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This experiment was conducted to clarify difference of arterial pressure regulatory mechanism between awake and anesthetized human subjects. In 18 subjects who were scheduled for surgical operations, passive tilting test was performed both in awake and anesthetized conditions. Arterial pressure and heart rate were measured during four types of tilting test, i.e., 1. supine-10 degrees head down tilt 2. 10 degrees head down tilt-supine 3. supine-10 degrees head up tilt 4. 10 degrees head up tilt-supine. Relative changes in arterial pressure and heart rate in response to these four tilting tests were compared. After postural changes, all anesthetized subjects showed significant arterial pressure changes followed by restoration of arterial pressure towards control level with opposite changes of heart rate. This initial arterial pressure changes were mainly induced by shift of blood due to gravity and subsequent arterial pressure and heart rate changes were mainly by baro-receptor reflex. On the other hand, awake subjects showed transient increase of heart rate immediately after tilting followed by arterial pressure rise 2 to 3 seconds later in all four tilting tests. However, arterial pressure did not change so remarkably as in anesthetized condition and remained almost constant during tilting test. In awake subjects, their arterial pressure was regulated rapidly and reflex control of arterial pressure was masked. This rapid regulation of arterial pressure may be induced directly by higher central nervous system.

A partir de dihydro-3,4 methyl-1 β-carboline, synthese de la decahydro methyl-3 indolo [2,3-a] pyranno [3,4-g] quinolizinone-2 qui a deja ete transformee en (±)-ajmalicine

Irradiation des composes du titre en presence de NaBH 4 ou KOH: obtention de tetrahydro-5,6,7,8- et 5,6,6a,10a phenanthridones-6, de 5H-phenanthridones-6 et d'aryl-2 N-methyl anilines

Sur l'exemple de la synthese d'hexahydro-2,3,4,4a,5,6 methyl-4 benzo [f] quinoleinemethanol-2(depyrrololysergol) a partir du trans-aldol hydroxy-1 methyl-4 octahydro-1,2,3,4,4a,5,6,10b benzo [f] quinoleinecarbaldehyde-2, synthese du (±)-lysergol a partir du trans-aldol benzyl-1 hydroxy-9 methyl-6 ergolinecarbaldehyde-8

Effects of peripheral and central thermoreceptor reflexes on sympathetic nerve activity to the skin (SkNA) and kidney (RNA) were compared in anesthetized cats. Sudden warming of the skin produced a rapid increase of RNA, wheras sudden cooling produced a rapid increase of SkNA. When the bath temperature (TB) was 17.6, 29.7, and 41.9 degrees C, the normalized SkNA was 100, 82, and 48%, while the normalized RNA was 81, 90, and 100%, respectively. Similarly, under open baroceptor loop conditions, SkNA changed inversely with TB, while RNA changed proportionally to TB. Changes in the temperature of the whole brain including hypothalamus (Thy) modified the amplitude of grouped RNA and SkNA synchronously with the cardiac cycle. At TB of 32.4 degrees C, when Thy was altered in a range of 30-42 degrees C, SkNA reached a maximum level at a Thy of 38.4 degrees C, whereas RNA reached a maximum above 42 degrees C. In a Thy range of 38-42 degrees C, the slopes of the Thy-SkNA curve and Thy-RNA curve were 30 and +4%/degrees C, respectively. At Thy below 38 degrees C, SkNA and RNA changed in parallel with Thy. Continuous cooling of the skin modified the slope of the TB-SkNA curve, but a small change of Thy caused a shift of the TB-SkNA curve.

Renal sympathetic nerve activity (RNA), arterial blood pressure (AP), and heart rate (HR) were simultaneously measured before and after administration of pentobarbital sodium (PB), chloralose (CHL), or urethan (URE) in conscious cats. We examined the time courses and magnitudes of the changes in RNA, AP, and HR over a period of 5 h under anesthesia with spontaneous or artificial respiration. In both respiratory conditions, PB initially decreased and then increased RNA, AP, and HR; CHL sustainedly increased RNA but had almost no effect on AP and HR. Under artificial respiration, URE transiently decreased RNA but had no effect on AP and HR. To examine the baroreflex response of RNA, AP was increased to 150 mmHg by norepinephrine and decreased to 65 mmHg by nitroprusside. RNA responded inversely to the alterations of AP in both awake and anesthetized states. Compared with the awake state, the inverse AP-RNA relationship curve initially shifted downward and then upward under PB, and the slope of the relation curve was initially decreased. On the other hand, under CHL the relationship curve shifted only upward, and the slope increased. Thus the anesthetic drugs affected differently and time dependently tonic and reflex renal sympathetic nerve activity in the conscious cat.

Das aus dem 5-Bromprotocatechualdehyd (I) in einer Reihe von Zwischenstufen hergestellte Saurechlorid (II) wird mit dem Tetralonimin (III) zum Amid (IV) umgesetzt und durch Bestrahlung mit einer Quecksilberdampflampe zum Oxychelirubin (V) cyclisiert.

The hypothalamic area was stimulated in anesthetized rabbits at a large number of selected points, and the effects on the simultaneously recorded right cardiac sympathetic nerve activity (CSNA) and renal nerve activity (RNA) were analyzed quantitatively. Four characteristic patterns of CSNA and RNA responses could be observed. The most striking finding was the presence of opposite responses of CSNA and RNA at many hypothalamic stimulus points, in addition to the conventionally observed CSNA and RNA responses in the same direction. By a new method, we drew hypothalamic maps for CSNA and RNA response magnitudes. These maps show that the excitatory areas of CSNA and RNA are surrounded by respective inhibitory areas. Although the excitatory areas of CSNA and RNA correspond with each other on the right side, they are not identical on the left side. These data suggest that the heart and kidney are controlled by sympathetic nerve activities originating from different hypothalamic neural groups in the rabbit.

We determined the effect of pharmacological blood of the pericoronary nerve either along the experimentally occluded left circumflex (CX) or the nonoccluded left anterior descending coronary artery (LAD) on the reflex inhibition of renal nerve activity (RNA) during a brief CX occlusion. In 15 pentobarbital-anesthetized dogs with carotid sinuses denervated, CX was occluded under four different conditions of the pericoronary nerves. With intact pericoronary nerves, CX occlusion resulted in a significant decrease [-44 +/- 6.4 (SE) %] in RNA. The decrease in RNA remained basically the same (-34 +/- 10.0%) after block of the pericoronary nerve along LAD with local infiltration of 2% lidocaine. However, the reduction of RNA was abolished after block of the pericoronary nerve along CX (-6 +/- 4.9%) and after block of the pericoronary nerves along both LAD and CX (3 +/- 2.6%). These results indicate that the afferent input transmitted via the pericoronary nerve along the experimentally occluded coronary artery plays a dominant role in mediating the reflex inhibition of RNA during the coronary occlusion.

1. Renal sympathetic nerve activity, heart rate and arterial blood pressure were simultaneously measured in thirteen awake cats before, during and after eating which was evoked by presenting food for a period of 10-15 s. 2. With food presentation, eating behaviour occurred in 93% (191) of 205 trials, and renal sympathetic nerve activity significantly increased in 65% of the 191 trials. On the other hand, in many of food presentation trials when no eating occurred, or with presentation of an empty food box, renal sympathetic nerve activity did not change significantly. 3. Eating started 1-8 s after the food presentation. The increase in renal sympathetic nerve activity was closely related to the beginning of eating but not to the onset of food presentation. Renal sympathetic nerve activity and heart rate increased with a slight time lag of 0.5-1.5 s from the onset of eating, whereas an increase in arterial blood pressure followed the onset of eating by 5.5 s. After the beginning of eating, renal sympathetic nerve activity, heart rate and arterial blood pressure increased at a maximum of 61 +/- 18% (mean +/- S.E. of mean), 26 +/- 4.0 beats/min, and 17 +/- 4.9 mmHg from the control values at 1.0, 5.5 and 11.5 s, respectively. 4. Cardiac-related grouped discharges of renal sympathetic nerve activity, which were observed at rest, increased during eating. 5. When arterial blood pressure was elevated by noradrenaline (2-5 micrograms/kg I.V.), renal sympathetic nerve activity during resting was almost completely inhibited and the increase in renal sympathetic nerve activity during eating was not induced. 6. We conclude that renal sympathetic nerve activity increases in association with eating behaviour but not as firmly with the food presentation, and that the increase in renal sympathetic nerve activity is initiated by descending input from the higher central nervous system rather than either by the viscero-autonomic reflex due to food intake or by the baroreflex due to a decrease in arterial blood pressure.