Induction of anaesthesia in patients undergoing aortocoronary bypass surgery: propofol versus etomidate.
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Biomedical subjects
Publications and source records attributed to I Keller.
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Experimental evidence from various neuropsychological and neurophysiological fields indicates that an oscillatory brain mechanism in a frequency range of 30-40 Hz is necessary for adequate sensory information processing. An oscillatory component of that particular frequency range can also be observed in the mid-latency auditory evoked potentials. Thus general anesthesia can be defined as a suppression of sensory information processing, and the effect of the i.v. anesthetics, Propofol and ketamine, on auditory perception and auditory-evoked potentials was therefore studied. In 22 patients anesthesia was induced with Propofol (2.5 mg/kg body weight, group I: n = 10) or ketamine (2 mg/kg body weight, group II: n = 12). Auditory-evoked potentials were recorded before, during, and after induction of general anesthesia. In the awake state, an oscillatory component with an energetically dominant 30-40 Hz frequency was present between 20 and 100 ms poststimulus latency. Propofol suppressed the mid-latency oscillatory component, whereas the component persisted under ketamine. Under Propofol, the 30-40 Hz leading frequency shifted to the lower frequency range, whereas under ketamine, the AEP were still dominated by a 30-40 Hz oscillation. Propofol suppresses the oscillatory brain mechanism necessary for adequate sensory information processing like various other general anesthetics. In contrast to Propofol, ketamine does not alter auditory perception. Suppression of sensory information processing must take place at a higher cortical level in a dissociative manner. The persistence of a 30-40 Hz oscillation must be seen in connection with dreams and hallucinations as reported for the drug and may be interpreted as insufficient suppression of sensory information processing under ketamine anesthesia.
Selectivity for the carboxy-terminus of angiotensin II (Ang II) and the high affinity of antibodies are prerequisites for clinical assays that evaluate Ang II in the presence of Ang I. A high-affinity monoclonal antibody (Kd = 7.1 X 10(-11) mol/l) was produced and used for the measurement of plasma Ang II. C3H mice were immunized with Ang II coupled by its carboxy-terminus to thyroglobulin. Somatic cell fusion between spleen cells and SP 2/0 myeloma cells, repeated subcloning and re-injection into mice yielded ascites containing sufficient antibody at a 2 X 10(7)-fold dilution. Radioassay standard curves show 50% tracer displacement when 32 fmol unlabelled Ang II is added and 2 fmol Ang II can be detected. Cross-reactivities, taking the reactivity with Ang II as 1.00 are: Ang I 0.003, Ang (1-7) 0.00001, Ang III 1.05, Ang(3-8) 0.88 and Ang(4-8) 0.75. Fast extraction of angiotensin from 2 ml plasma by reversible adsorption to phenylsilylsilica (Bondelut PH) provides recoveries of 96-102%. During angiotensin converting enzyme inhibition with 25 mg intravenous captopril, plasma immunoreactive Ang II decreased in supine normal volunteers from 8.6 +/- 3.6 to 4.5 +/- 3.4 fmol/ml (P less than 0.01, n = 8). It thus appears that plasma immunoreactive Ang II can now be measured after a simple extraction procedure by using monoclonal antibodies.
We examined the effects of unilateral radiofrequency lesions in the preoptic area on lateral hypothalamic self-stimulation in 15 rats. The animals were tested for self-stimulation in the lateral hypothalamus at 3 different current intensities from electrodes placed in both hemispheres, and then received a unilateral lesion in the preoptic area. Four hours later they were again tested for self-stimulation at the 3 current intensities and then daily over the following 14 days, or until they recovered their presurgical rates of self-stimulation. Rate of self-stimulation decreased in the damaged hemisphere, and recovered to prelesion levels within 2 weeks in 6 of 9 rats. In the intact hemisphere rate of self-stimulation increased above the prelesion level during a period from 1 to 2 weeks after the lesion. These results suggest that the preoptic area is involved in lateral hypothalamic self-stimulation. The effects of D-amphetamine (1 mg/kg) and apomorphine (2 mg/kg) injections on turning behavior were also studied in an open field and in a rotometer. Apomorphine induced contraversive turning to the lesion side in the open field and D-amphetamine induced ipsiversive turning in the rotometer.
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1 MK 421 and its lysine analogue are two new inhibitors of angiotensin converting enzyme. Ten mg of both compounds were each given p.o. to 12 normotensive volunteers to determine their effect on the various components of the renin angiotensin aldosterone system. 2 Plasma converting enzyme activity decreased to very low levels within 3 to 4 h to recover only slowly over the next 72 h. Plasma angiotensin II and aldosterone also fell but returned to baseline within 24 h, whereas plasma renin activity rose reflecting the low angiotensin II levels. 3 There was a close correlation between both angiotensin II and aldosterone levels and the logarithm of plasma converting enzyme activity demonstrating that angiotensin II and aldosterone fell only when converting enzyme activity was reduced to very low levels. 4 Mean hourly urinary sodium excretion increased markedly 6 to 10 h post-drug, while blood pressure decreased slightly. Both drugs were well tolerated. 5 Thus 10 mg of MK 421 or its lysine analogue given orally are effective and long acting angiotensin converting enzyme inhibitors.
Repeated administration of thyroxine (T4) in vivo (2 microgram/100 g body wt for 6 days) lowered by 2.3 times (P less than 0.025, df = 18) the basal rate of Na+ transport measured by the short-circuit current (SCC) in vitro in the urinary bladder of the toad (Bufo marinus). This difference was not accounted for by a change in the plasma aldosterone concentration. Moreover the response of the SCC to aldosterone in vitro was markedly inhibited in bladders from T4-treated animals (P less than 0.001, df = 18). These findings raised the possibility of a direct interaction between thyroid hormone and aldosterone in the target cell. The effects of L-triiodothyronine (T3) and aldosterone were examined in vitro. T3 alone (60 nM) had no significant effect on the base-line SCC (deltamuA = -14 +/- 11 (SE) muA per hemibladder; P greater than 0.3, n = 10). By contrast, T3 (60 nM) inhibited the response of the SCC to aldosterone from 6 to 8 h after its addition (deltamuA = -98 +/- 19 muA per hemibladder; P less than 0.001, n = 10). The inhibition by T3 was present at 6 nM (P less than 0.01, n = 10) and became not significant at 0.6 nM. T3 had no significant effect on base-line or aldosterone-stimulated H+ transport. Thyroid hormone might therefore regulate the late response of the SCC to aldosterone at the level of its target cell.
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The shape and thickness of the third ventricles were studied with magnetic resonance imaging in 46 patients under evaluation for memory impairment. We compared this population with 23 subjects imaged for other reasons. The study group consisted of patients with diagnoses of probable dementia of the Alzheimer's type (DAT; 35.6%), multi-infarct dementia (MID; 22.2%), depression (8.9%), alcoholic dementia (6.7%), other dementias (OD; 13.2%) and no dementia (6.7%). Within the study group, there were no significant differences across diagnostic categories for duration of symptoms or level of education. Patients with DAT were, however, more impaired than others (Mini-Mental State Examination scores: DAT 14.6 [+/- 8.2] versus MID 17.4 [+/- 6.2] versus OD 21.2 [+/- 6.4]). Demented subjects were more likely than nondemented individuals to have a convex third ventricle and greater wall separation. The results suggest that the shape of the third ventricle may correlate with dementia. Possibly, the dorsal medial nucleus of the thalamus is involved in the dementia.
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