Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity

BACKGROUND: Venodilation is thought to be one of the mechanisms underlying propofol-induced hypotension. The purpose of this study is to test two hypotheses: (1) propofol increases systemic vascular capacitance, and (2) the capacitance change produced by propofol is a result of an inhibition of sympathetic vasoconstrictor activity. METHODS: In 33 Wistar rats previously anesthetized with urethane and ketamine, vascular capacitance was examined before and after propofol infusion by measuring mean circulatory filling pressure (Pmcf). The Pmcf was measured during a brief period of circulatory arrest produced by inflating an indwelling balloon in the right atrium. Rats were assigned into four groups: an intact group, a sympathetic nervous system (SNS)-block group produced by hexamethonium infusion, a SNS-block + noradrenaline (NA) group, and a hypovolemic group. The Pmcf was measured at a control state and 2 min after a bolus administration of 2, 10, and 20 mg/kg of propofol. RESULTS: The mean arterial pressure (MAP) was decreased by propofol dose-dependently in intact, hypovolemic, and SNS-block groups, but the decrease in MAP was less in the SNS-block group (-25%) than in the intact (-50%) and hypovolemic (-61%) groups. In the SNS-block + NA group, MAP decreased only at 20 mg/kg of propofol (-18%). The Pmcf decreased in intact and hypovolemic groups in a dose-dependent fashion but was unchanged in the SNS-block and SNS-block + NA groups. CONCLUSIONS: The results have provided two principal findings: (1) propofol decreases Pmcf dose-dependently, and (2) the decrease in Pmcf by propofol is elicited only when the sympathetic nervous system is intact, suggesting that propofol increases systemic vascular capacitance as a result of an inhibition of sympathetic nervous system.     

Deriving protocol specifications from service specifications written in LOTOS

Summary.  A complete communication system is broken down into a number of protocol layers each of which provides services to the layer above it and uses services provided by its underlying layer. A service specification defines a particular ordering of the operations that a given layer provides to the layer above it. The active elements in each layer are called entities and they use a protocol in order to implement their service definition. On the basis of this relation between the service and protocol concepts we have developed algorithms for deriving protocol entity specifications from a formal service specification. The derived protocol entities ensure the correct ordering of the service primitives by exchanging synchronization messages through an underlying communication medium. This paper presents an extended version of our earlier derivation algorithms. This version of the algorithm can handle all operators and unrestricted process invocation and recursion as defined by basis LOTOS. The correctness of this derivation algorithm is formally proved. Received: January 1992 / Accepted: February 1996     

Activation of the protein kinase p38 in the spindle assembly checkpoint and mitotic arrest

The mitogen-activated protein kinase (MAPK) superfamily comprises classical MAPK (also called ERK), c-Jun amino-terminal or stress-activated protein kinase (JNK or SAPK), and p38. Although MAPK is essential for meiotic processes in Xenopus oocytes and the spindle assembly checkpoint in Xenopus egg extracts, the role of members of the MAPK superfamily in M phase or the spindle assembly checkpoint during somatic cell cycles has not been elucidated. The kinase p38, but not MAPK or JNK, was activated in mammalian cultured cells when the cells were arrested in M phase by disruption of the spindle with nocodazole. Addition of activated recombinant p38 to Xenopus cell-free extracts caused arrest of the extracts in M phase, and injection of activated p38 into cleaving embryos induced mitotic arrest. Treatment of NIH 3T3 cells with a specific inhibitor of p38 suppressed activation of the checkpoint by nocodazole. Thus, p38 functions as a component of the spindle assembly checkpoint in somatic cell cycles.     

Dynamics of an HVDC system in the presence of unbalanced AC transmission line faults and a stabilization scheme

The introduction of an HVDC system into the trunk power supply system requires transmitting as much dc power as possible for improving the whole ac/dc system stability. The continued operation scheme of an HVDC system which makes it possible to operate even under very low commutation bus voltage is adopted to cope with such system requirement. Further stability improvement can be achieved by adding damping control which modulates converter active and/or reactive power. To take full advantage of these control effects, it is essential that the HVDC system can maintain stable operation during the ac system faults and reclosing. Particular attention should be given to a repetitive commutation failure following the unbalanced ac transmission line faults. This paper discusses first the cause of the repetitive commutation failure when supplied with unbalanced ac system voltage based on an experiment using the CRIEPI AC-DC Power System Simulator. Then a stabilization control scheme with an on-line extinction angle estimation is proposed and the effect is verified by digital simulation.     

Microwave switch: LAMPS (light-activated microwave photoconductive switch)

A new microwave switch, the light-activated microwave photoconductive switch consisting of a heterostructure photoconductive switch (HPCS) with a flip-chip bonded vertical-cavity surface-emitting laser is reported. An insertion loss of 0.17 dB at a laser power of 15 mW and an isolation of 25 dB were obtained at 1 GHz. Excellent linearity was obtained with second and third order intercepts measured at 960 MHz of SOI=115 dBm and TOI=65 dBm at 960 MHz, respectively.     

Transesophageal pacing and recording

Identification of P wave is essential for the diagnosis of various arrhythmias. The transesophageal ECG is useful for obtaining the relationship of atrial-ventricular activation when P wave is difficult to recognize on the surface ECG. Transesophageal pacing is also helpful to evaluate the function of the conduction system and to clarify the mechanism of arrhythmias. Thus, transesophageal pacing and recording can be used as beside electrophysiologic studies in patients with sick sinus syndrome, atrial-ventricular block, atrial flutter, and paroxysmal supraventricular tachycardia.