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[Methods of evaluation of disorders of the cerebrospinal fluid outflow resistance].

Diagnostic methods for estimating the disturbances of the intracranial fluid resorption process were presented. The following tests are described: constant rate infusion test, boluses, perfusion test, constant pressure infusion test. The methods were compared in the face of the concept of nonlinear outflow resistance--pressure relationship. The author presents his concept of the test for complex examination of outflow resistance--pressure relationship.

Cerebrospinal Fluid↗
PubMed1991

[Effects of thyrotropin-releasing hormone (TRH) on status epilepticus in rats].

Recent studies have demonstrated that intramuscular administration of thyrotropin-releasing hormone (TRH) or its analogue improves various clinical aspects of intractable epilepsy such as Lennox-Gastaut syndrome, West syndrome, and myoclonus epilepsy. Other clinical studies reported efficient property of intravenous TRH against status epilepticus. However, it is also true that intravenous TRH produces epileptic seizures in patients with epilepsy or organic brain damage. Thus, the utility of intravenous TRH for the treatment of status epilepticus seems to be equivocal. To further explore the problem in this regard, we examined the effect of TRH on limbic status epilepticus in rats. Thirty-eight male Wistar rats weighing 180-220g were used. Status epilepticus was induced by intracerebral injection of a combination of 200 micrograms of dibutyryl-cAMP (db-cAMP) and 67.2ng of ethylenediaminetetraacetic acid (EDTA) into the amygdala (AM) through an implanted cannula. 30 min later, TRH or vehicle (distilled water) was administered intravenously (i.v.) or intracerebroventricularly (i.c.v.). Although 3 mg/kg of TRH (n = 9), when injected i.v., did not alter the pattern of electroclinical ictal responses induced by db-cAMP/EDTA, 25 mg/kg (n = 5) and 50 mg/kg (n = 5) of TRH significantly exaggerated EEG and/or behavioral ictal seizures, beginning immediately after the injection and lasting for more than 30 min. With 50 mg/kg of TRH, the exaggerated seizure patterns were followed by marked suppression of electroclinical seizures. 50 micrograms of i.c.v. TRH (n = 5), like higher doses of i.v. TRH, caused a slight, but not a significant, build up of electroclinical ictal seizures, beginning immediately after the injection and lasting for about 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Possibility for induction of convulsion by fleroxacin and its disposition in the central nervous system in animals.

Fleroxacin and its metabolites were examined for their possibility of the induction of convulsion in mice, inhibitory activity on GABA receptor binding, and disposition in the central nervous system of mice, rats and dogs. No convulsion was evoked in mice at high oral combination doses of fleroxacin and fenbufen. Brain-to-serum concentration ratios of fleroxacin after oral dose were 0.13 in mice, 0.19 in rats and 0.28 in dogs. Rats showed no accumulation of fleroxacin in brain and similar elimination from brain to that from serum after the oral dose. Dogs exhibited the similar distribution of fleroxacin into various brain regions. The inhibitory effect of fleroxacin on GABA receptor binding was relatively weak and slightly potentiated in the presence of 4-biphenylacetic acid. Demethyl fleroxacin showed more potent inhibitory activity on GABA receptor binding and potentiation with 4-biphenylacetic acid. The combination of intravenous demethyl fleroxacin and oral fenbufen showed no convulsion in mice. Fleroxacin N-oxide showed only slight inhibitory activity on GABA receptor binding, being not influenced with 4-biphenylacetic acid.

Animals↗
PubMed1990

[Antifungal agents].

Explore the source record for details and available documents.

Administration, Oral↗
PubMed1985

Opposing central and peripheral actions of brain-gut peptides: a basis for regulation of gastric function.

The existence of an increasing number of peptides in both the gut and the brain provides the basis for the concept of a brain-gut axis. However, to date, no unifying hypothesis has been put forward to explain the physiologic significance of this remarkable phenomenon. The present study examines the central and peripheral actions on gastric function of cholecystokinin octapeptide (CCK-8), somatostatin, and bombesin, all of which exist in both the gut and brain. Intravenous infusion of CCK-8, in doses of 50, 100, and 200 pmol X kg-1 X hr-1, caused 28%, 38%, and 52% inhibition, respectively, of the rate of gastric emptying of a liquid meal in dogs. By contrast, the injection of 32, 64, and 128 pmol X kg-1 into the lateral cerebral ventricle of these dogs accelerated gastric emptying by 6%, 26%, and 32%, respectively. Bombesin, which stimulated gastric acid secretion in a dose-dependent manner but which had no effect on the submaximal acid response to pentagastrin when administered peripherally, inhibited in a dose-dependent manner the submaximal response to pentagastrin when given centrally, with a maximal inhibition of 66% +/- 5%, at a dose of bombesin of 180 pmol X kg-1. Similarly, somatostatin-14 caused graded inhibition of pentagastrin-stimulated acid secretion when it was administered peripherally but caused dose-dependent augmentation of the acid response when it was given centrally. Maximal inhibition of 51% of the pentagastrin response occurred with a peripheral dose of somatostatin of 800 pmol X kg-1 X hr-1. By contrast, maximal augmentation of the pentagastrin response of 78% occurred when a dose of 400 pmol X kg-1 of the peptide was injected into the lateral ventricle. We conclude that CCK-8, bombesin, and somatostatin have opposing actions on gastric function when administered centrally and peripherally. We propose that this phenomenon may be common to all neuropeptides of the brain-gut axis and may provide a basis for central regulation of gut function.

Animals↗
PubMed1985

Factors influencing the secretion of vasopressin into cerebrospinal fluid.

Vasopressin (VP) has been found in the cerebrospinal fluid (CSF) of several species of animals. Although it is known that hemorrhage, hypertonicity of body fluid, hypoxia, and hypercapnia all increase VP in plasma, little is known regarding the stimuli that cause the secretion of VP into the CSF. We therefore performed several studies to examine whether stimuli capable of increasing plasma levels of VP can also increase VP in the CSF of anesthetized dogs. We found that hemorrhage, intracerebroventricular infusion of hypertonic artificial CSF, hypoxia, and hypercapnia all produced increases in the concentration of VP in plasma and in CSF, but the time courses and the magnitude of the increases in the two compartments were different. In addition, an i.v. infusion of hypertonic saline or of hydrochloric acid produced an increase in plasma VP without significantly changing CSF VP. Thus, although the secretion of VP into plasma and CSF may be influenced by the same stimuli, changes in one compartment do not necessarily correlate with changes in the other. Taken together, our results are consistent with the hypothesis that the plasma and CSF VP may derive from different sources.

Acidosis↗
PubMed1985

Study of central regulation of intraocular pressure using ventriculocisternal perfusion.

The ability of hypoosmotic solution, prostaglandin E1 (PGE1) and clonidine to influence intraocular pressure (IOP) by a central mechanism was studied using the technique of ventriculocisternal perfusion in conscious rabbits. IOP remained unchanged during the perfusion of 150 mOsm artificial cerebrospinal fluid. IOP rapidly increased by 15 mmHg during the perfusion of PGE1 at the dose of 1 or 3 micrograms/min. However, when PGE1 was perfused intravenously at the dose of 1 microgram/min, a similar IOP response was observed. Furthermore, during the ventriculocisternal perfusion of PGE1 a significant systemic absorption occurred. These observations indicate that the ocular hypertension during the ventriculocisternal perfusion of PGE1 is primarily due to the peripheral action of systematically absorbed PGE1. IOP gradually decreased by 3 mmHg during the ventriculocisternal perfusion of clonidine at the dose of 0.1 or 0.33 micrograms/min. Intravenous perfusion of clonidine at the same doses did not change the IOP. These results indicate that clonidine can lower IOP by a centrally mediated mechanism. Ventriculocisternal perfusion of clonidine (0.1 micrograms/min) in rabbits with unilateral superior cervical ganglionectomy lowered IOP in both eyes, indicating that ocular adrenergic innervation does not participate in this centrally mediated IOP response. However, the cardiovascular parameters of anesthetized rabbits were altered by the ventriculocisternal perfusion of clonidine (0.1 micrograms/min), suggesting that a change in systemic hemodynamics is involved in the central IOP effect of clonidine.

Alprostadil↗
PubMed1979

Steady-state disposition of propranolol and its total metabolites in the spontaneously hypertensive rat: chronic subcutaneous vs. intracerebroventricular infusion with osmotic minipumps.

The steady-state disposition of propranolol and its total metabolites was measured after 6 day continuous subcutaneous (1 mg/kg/day) or intracerebroventricular (i.c.v., 0.01 and 1 mg/kg/day) infusion of dl-[3H]propranolol with osmotic minipumps in spontaneously hypertensive rats. After 2 days daily excretion of total radioactivity was 70% or more of the total dose infused each day. Steady-state plasma concentrations (day 3 and 6) of propranolol and its total metabolites did not differ significantly during subcutaneous or i.c.v. infusion of 1 mg/kg/day. During i.c.v. infusion with 0.01 mg/kg/day these concentrations were only 0.01 to 0.02 times as high. Propranolol and its total metabolite concentrations did not differ significantly in peripheral tissues during subcutaneous or i.c.v. infusion of 1 mg/kg/day, whereas brain propranolol concentrations were 40- to 600-fold higher during i.c.v. infusion. During i.c.v. infusion with 0.001 mg/kg/day, peripheral propranolol and total metabolite concentrations were only 0.003 to 0.02 times those following 1 mg/kg/day. Brain propranolol concentrations after 0.01 mg/kg/day i.c.v. were in the same range as those following 1 mg/kg/day subcutaneously. The data suggest that the osmotic minipump is a useful tool for creating and maintaining a steady-state for propranolol in spontaneously hypertensive rats. Moreover, by i.c.v. placement of the pump outlet the brain can be selectively perfused with this agent for a prolonged period of time.

Animals↗
PubMed1979

Intraventricular pressure and CSF dynamics in chronic adult hydrocephalus.

The authors present their experience with continuous intraventricular pressure measurements and the constant infusion test in 50 adult patients suffering from chronic communicating hydrocephalus. A good correlation has been found in 27 cases between the response to CSF shunting and the actual state of the CSF hydrodynamics. The importance of such investigations in selecting adult hydrocephalic patients for shunt therapy is emphasized.

Adolescent↗
PubMed1981

Induction of hyperphagia in rats by intracerebroventricular infusion of sodium pentobarbital. A method for testing anorexigenic compounds.

In rats hyperphagia could be reversibly induced by intracerebroventricular infusion of sodium pentobarbital. Hyperphagia was elicited in a dose dependent manner, the optimal infusion rate being 1000 micrograms/h sodium pentobarbital. At this rate, feeding behaviour was induced selectively, with only minor side effects being apparent. Systemic application of d-methamphetamine or propylhexedrine given prior to infusion resulted in a dose dependent reduction of hyperphagia. The method, therefore, could be useful for testing putative anorexigenic compounds in hyperphagic rats.

Animals↗
PubMed1981

Reductions in blood pressure, heart rate and renal sympathetic nervous discharge after imidazole-4-acetic acid: mediation through central gamma-aminobutyric acid (GABA) receptor stimulation.

Intracerebroventricular administration of imidazole-4-acetic acid (IAA) (0.3--10 microgram/kg) significantly reduced mean arterial pressure, heart rate and renal sympathetic nerve discharge in chloralose-anesthetized cats. In contrast, i.v. administration of IAA did not lower arterial pressure or heart rate. This would suggest that the hypotensive and bradycardic effects of IAA were centrally mediated. The cardiovascular effects of IAA were attenuated by the central administration of bicuculline methiodide (15 microgram/kg), a gamma-aminobutyric acid receptor antagonist. Reflex bradycardia evoked during the pressor response to norepinephrine (0.03--1.0 microgram/kg i.v.) was reversed to tachycardia after only the central administration of IAA. The vasoconstrictor response evoked during a 20-sec period of bilateral occlusion of carotid arteries was not altered by IAA. These results suggest that the cardiovascular effects of IAA are mediated through the activation of central gamma-aminobutyric acid receptors, to inhibit sympathetic vasomotor outflow.

Animals↗
PubMed1981

Behavioral and electrocortical effects of beta-endorphin after intracerebral infusion in rats.

In rats with cannulae chronically implanted into specific areas of the brain, the effects of beta-endorphin were studied on behavior and electrocortical activity. It has been shown that analgesia and catatonia were evoked after infusing beta-endorphin into the III cerebral ventricle or into the hypothalamus. On the contrary, beta-endorphin microinjected into the caudate nucleus or into the substantia nigra produced an intense pattern of stereotyped movements, occasional contralateral circling, contralateral myoclonic jerks and asymmetric posture. Stereotyped gnawing, grooming and "wet-dog" syndrome preceded catatonia after intrahypothalamic administration of beta-endorphin. Bilateral (III ventricle) or ipsilateral (hypothalamus, caudate nucleus and substantia nigra) high voltage electrocortical spikes and other ECoG pathological changes accompanied by motor disorders (stereotypies, myoclonic jerks) or without any overt behavioral change were constantly observed. Behavioral and electrocortical changes evoked by beta-endorphin were long-lasting and rapidly reversed by the specific opiate antagonist, naloxone.

Animals↗
PubMed1983

[Hypertrophic non-obstructive apical cardiomyopathy. A case report].

A 53-year old patient with recurrent atrial fibrillation and atypical angina was found to have hypertrophic non-obstructive apical cardiomyopathy. His electrocardiogram recorded left ventricular hypertrophy and giant inverted T waves. Cross-sectional echocardiography revealed a typical ace-of-spade configuration of the left ventricular apex. This feature was confirmed at cardiac catheterization, which failed, however, to detect any intraventricular pressure gradient even after isoproterenol infusion. The apex of the right ventricle was also obliterated by hypertrophied muscle. Thus this case had all the typical findings of hypertrophic non-obstructive apical cardiomyopathy, which were best displayed by electrocardiography, bidimensional echocardiography and left ventriculography.

Angiocardiography↗
PubMed1995

Comparison between the effects of central and systemic hypertonic NaCl on hemodynamic responses to hemorrhage in sheep.

Effects of treatment with systemic hypertonic (1.2M, 4 mL kg-1) NaCl (SHTNa) on tolerance to hemorrhage, accompanying systemic hemodynamics, and regional blood flow were investigated in conscious sheep. The results were compared with those obtained in animals subjected to hemorrhage during intracerebroventricular (ICV) administration of hypertonic (.5 M, .02 mL min -1) NaCl (CHTNa). Corresponding bleeding during ICV infusion of isotonic saline served as control. All treatments were started 30 min before commencement of a slow (.7 mL kg-1 min-1) hemorrhage, which was continued until the mean systemic arterial pressure (MSAP) suddenly dropped to about 50 mmHg. To reach the distinct fall in MSAP significantly more blood had to be withdrawn in the CHTNa (27.8 +/- 2.2 mL kg-1, p < .05) than in the SHTNa group (21.5 +/- 1.7 mL kg-1), which in turn showed a significantly higher tolerance to hemorrhage than the controls (15.1 +/- .7 mL kg-1, p < .01). The hemorrhage-induced reduction of cardiac output (CO) below basal level was less pronounced in the CHTNa group, where also the posthemorrhage CO recovery was most rapid. Spontaneous recovery of MSAP after bleeding was equally improved in both treatment groups with the central venous pressure being significantly higher in the SHTNa group. The hemorrhage-induced fall in renal blood flow (RBF) was more pronounced in the CHTNa group, which also had an impaired posthemorrhage recovery of RBF. In comparison to the SHTNa and control groups the renovascular resistance was significantly higher in the CHTNa group already during the prehemorrhage infusion period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Overproduction of corticotropin-releasing factor in transgenic mice: a genetic model of anxiogenic behavior.

Corticotropin-releasing factor (CRF) is released in response to various stressors and regulates adrenocorticotropin secretion and glucocorticoid production. In addition to its endocrine functions, CRF acts as a neuromodulator in extra-hypothalamic systems and has been shown to play a role in behavioral responses to stress. CRF overproduction has been implicated in affective disorders such as depression and anorexia nervosa. A transgenic mouse model of CRF overproduction has been developed in order to examine the endocrine and behavioral effects of chronic CRF excess. CRF transgenic animals exhibit endocrine abnormalities involving the hypothalamic-pituitary-adrenal axis such as elevated plasma levels of ACTH and glucocorticoids. The present series of experiments tested the hypothesis that chronic overproduction of CRF throughout the life-span of these animals may lead to an anxiogenic behavioral state. CRF transgenic mice and normal littermate controls were tested by measuring locomotor activity in a novel environment and through the use of an elevated plus-maze as indices of anxiety. CRF transgenic animals exhibited an increase in anxiogenic behavior, an effect known to occur following central administration of CRF in mice and rats. Injection of the CRF antagonist alpha-helical CRF 9-41 into the lateral cerebral ventricles reversed the anxiogenic state observed in the CRF transgenics. This finding supports the possibility that central CRF overproduction may mediate the anxiogenic behavior exhibited in this animal model. Thus, CRF transgenic mice represent a genetic model of CRF overproduction that provides a valuable tool for investigating the long-term effects of CRF excess and dysregulation in the CNS.

Adrenocorticotropic Hormone↗
PubMed1997

Renal excretory responses produced by central administration of opioid agonists in ketamine and xylazine-anesthetized rats.

This study examined the renal excretory responses produced by the intravenous (i.v.) infusion of the alpha-2 agonist, xylazine, in ketamine-anesthetized rats. In addition, the renal responses produced by the intracerebroventricular (i.c.v.) injection of opioid agonists were also examined with use of this anesthetic paradigm. In male Sprague-Dawley rats, the i.v. infusion of isotonic saline (55 microl/min) containing ketamine alone (1.0 mg/kg/min) produced low levels of urine flow rate (6.3 +/- 1.3 microl/min/gkw) and urinary sodium excretion (0.28 +/- 0.08 microeq/min/gkw). However, after adding xylazine (50 microg/kg/min) to the ketamine infusate, these renal excretory responses were significantly augmented. Steady-state levels of urine flow rate and urinary sodium excretion were attained approximately 120 min after starting the xylazine infusion and were similar in magnitude to the levels of water and sodium excretion previously observed in untreated, conscious rats. In ketamine/xylazine-anesthetized rats, the i.c.v. injection of the mu opioid agonist, dermorphin (0.1 nmol/kg), or the kappa opioid agonist, U-50488H (1 microg total), produced profound and concurrent diuretic and antinatriuretic responses. The pattern (direction and magnitude) of these opioid-induced renal excretory responses was similar to those previously reported in conscious rats. Together, these results indicate that the i.v. infusion of xylazine enhances the renal excretion of water and sodium in ketamine-anesthetized rats. Moreover, the renal responses produced by i.c.v. administration of opioids are similar in ketamine/xylazine-anesthetized and conscious rats. Thus, it appears that the ketamine/xylazine infusion protocol may provide a valid and useful approach to investigate various aspects of the central opioid control of renal function in rats during experimental procedures that require anesthesia.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗