic factors in the context of atherosclerosis prevention.
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PMID:Mechanisms responsible for inhibition of vein-graft arteriosclerosis by fish oil. 276 20


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