Formation of nanoparticles by ion beam irradiation of thin films.

The possibility of fabricating nanoparticles by ion bombardment was investigated by the ion bombardment of indium films on oxide covered Si and Cr surfaces. The different masses of implanting specimen ensured the different energy transfer while the same Si substrate ensured the same thermal conductivity for the In and Cr layers. Chromium served as a reference for the effect of ion bombardment and as a substrate as well. The SRIM program was used to simulate the ion surface interaction process. The nanoparticles were detected by scanning electron microscopy (SEM). We found that the melting of the In layer results in the formation of nanoparticles of 50-300 nm diameter and 5-10 nm height. This method can be promising for nanoparticle formation of materials with low melting point.

[Central presynaptic receptors]. / Zentrale präsynaptische Rezeptoren.

Experiments on two different inhibitory presynaptic receptor systems are presented. 1. Superfused and electrically stimulated brain slices are a widely used experimental model to study the release of noradrenaline and its modulation by inhibitory alpha-2 adrenoceptors. By using a minisuperfusion chamber we succeeded in studying the simplest case of autoinhibition, i.e. the release of transmitter induced by a single pulse and two consecutive pulses, respectively. When electrical stimulation is performed using a single pulse, no autoinhibition is possible, whereas following stimulation with two pulses the transmitter released by the first pulse will inhibit the effect of the second pulse. By systemically varying the time interval between the two pulses the minimal time requirement for development of autoinhibition was determined to be 100 ms. Short pulse trains of high frequency such as 4 pulses within 30 ms circumvent autoinhibition and cause inhibition-free release by each applied pulse. The release of transmitter evoked in this way is not only free from autoinhibition but, in addition, easily measurable, which makes this method of stimulation very suitable for analyses at presynaptic receptors. By using this approach it became possible, for the first time, to determine dissociation constants of antagonists and agonists at the central presynaptic alpha-2 adrenoceptor without the distortion introduced by autoinhibition occurring during release. 2. There is a substantial body of evidence for a role of medullary serotonergic nerve cells in the regulation of blood pressure and heart rate. It is hypothesized that the serotonergic neurons project to the thoracic spinal cord exerting a tonic excitatory influence on presynaptic sympathetic neurons of the intermediolateral cell column. Experiments were performed in pentobarbital anaesthetized rats to reduce this excitatory tone by activating inhibitory autoreceptors which are located on the perikarya and dendrites on the serotonergic cells and which have been shown to belong to the 5-HT1A subtype. Local stereotactic injection of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) caused a decrease in mean arterial blood pressure (MAP) and heart rate (HR). The effects were blocked by pretreatment of the animals with the 5-HT1A antagonist spiroxatrine. Moreover, neurochemical lesioning of serotonergic neurons by intracisternal injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) abolished the effects of 8-OH-DPAT. Bilateral intraspinal injection of 5,7-DHT, which interrupts the medullo-spinal serotonergic pathway, markedly attenuated the effects of local intramedullary injection of 8-OH-DPAT.(ABSTRACT TRUNCATED AT 400 WORDS)

Influence of urapidil and 8-OH-DPAT on brain 5-HT turnover and blood pressure in rats.

The effects of urapidil, of the selective 5-HT1A receptor agonist (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), and of the alpha 2-adrenoceptor agonist clonidine on the in vivo rate of synthesis of 5-hydroxytryptamine (5-HT) were determined in rat brain cortex and hypothalamus. Urapidil (10 mg/kg), 8-OH-DPAT (0.3 mg/kg) or clonidine (0.3 mg/kg; all drugs i.p.) caused significant reductions in 5-HT synthesis rate. Pretreatment with the selective 5-HT1A receptor antagonist spiroxatrine (SPX; 1 mg/kg s.c.) or the nonselective 5-HT1 receptor antagonist metitepine (1 mg/kg i.p.) abolished the effects of urapidil and 8-OH-DPAT, but not of clonidine. The effects of urapidil and 8-OH-DPAT on mean arterial blood pressure (MAP) and heart rate (HR) of pentobarbital-anesthetized, normotensive rats were measured following stereotaxic microinjection into the B1/B3 cell region of the ventral medulla. The mean percentage decreases induced by urapidil (3 micrograms) and 8-OH-DPAT (0.2 micrograms) amounted to (MAP/HR) -13%/-6% and -19%/-25%, respectively. The following pretreatments markedly attenuated or prevented the effects of intramedullary injections of urapidil or 8-OH-DPAT: (a) SPX (1 mg/kg s.c., 60 min): (b) intracisternal injection of the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT; 0.2 mg; 7-10 days); (c) bilateral injection of 5,7-DHT at the cervical level of the spinal cord (each side 5 micrograms; 7-10 days). The present results are compatible with an action of urapidil as agonist at central 5-HT1A receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Enflurane alters compensatory hemodynamic and humoral responses to hemorrhage.

This study examined the impact of enflurane (3%) on the hemodynamic and humoral defense mechanisms in a canine model of hemorrhagic shock. In order to obtain reasonable reference values with confounding influences of anesthesia and recent surgical preparation, the dogs were chronically instrumented 8-10 days prior to the experiments enabling measurements in the conscious state. While arterial pressure, cardiac output, and the corresponding derivatives were recorded continuously, plasma catecholamines and plasma renin activity were determined intermittently. As anticipated, the conscious dogs were able to tolerate considerable more severe levels of hemorrhage than the dogs anesthetized with enflurane. This finding is associated with reciprocal responses of both the renin-angiotensin system and the sympathoadrenal system in the conscious and anesthetized states. While the sympathoadrenal system prevailed in the conscious dogs, the renin-angiotensin system predominated during enflurane anesthesia. Despite the augmented response of the renin-angiotensin system, the activation of this defense mechanism was not sufficiently powerful enough to prevent overall hemodynamic deterioration with hemorrhage in the animals anesthetized with enflurane.

[Effect of morphine on circulatory control in acute progressive hemorrhage]. / Einfluss von Morphin auf die Kreislaufkontrolle bei akuter progressiver Hämorrhagie.

The effects of acute, progressive haemorrhage, 1 ml/s were examined in the same mongrel dogs on separate days, unanaesthetized and anaesthetized with morphine (2 mg/kg i.v.) and with administration of nasal oxygen to maintain arterial blood gases at physiological levels. In normal, unanaesthetized dogs mean arterial pressure was well maintained through 30 ml/kg of blood loss. Cardiac output fell with haemorrhage (70 +/- 2%; mean +/- S.E.M.) but heart rate and total peripheral resistance rose by 72 +/- 11% and by 124 +/- 11%, respectively. Morphine induced slight but significant changes in heart rate and mean arterial pressure but did not affect the ability to withstand hemorrhage. Thus, in contrast to barbiturates and volatile anaesthetics, morphine does not seem to comprise the efficacy of the rapidly acting pressure control system in response to progressive hemorrhage. The results of the present investigation are not consistent with the hypothesis that opioids are hypotensive factors in hypovolaemic shock.