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PubMed1989

Clinical studies on aclacinomycin A cardiotoxicity in adult patients with acute non lymphoblastic leukaemia.

Nine patients with acute non lymphoblastic leukaemia (ANLL) were treated with Aclacinomycin in the doses of 20 mg/m2/day x 7 days in 30' lasting intravenous infusion and Cytosin arabinosid 100 mg/m2/day x 7 days in continuous infusion as well as control group consisted of 30 healthy people were examined by means of 24 hrs Holter ECG monitoring and ultrasonocardiography (UCG) to evaluate the influence of Aclacinomycin A (Aclaplastin - Behring) on cardiac rhythm and function. The UCG and Holter examinations were performed before Aclacinomycin and after 7-10 days from the beginning of the therapy. There were no statistical differences between the results of UCG examination in Aclacinomycin-treated group before the therapy and the control group. A slight nonsignificant decrease in left ventricular stroke volume and ejection fraction were observed after Aclacinomycin. Cardiac index decreased after the therapy (p less than 0.05) but was of normal value. The only true significant (p less than 0.001) decrease was observed in the contractility of cardiac fibres but the cardiac failure was not observed. No alterations in left ventricular posterior wall and intraventricular septum thickness were found. The effusion to pericardium was observed in 2 pts in the initial study and in 1 of them also after the therapy. The obtained results supported the clinical observations that Aclacinomycin A is promising agent for the treatment of ANLL because of its low cardiotoxicity.

Aclarubicin↗

PubMed1986

Electrocardiographic changes during microlaryngoscopy in practolol-pretreated patients under balanced anaesthesia.

Electrocardiographic (ECG) changes were studied in 82 adult patients with a mean age of 49 years undergoing microlaryngoscopy. The patients were pretreated with practolol 0.15 mg/kg i.v. 5 min before induction of anaesthesia with thiopental. Anaesthesia was maintained with nitrous oxide in oxygen, fentanyl and suxamethonium-infusion. ECG changes occurred in 49% of the patients before anaesthesia and procedure. Pre-existing ECG changes increased or new changes occurred in 39% of the patients during intubation and in 38% during the procedure. The most common preanaesthetic ECG changes were flat or negative T-wave (18%), sinus tachycardia (13%), ischaemic S-T segment depression (8.5%) and intraventricular conduction disturbance (8.5%). ECG changes during intubation were sinus tachycardia (16%), ventricular ectopic beats (12%), supraventricular ectopic beats (10%) and ischaemic S-T segment depression (10%). The most common changes during microlaryngoscopy were supraventricular ectopic beats (16%), T-wave flattening or inversion (15%), ischaemic S-T segment depression (11%) and sinus bradycardia (10%). In all patients ECG changes disappeared without any special treatment. Unlike our earlier identical study without practolol pretreatment, neither sinus tachycardia nor junctional rhythm occurred during microlaryngoscopy in the present study. The results suggest that practolol pretreatment before microlaryngoscopy is especially useful when sinus tachycardia and junctional rhythm should be avoided.

Adult↗

PubMed1993

Mechanisms of atrial and brain natriuretic peptide release from rat ventricular myocardium: effect of stretching.

Ventricular hypertrophy is characterized by augmentation of the synthesis and storage of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). To evaluate in vitro the cellular mechanisms of immunoreactive ANP (IR-ANP) and BNP (IR-BNP) release from ventricular cardiocytes, we measured the secretory response to graded passive myocardial stretch in isolated atrialectomized perfused hypertrophied hearts of 14- to 18-month-old spontaneously hypertensive rats. At this age, the ventricular levels of both IR-ANP and IR-BNP were markedly higher in spontaneously hypertensive (182 +/- 27 and 32 +/- 3 pmol/ventricle, respectively) than in age-matched normotensive Wistar-Kyoto rats (35 +/- 4 and 12 +/- 1 pmol/ventricle, respectively; P < 0.001), whereas the differences between the strains in atrial levels of these peptides were small. The release of natriuretic peptides from ventricles in response to stretch was examined by increasing the volume of the intraventricular balloon for 10 min. Stretching of the hypertrophied ventricles produced a rapid transient (from 1-5 min) increase in both IR-ANP and IR-BNP secretion. As left ventricular pressure rose from 0 to 26 +/- 1 mm Hg, IR-ANP and IR-BNP release into the perfusion fluid increased 1.8 +/- 0.4- and 2.5 +/- 0.2-fold, respectively. Infusion of staurosporine, known to inhibit protein kinase-C activity in heart cells, blocked the stretch-induced increase in IR-ANP release (F = 3.10; P < 0.001, by analysis of variance), but had no effect on basal ventricular IR-ANP secretion (F = 0.87; P = NS). An L-type calcium channel antagonist, diltiazem, had no significant effect on basal (F = 1.20; P = NS) or stretch-stimulated (F = 1.47; P = NS) IR-ANP release from hypertrophied rat myocardium. Chromatographical analysis revealed that the ventricles primarily release the active processed 28- and 45- amino acid ANP- and BNP-like peptides, respectively, both before and during stretch. This study indicates that stretch stimulates both ANP and BNP secretion from hypertropic ventricular myocytes. The results further suggest that protein kinase-C may be involved in stretch-induced ventricular ANP release, whereas the influx of extracellular calcium may not be necessary.

Alkaloids↗

PubMed2001

Lack of dependence and rewarding effects of deltorphin II in mu-opioid receptor-deficient mice.

We have previously shown that the antinociceptive effects produced by the delta opioid-selective agonist deltorphin II are preserved in mu-opioid receptor (MOR)-deficient mice. We have now investigated rewarding effects and physical dependence produced by deltorphin II in these animals. Wild-type and MOR-deficient mice were implanted with a cannula into the third ventricle and deltorphin II was administered centrally. The rewarding effects induced by deltorphin II were then investigated using the place preference paradigm. Wild-type mice showed place preference for the compartment previously associated with deltorphin II and this effect was not observed in MOR-deficient mice. In a second experiment, mice received a chronic perfusion of deltorphin II over 6 days, via an Alzet minipump connected to the intraventricular cannula, and withdrawal was precipitated by naloxone administration. Wild-type animals showed a moderate but significant incidence of several somatic signs of withdrawal. This withdrawal response was suppressed in MOR-deficient mice. Analysis of the immunoreactivity levels of PKC-alpha, PKC-beta (I and II) and PKC-gamma isozymes in the cerebral cortex of mice infused chronically with deltorphin II showed a significant up-regulation of all these isozymes in the soluble fraction in wild-type but not in MOR-deficient mice. In conclusion, mu-opioid receptors, which are not involved in deltorphin II antinociception, appear to mediate the effects of chronic deltorphin II on rewarding responses, physical dependence and adaptive changes to PKC.

Animals↗

PubMed1975

The brain as a possible site for the cardiovascular effects of beta-adrenoceptor blocking agents in cats.

1. DL-Propranolol, L-propranolol, DL-alprenolol, pindolol (LB46), practolol, ICI 66082, sotalol and oxprenolol all produced prolonged falls in blood pressure and heart rate after intracerebroventricular administration in conscious normotensive cats. 2. Transient initial pressor responses and tachycardias were observed after intracerebroventricular infusions of all the beta-adrenoceptor antagonists used, except ICI 66082. 3. D-Propranolol, D-alphrenolol, procaine and lignocaine all produced initial increases in blood pressure and heart rate but did not subsequently cause any reduction in either blood pressure or heart rate. 4. The time of maximum hypotension and bradycardia after intracerebroventricular infusion of beta-adrenoceptor antagonists coincided with the maximum inhibition of the centrally mediated tachycardia observed after intracerebroventricular isoprenaline.

Adrenergic beta-Antagonists↗

PubMed1990

Pressor and sympathetic responses to dorsal raphe nucleus infusions of TRH in rats.

Pressor, tachycardic, and sympathoexcitatory responses to intracerebroventricularly (icv) infused thyrotropin-releasing hormone (TRH) were recorded in urethan-anesthetized rats to identify where centrally administered TRH acts in the brain. None of these responses was altered either by electrolytic lesions in the medial preoptic, posterior, or paraventricular hypothalamus or by chemical lesions produced by destroying catecholaminergic neurons with icv infused 6-hydroxydopamine. By contrast, when serotonergic neurons were similarly destroyed with 5,7-dihydroxytryptamine, TRH-induced tachycardia was inhibited. Attendant pressor responses were also inhibited by electrolytic lesions of the dorsal, but not of the median, raphe nucleus. Pressor and sympathoexcitatory responses elicited by infusing TRH directly into the dorsal raphe nucleus resembled those produced by icv infusion, and their magnitude diminished after pentolinium-induced ganglioplegia. These results are compatible with the interpretation that icv infused TRH may produce its cardiovascular and sympathetic effects by acting, at least in part, on serotonergic mechanisms located in the dorsal raphe nucleus.

5,7-Dihydroxytryptamine↗

PubMed2005

Neuropeptide W as a stress mediator in the hypothalamus.

Neuropeptide W (NPW) was isolated and found to be an endogenous peptide ligand for the orphan receptors GPR7 and GPR8. Centrally administered NPW caused a dose-dependent increase in corticosterone levels in rats. This observation indicates that NPW may play an important role in the hypothalamic organization of the endocrine response to stress. We examined the effects of immobilization stress and cold exposure on NPW-containing neurons in the hypothalamus of the rat, using dual immunostaining for NPW and Fos. In addition, to analyze the function of NPW, we studied the effect of intracerebroventricular (icv) NPW administration on Fos protein accumulation in the brain. Double immunohistochemistry for NPW and Fos showed that the percentage of Fos expression in the NPW-immunoreactive cells of the perifornical nucleus was significantly increased by immobilization stress compared with that in nonstressed rats. Similarly, the results indicated that cold exposure activates NPW-immunoreactive neurons in the perifornical nucleus. An icv administration of NPW resulted in significant Fos expression in the paraventricular nucleus, as compared with saline-infused controls. These results suggest that NPW is related to stress-responsive signal transduction, and that NPW may modulate the hypothalamus-pituitary-adrenal axis.

Animals↗

PubMed1987

Intracerebroventricular cholinergic drug administration in Alzheimer's disease: preliminary results of a double-blind study.

In June 1983, we began evaluating intracerebroventricular (ICV) cholinergic drug infusion in patients with biopsy-documented Alzheimer's disease (AD). An initial trial in four patients showed this treatment approach to be feasible, but objective improvement in cognitive or social function was not documented (Harbaugh et al., 1984; Harbaugh, 1986). A double-blind, placebo-controlled crossover study involving a larger number of patients has since been done. The results of this study, presented here, document a statistically significant improvement in some cognitive test results during periods of drug infusion. However, the clinical applicability of this treatment approach is still questionable. A collaborative, double-blind study evaluating activities of daily living and cognitive test results during drug and placebo infusion is presently underway and should better define the safety and efficacy of this treatment approach for patients with AD.

Aged↗

PubMed1984

Improved myocardial recovery from ischemia. Treatment with low-dose adenosine triphosphate-magnesium chloride.

To evaluate the effects of adenosine 5-triphosphate-magnesium chloride (ATP-MgCl2) on myocardial function following ischemia, mongrel dogs were placed on cardiopulmonary bypass with separate coronary perfusion pressures at 80 mm Hg. An intraventricular balloon was used to assess cardiac function as the area under the pressure-volume curve (PV), compliance (C), and cardiac contractility (dP/dT). Control measurements were made of coronary flow (Q), myocardial oxygen consumption and PV, C, and dP/dT. Myocardial ischemia was then induced for 45 minutes, followed by reperfusion (R). In group 1 (n = 5), no ATP-MgCl2 was infused into the coronary perfusion line. In group 2 (n = 5), low-dose ATP-MgCl2 (0.13 mg/min/kg) was infused during the first 30 minutes of reperfusion (R0 to R30), and in group 3 (n = 5), high-dose ATP-MgCl2 (3.2 mg/min/kg) was infused from R0 to R30. Use of ATP-MgCl2 therapy produced marked coronary vasodilation. After 20 minutes of reperfusion (R20), coronary resistance was 81% +/- 12%, 55% +/- 15%, and 31% +/- 3% of control in groups 1, 2, and 3, respectively. The high-dose ATP-MgCl2 (group 3) caused a marked systemic hypotension, but the low-dose ATP-MgCl2 (group 2) did not. After 75 minutes of reperfusion (R75), compliance was decreased in all groups. In groups 1 and 3, both function (PV) and dP/dT were significantly decreased. However, for group 2 (low-dose ATP-MgCl2), function (PV), and dP/dT were not different from the control group, indicating an excellent recovery. Thus, at low doses, ATP-MgCl2 appears to be a promising adjunct to the treatment of the ischemic myocardium.

Adenosine Triphosphate↗

PubMed2000

Emergency management of deeply comatose children with acute rupture of cerebral arteriovenous malformations.

PURPOSE: To assess the impact of emergency management on mortality and morbidity of acute rupture of cerebral arteriovenous malformations resulting in deep coma in children, and the factors predicting outcome. METHODS: Retrospective chart review of 20 children with a Glasgow Coma Scale < or = 8 with acute hemorrhagic stroke from a cerebral arteriovenous malformation rupture was conducted. Protocol included: early resuscitation with tracheal intubation and ventilation after induction of anesthesia with sufentanil, and benzodiazepine, and mannitol 20% or hypertonic saline 7.5% infusion for life-threatening brain herniation. Radiological exploration was limited to contrast-enhanced CT scan preceding immediate surgical decompression. Postoperatively, children were deeply sedated and intracranial pressure monitoring allowed titration with osmotherapy, vasopressors, hyperventilation or barbiturate coma to control cerebral perfusion pressure. Analysis used stratification of the type of hemorrhage (supra or infra tentorial), location (intraparenchymal and subarachnoid, intraparenchymal and intraventricular or intraventricular alone) and relationship between presentation, evolution with resuscitation, type of cerebral lesion, and outcome. RESULTS: Patients had a severe initial presentation (median Glasgow Coma Scale five), eight had unilateral and eight bilateral third nerve palsy. Compressive hematoma in supratentorial localisation represented 75% of the cases. Global mortality was 40%. Persistence of mydriasis after resuscitation increased mortality to 75%. Massive intraventricular flooding was associated with increased mortality. Good functional outcome was achieved in survivors. CONCLUSION: Acute rupture of an AVM can result in rapidly progressing coma. Emergency management with early resuscitation, minimal radiological exploration before rapid surgical decompression results in a mortality rate of 40%, but a good functional outcome can be expected in the survivors.

Acute Disease↗

PubMed1995

Inhibition of long-term potentiation in the dentate gyrus of freely moving rats by the metabotropic glutamate receptor antagonist MCPG.

Metabotropic glutamate receptors (mGluRs) are critically involved in the maintenance of long-term potentiation (LTP) (Reymann and Matthies, 1989; Behnisch et al., 1991; Izumi et al., 1991; Bashir et al., 1993). In order to assess further the physiological role of MGluRs in LTP, we injected freely moving rats with the recently available, competitive mGluR antagonist (R,S)-alpha-methyl-4-carboxyphenylglycine (MCPG) intraventricularly and recorded extracellularly the population spike (PS) as well as the field excitatory postsynaptic potential (fEPSP) of the granule cells of the dentate gyrus in response to stimulation of fibers of the perforant path. MCPG was administered in two concentrations (A = 20 mM/5 microliters; B = 200 mM/5 microliters) either 30 min prior to or 5 min after LTP induction. Sodium chloride infusion served as a control. Normal synaptic transmission was not altered by MCPG. However, the mGluR antagonist inhibited LTP in a concentration-dependent manner. Concentration A did not influence the potentiation shortly after the tetanus. In the PS, short-term potentiation (STP), which is decremental in its time course, occurred normally, but in contrast to controls the potentiation declined back to baseline values after 2-3 hr. This dose also reduced the posttetanic increase in the slope function of the fEPSP, and led to a time course of potentiation similar to that for the PS. Concentration B completely abolished the tetanus-induced potentiation. This block was similar to that obtained for the NMDA antagonist 2-amino-5-phosphonopentanoate (AP5). Both MCPG concentrations had no influence on the time course of preestablished LTP. These effects seem to be due to the action of the (+)-isomer of MCPG, since intracerebroventricular application of the (-)-isomer was without effect on the duration and magnitude of LTP. In addition, we were interested in the mGluR subtypes involved in the blocking mechanism of MCPG. 1S,3R-aminocyclopentane-1,3-dicarboxic acid (ACPD)-activated PPI hydrolysis in hippocampal slices was competitively inhibited by MCPG at a concentration of 1 mM or higher. In contrast, this concentration of MCPG did not affect the reduction of forskolin-stimulated cAMP formation by ACPD. These results corroborate recent findings that mGluRs are required for the induction of LTP in CA1 and CA3 in vitro (Bashir et al., 1993; Sergueeva et al., 1993) and in vivo (Riedel and Reymann, 1993). The process of STP is found to be independent of mGluR activation.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1992

Increase in cortical and midbrain tryptophan hydroxylase activity by intracerebroventricular administration of corticotropin releasing factor: block by adrenalectomy, by RU 38486 and by bilateral lesions to the central nucleus of the amygdala.

Corticotropin releasing factor (CRF) infused bilaterally into the lateral ventricles of awake, chronically cannulated, male Sprague-Dawley rats produced a dose-dependent increase in the in vitro activity of cortical and midbrain tryptophan hydroxylase after 60 min. The maximal increase in enzyme activity of 60% over that of vehicle-treated controls was reached 45 min after an infusion of 3 micrograms CRF. The increase in enzyme activity after a single dose of CRF resembled that seen after exposure of rats to an acute sound stress: it was reversed by preincubation of the enzyme preparation with alkaline phosphatase and was nonadditive with the increase in activity obtained in the presence of phosphorylating conditions. The response to intracerebroventricularly administered CRF was abolished by bilateral adrenalectomy, but restored by repeated daily systemic administration of the synthetic glucocorticoid, dexamethasone (500 micrograms/day, i.p. for 3 days), to the adrenalectomized rats. Intracerebroventricular administration of the glucocorticoid antagonist, RU 38486 (200 micrograms/day for 4 days), also blocked the acute increase in tryptophan hydroxylase activity in response to CRF. Finally, bilateral lesions to the central nucleus of the amygdala, a region involved in mediating behavioral, endocrine and autonomic responses to stressful stimuli, abolished the increase in enzyme activity in response to intraventricular CRF. The glucocorticoid sensitivity of the response to CRF, as well as the involvement of the central nucleus of the amygdala support the view that CRF may have a role in mediating the enhancement of tryptophan hydroxylase activity by acute sound stress.

Adrenalectomy↗

PubMed1988

Local asymptomatic status epilepticus induced by withdrawal of GABA infusion into limbic structures.

Most of the experimental models of status epilepticus result either from administration of a variety of excitatory neurotoxins or repeated electrical stimulation. Here we propose a new model based on the withdrawal of chronic gamma-aminobutyric acid (GABA) infusion into limbic structures via osmotic minipumps. Appearing with a latency of about 50 min, continuous pseudo-rhythmic EEG epileptic spiking was elicited for about 12-24 h after removal of GABA infusion in hippocampus or amygdala. No apparent distant brain damage was observed. This model differs from many others by several features and could result from different mechanisms.

Amygdala↗

PubMed1985

The role of caudate nucleus in dermorphin-induced catalepsy in rats.

Bilateral electrolytic lesions of caudate nucleus were observed to potentiate the cataleptic response, and to prevent the muscular rigidity produced by intracerebroventricular injection or infusion of dermorphin. These results suggest that caudate nucleus plays an inhibitory role in controlling the cataleptic response and its integrity is essential for full development of dermorphin-induced rigidity.

Animals↗

PubMed1996

Interleukin-6 prevents ischemia-induced learning disability and neuronal and synaptic loss in gerbils.

Interleukin-6 (IL-6) has been shown to have potent neurotrophic activity on peripheral and central neurons in vitro. However, it remains to be determined whether or not IL-6 rescues hippocampal CA1 neurons from lethal ischemia and prevents ischemia-induced learning disability. In the present in vivo study, we infused IL-6 continuously for 7 days into the lateral ventricle of gerbil starting 2 h before 3-min forebrain ischemia. IL-6 infusion prevented the occurrence of ischemia-induced learning disability in a dose-dependent manner as revealed by a step-down passive avoidance task. Subsequent light and electron microscopic examinations showed that pyramidal neurons in the CA1 region of the hippocampus as well as synapses within the strata moleculare, radiatum and oriens of the region were significantly more numerous in gerbils infused with IL-6 than in those receiving vehicle infusion. These findings suggest that IL-6 has a trophic effect on ischemic hippocampal neurons.

Animals↗

PubMed2005

ICV testosterone induces Fos in male Syrian hamster brain.

Previous studies in our laboratory have demonstrated intracerebroventricular (ICV) self-administration of testosterone in hamsters. This suggests that androgens are reinforcing, independent of their anabolic effects. Furthermore, pharmacologic testosterone acts as a depressant: ICV testosterone infusion acutely reduces respiration, locomotion and body temperature. However, with chronic exposure, males develop tolerance. To understand mechanisms for androgen action, we looked for Fos expression after acute and chronic ICV infusion of testosterone or vehicle. 32 castrated males with chronic physiologic testosterone replacement (n=8/group) were infused ICV for 4h/day with 40 microg testosterone or 40 microl vehicle. Half of the males were perfused after the first day of ICV infusion; the remaining males were perfused after 15 days of ICV infusion. 60 microm coronal brain slices were cut. Every fourth section was stained for Fos. Additional sections were stained for androgen receptors (AR) and estrogen receptors (ER). Testosterone infusion induced Fos above control in the posteromedial bed nucleus of the stria terminalis (BSTPM), posteromedial amygdala (MeP), lateral habenula (LHb), median raphe (MnR), lateral pontine nucleus (Pn), and ventral tegmental area (VTA). In particular, Fos was elevated in the BSTPM, MeP, LHb, and VTA only after 1 day of testosterone. 15 days of testosterone enhanced Fos expression above control in the MnR and lateral Pn. Importantly, Fos was not present in all brain areas involved in reward or in those with dense steroid receptors. Furthermore, AR and ER immunostaining was unaltered by testosterone infusion. We conclude that pharmacologic testosterone activates select steroid-sensitive brain regions, as well as midbrain areas involved in reinforcement of commonly-abused drugs.

Analysis of Variance↗

PubMed2001

Intracerebroventricular infusions of TNF-alpha preferentially recruit blood lymphocytes and induce a perivascular leukocyte infiltrate.

Tumour necrosis factor (TNF)-alpha is important in several central nervous system (CNS) inflammatory diseases, however, its role in the recruitment of leukocytes into the cerebral spinal fluid (CSF) and CNS is incompletely understood. Therefore, we examined the effect of intracerebroventricular (icv) and parenchymal infusions of TNF-alpha on the type of leukocyte, the pool and subset of lymphocytes recruited into CSF and brain parenchyma. Parenchymal injections of 500 ng of recombinant human TNF-alpha did not induce inflammation, whereas an icv infusion of TNF-alpha caused CSF leuckocytosis and a perivascular infiltrate. Twenty-four hours after the icv infusion neutrophils predominated, with CD4+ T cells being the major lymphocyte subset in CSF. By 48 h lymphocytes were the dominant cell type with CD8+ cells surpassing CD4+ cells in both the CSF and the perivascular infiltrate. The labeled recirculating lymphocyte pool prevailed in normal CSF, but after the infusion of TNF-alpha, the blood pool of lymphocytes was preferentially recruited. These results have implications for the immune surveillance of the CNS.

Animals↗

PubMed1997

Chronic ICV enterostatin preferentially reduced fat intake and lowered body weight.

The pancreatic peptide enterostatin will acutely reduce fat intake in rats provided a choice of diets. Chronic ICV infusions of enterostatin suppress the intake of high fat diet. However, the effects of chronic ICV enterostatin on diet choice has not previously been studied. To investigate this, enterostatin (0.5 microgram/h) or artificial cerebrospinal fluid (CSF) was infused for 9 days into the lateral ventricle of rats adapted to a two-choice high-fat (HF) and low-fat (LF) diet regime. Enterostatin reduced intake of HF diet with the maximum depression at day 4, but there was no compensatory increase in LF intake. The body weight of enterostatin-infused rats declined. This was associated with a reduction in fat pad and liver weights compared to the CSF-infused control rats. Serum triglycerides and insulin were decreased and corticosterone was elevated in enterostatin-infused rats. The data show that enterostatin will chronically reduce fat intake and body weight and suggest that enterostatin may attenuate the appetite for fat.

Animals↗