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PubMed1985

Effects of intraventricular growth hormone-releasing factor on growth hormone release: further evidence for ultrashort loop feedback.

We examined the effects of cerebroventricular injection of synthetic human GH-releasing factor [hGRF-(1-44)] on regulation of GH release in conscious male rats. These results were compared with the direct effects of hGRF on hormone released from dispersed anterior pituitary cells. Administration of two higher doses of hGRF (200 and 2000 ng) into the third ventricle (3V) produced a dose-related increase in plasma GH levels (P less than 0.001). Injection of hGRF into the 3V at two lower doses actually reduced GH release. Infusion of 20 ng (5 pmol) hGRF reduced plasma GH from 5-60 min (P less than 0.005), with a maximum suppression of 66%. The 2-ng (0.5-pmol) dose decreased GH secretion by 45% (P less than 0.05). hGRF stimulated a significant and dose-dependent release of GH from dispersed pituitary cells at concentrations of 10(-10) and 10(-9) M (P less than 0.025). The specificity of GRF for GH control, whether stimulatory or inhibitory, was seen by the failure of GRF to modify PRL, TSH, or LH release. Our results indicate that injection of larger doses of GRF into the 3V produce GH release, but at lower doses, 3V GRF may exert an action centrally to inhibit GH release. We propose that hypothalamic GRF may decrease its own neurosecretion by negative ultrashort loop feedback.

Animals↗

PubMed2004

Management of coagulopathy with recombinant factor VIIa in a neonate with echovirus type 7.

A 5-day-old newborn presented with neonatal enteroviral infection. The patient's hospital course was complicated by acute liver dysfunction, renal insufficiency, fluid overload, respiratory failure, hypertension, catheter related thrombosis, Klebsiella pneumoniae sepsis, intracerebral and intraventricular hemorrhage, and disseminated intravascular coagulation (DIC). Administration of fresh frozen plasma (FFP) and cryoprecipitate failed to control the patient's hemostasis and led to significant fluid overload. Recombinant activated factor VII (rFVIIa, Novoseven NovoNordisk, Bagsvaerd, Denmark) was given to the neonate as a bolus (rFVIIa at 60-80 microg/kg body weight), followed by a continuous infusion (2.5-16 microg/kg/hr). Recombinant activated factor VII controlled hemostasis, until the patient's liver function recovered. The patient's blood product requirement significantly decreased and his fluid overload resolved. Administration of rFVIIa appears to have stabilized the coagulation process. The patient appears to have fully recovered from the infection's complications.

Blood Coagulation Disorders↗

PubMed1976

Behavioural, electrocortical and body temperature effects of cholera toxin.

In young chicks intrahypothalamic infusion of cholera toxin produced a dramatic and dose-dependent increase in motor activity. Similar effects were also obtained in adult fowls after injection of cholera toxin into the third cerebral ventricle, the hypothalamus or the paleostriatum augmentatum. Electrocortical changes consisted of a slight desynchronization during the hypermotor activity and were preceded, when the highest intraventricular doses were used, by a short period of slower frequency and higher amplitude potentials. Intraventricular and intrahypothalamic but not intrastriatal injection of cholera toxin produced a typical biphasic hyperthermic response.

Animals↗

PubMed2001

The protective effect of ceramide in immature rat brain hypoxia-ischemia involves up-regulation of bcl-2 and reduction of TUNEL-positive cells.

Preconditioning brain with tumor necrosis factor alpha (TNF-alpha) can induce tolerance to experimental hypoxia and stroke and ceramide is a downstream messenger in the TNF-alpha signaling pathway. A hypoxic-ischemic (HI) insult in the immature rat injures brain primarily through apoptosis. Apoptosis is regulated by Bcl-2 family proteins. The authors explored whether ceramide protects against HI in the immature rat, and whether Bcl-2 family protein expression is involved. Hypoxia-ischemia was produced in seven-day-old rats by ligating the right carotid artery, followed by 2 hours of 8% oxygen exposure. Thirty minutes after HI, C2-ceramide (150 microg/kg) was injected intraventricularly. Infarct volume was measured 5 days later. C2-ceramide reduced HI-induced brain damage by 45% to 65% compared with HI/dimethyl sulfoxide (DMSO) (vehicle control) or HI only groups. In separate experiments, brains of sham-operated control and HI only animals and animals subjected to HI plus C2-ceramide or DMSO infusion were sampled 6 hours, 24 hours, and 5 days after treatments and analyzed for Bcl-2, Bcl-xl, and Bax expression (Western blotting), and apoptosis (TUNEL assay). Augmented Bcl-2 and Bcl-xl levels in the C2-ceramide treated group were associated with a significant decrease in TUNEL-positive cells. The results support a protective role for ceramide in neonatal HI.

Animals↗

PubMed1983

The efficacy of Ajmaline in ventricular arrhythmias after failure of lidocaine therapy in the acute phase of myocardial infarction.

Forty-three patients in the acute phase of myocardial infarction who were resistant to conventional doses of lidocaine received Ajmaline intravenously (50 mg bolus followed by constant infusion rate of 1-1.5 mg/min). Dangerous ventricular arrhythmias were abolished in 72% of this group of patients (group A). In the remaining patients (28%), Ajmaline was found to be ineffective (group B). There was no reduction of systolic or diastolic blood pressure and there was an insignificant increase in heart rate. Atrio-ventricular or intraventricular conduction defects appeared in 46% of the patients described. There was a statistically significant increase in occurrence of heart blocks in group B patients and among these complete left bundle branch block (CLBBB) was the most prevalent. Atrio-ventricular or intraventricular conduction defects were transient, appearing between 8-36 h (mean 23 h), and were not accompanied by reduction of ventricular rate. Conduction defects disappeared within several hours (up to 24 hours) after Ajmaline was discontinued. It is concluded that Ajmaline administered by this regimen is an effective alternative agent for patients with ventricular arrhythmia not controlled by lidocaine in the acute phase of myocardial infarction.

Ajmaline↗

PubMed1985

The effect of chronic in vivo infusion of forskolin on noradrenergic receptor sensitivity.

Forskolin, a diterpene isolated from the plant Coleus forskolii, activates the catalytic subunit of adenylate cyclase, resulting in a hormone receptor-independent increase in the intracellular production of cyclic AMP. This study was undertaken to assess the effect of chronic in vivo infusion of forskolin on noradrenergic neuronal activity. Forskolin was infused into the right lateral ventricle of male Sprague Dawley rats via Alzet osmotic minipumps (model 2001) for 7 days. Chronic infusion of forskolin resulted in a decrease in norepinephrine-stimulated cyclic AMP accumulation in the limbic forebrain. Chronic infusion of forskolin also resulted in a decrease in the Bmax for 3H-dihydroalprenolol (3H-DHA) binding to beta-adrenergic receptors in the cerebral cortex and hippocampus, with no apparent change in the Kd values. These data suggest the possibility of a novel therapeutic approach to modulating receptor sensitivity, and that chronic infusion of forskolin may be a useful model for studying the role of cyclic AMP in the control of neuronal activity.

Animals↗

PubMed1996

Intracerebroventricular infusion of the CCKB receptor agonist pentagastrin potentiates acoustic startle.

The acoustic startle reflex is increased by stimuli associated with aversive events (such as the delivery of shock) and so has been used as a sensitive index of 'anxiety' or 'fear'. Administration of cholecystokininB (CCKB) receptor agonists produces a constellation of behaviors associated with 'anxiety' in laboratory animals and humans. Here, intracerebroventricular infusions of the CCKB agonist, pentagastrin (0, 1, 10, 100 nM), produced a long-lasting, dose-related potentiation of acoustic startle responses. Similar infusions of pentagastrin had no effect on locomotor activity over the same time course, showing that changes in startle responses following infusions of pentagastrin are not due to nonspecific changes in motor activity.

Acoustic Stimulation↗

PubMed1983

New multi-cannula pedestal device for micro-injection of drugs into brain tissue or cerebral ventricle.

A new multiple-cannula-pedestal system for micro-injection of drugs directly into either brain tissue or cerebral ventricle is described. Its features include ease of construction from commonly available materials, no specialized machining required, durability and economy. A special aspect of the cannula system is a protective cap containing a bolt which threads onto a nut fixed within the pedestal base. Since the cap cannot be dislodged, potential damage to indwelling stylets and exposed guide tubes is prevented. Moreover, an aseptic preparation is therefore provided so that test compounds can be infused repeatedly over a prolonged period. Finally, the protective caps are interchangeable and the pedestal base itself can be re-cycled for usage in different animals.

Animals↗

PubMed1995

Modest reduction of benzodiazepine binding in rat brain in vivo induced by antisense oligonucleotide to GABAA receptor gamma 2 subunit subtype.

The GABAA (gamma-aminobutyric acid-A) receptor gamma 2 subunit subtype is probably a functionally integral part of the benzodiazepine binding site of the GABAA receptor complex, important for benzodiazepine pharmacology. We have evaluated the possibility of specifically reducing benzodiazepine receptor binding properties in vivo using phosphorothioate antisense oligodeoxynucleotides to inhibit the expression of GABAA receptor gamma 2 subunit subtype. Intracerebroventricular infusions of an antisense oligonucleotide reduced benzodiazepine receptor radioligand binding by 9-15% in specific rat brain regions.

Animals↗

PubMed1995

Continuous infusion of neuropeptide Y in the SCN decreases food intake in rats.

We investigated the effect of chronic infusion of neuropeptide Y (NPY) aimed at the hypothalamic suprachiasmatic nucleus (SCN) or the lateral cerebral ventricle (LCV) on food intake. The experiments were performed in adult male Wistar rats infused for 7 days with saline or NPY (10 and 100 pmol microliters-1 h-1) into the SCN (n = 18) or LCV (n = 17). Infusion of the lower dose of NPY in the SCN significantly decreased food intake, whereas infusion of the higher dose did not. There was no change in food intake specific to saline or either dose of NPY with infusion in the LCV. It is concluded that chronic infusion of NPY into the SCN at a dose of 10 pmol h-1 inhibits food intake in rats.

Animals↗

PubMed1998

Nociceptin fails to affect heroin self-administration in the rat.

The recently isolated peptide nociceptin has a primary structure similar to that of opioid peptides. Early functional studies suggested that it may act in opposition to opioid systems. To determine whether nociceptin influences the rewarding properties of heroin, nociceptin was given intracerebroventricularly (i.c.v.) to rats trained to self-administer heroin. Rats (n = 8) were given doses of 0.01 microg, 0.1 microg, 1.0 microg and 10.0 microg in a Latin square design. None of the doses significantly affected heroin self-administration rates compared to vehicle. The highest dose of nociceptin used inhibited spontaneous locomotor activity, evidence that the peptide retained its biological activity after i.c.v. infusion. These studies suggest that nociceptin does not affect the rewarding value of heroin.

Animals↗

PubMedDate not supplied

Sustained protection by iloprost of the porcine heart in the acute and chronic phases of myocardial infarction.

The effects of iloprost (ZK 36 374) on myocardial ischemia and infarction were studied in three groups of four anesthetized and heparinized pigs. Coronary microembolization was evoked by the injection of microspheres (50 microM) into the left coronary artery. A dose of 12 million beads/kg was followed by ventricular fibrillation and death after 11 +/- 5 min (group A). In group B, ischemia was evident at 15 min after the injection of 6 million beads/kg from an ST segment elevation in the precordial electrocardiogram (2.9 +/- 1.1 mV; p less than 0.05) and from an arterial-coronary venous difference in inosine concentration of -8.5 +/- 0.3 microM (p less than 0.05). However, in the presence of iloprost--an infusion of 0.18 micrograms/kg/min started 30 min before embolization--no ST segment elevation (0.45 +/- 0.23 mV; NS) or inosine release (-1.5 +/- 1.0 microM) was detected after the injection of 12 million beads/kg (group C). After 7 days, the animals from group B had more frequent spontaneous ventricular arrhythmias than those from group C. Programmed electrical stimulation induced intraventricular reentry in some animals of both groups (3 of 4 in B and 2 of 4 in C). Ventricular tachycardia was induced in two animals from group B. Postmortem examination revealed small myocardial infarcts in all group B animals; however, in group C no infarcts were detected. These data corroborate the view that prostacyclin-mimetic compounds are beneficial in the acute and in the chronic phases of myocardial infarction.

Animals↗

PubMed2004

Central Tempol alters basal sympathetic nerve discharge and attenuates sympathetic excitation to central ANG II.

In the present study, we established dose-response relationships between central administration of 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (Tempol, a superoxide dismutase mimetic) and the level of renal sympathetic nerve discharge (SND) and tested the hypothesis that intracerebroventricular (icv) Tempol pretreatment would attenuate centrally mediated changes in SND produced by icv ANG II administration. Urethane-chloralose-anesthetized, baroreceptor-denervated, normotensive rats were used. We found that icv Tempol administration produced dose-dependent sympathoinhibitory, hypotensive, and bradycardic responses. Mean arterial pressure and SND values were significantly increased after icv ANG II (150 ng/kg) administration, and these responses were abrogated after icv pretreatment with Tempol (75 micromol/kg) or losartan. Brain superoxide levels tended to be higher in ANG II-treated rats compared with rats treated with Tempol and ANG II. Tempol pretreatment did not prevent increases in SND level that were produced by acute heat stress, which indicates specificity in the effect of Tempol in reducing sympathoexcitation. These results demonstrate that icv Tempol administration influences central sympathetic neural circuits in a dose-dependent manner and attenuates SND responses to central ANG II infusion.

Angiotensin II↗

PubMed1994

Inhibitory effect of arginine-vasopressin on LH secretion in the ovariectomized rhesus monkey.

Arginine-vasopressin (AVP) has been previously shown to act in synergism with corticotropin-releasing hormone (CRH) in mediating stress-induced changes in the hypothalamo-pituitary-adrenal (HPA) axis. We have previously shown that both AVP and CRH play a role in mediating IL-1 alpha-induced changes in gonadotropin secretion. In this study, we investigate the effects of exogenously administered AVP on luteinizing hormone (LH) secretion in the ovariectomized (OVX) rhesus monkey. Adult OVX rhesus monkeys were given an intracerebroventricular (ICV) infusion of AVP (15 micrograms/h, n = 8; 50 micrograms/h, n = 5). Control animals received an ICV infusion of physiological saline at a rate 30 microliters/h (n = 12). LH concentrations were measured at 15-min intervals during a 3-hour preinfusion morning baseline and 5-hour postinfusion period. Cortisol concentrations were determined at 45-min intervals. Pulsatile LH release remained unchanged after a control saline infusion. After an AVP infusion, however, LH concentrations (ng/ml) significantly decreased (15 micrograms: from 172.9 +/- 6.4 baseline to 129.4 +/- 5.3; 50 micrograms: from 142.8 +/- 8.3 to 106.7 +/- 6.0, mean +/- SE; p < 0.05). By the fifth hour of the AVP infusion, areas under the LH curve were 64.3 +/- 10.5 and 62.9 +/- 11.0% of morning baseline for 15 and 50 micrograms hourly infusion rate, respectively. While cortisol concentrations decreased throughout the experimental period in the animals receiving saline (a.m.: 35.4 +/- 2.4 micrograms/dl vs. p.m.: 27.7 +/- 1.9 micrograms/dl), they increased after AVP infusion (15 micrograms/h: 42.3 +/- 2.4 vs. 54.6 +/- 2.0 micrograms/dl; 50 micrograms/h: 41.9 +/- 6.6 vs. 50.8 +/- 8.5 micrograms/dl).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Sustained radiographic and clinical response in patient with bifrontal recurrent glioblastoma multiforme with intracerebral infusion of the recombinant targeted toxin TP-38: case study.

Glioblastoma multiforme remains refractory to conventional therapy, and novel therapeutic modalities are desperately needed. TP-38 is a recombinant chimeric protein containing a genetically engineered form of the cytotoxic Pseudomonas exotoxin fused to transforming growth factor (TGF)-alpha. TGF-alpha binds with high affinity to the epidermal growth factor receptor, which is uniformly overexpressed in malignant gliomas, often because of gene amplification. Prior to therapy with TP-38, the patient described here was completely refractory to multiple other therapies, with radiographic and pathologic evidence of tumor progression. After therapy, she improved clinically, was weaned off steroids and anti-convulsants, and experienced a progressive decrease in enhancing tumor volume. Despite multiple prior recurrences, she has not progressed for >43 months after TP-38 therapy. Small remaining areas of enhancement demonstrate no evidence of tumor histologically and are hypometabolic on positron emission tomography. This report describes a dramatic and sustained clinical and radiographic response in a patient with a bifrontal glioblastoma multiforme treated with intratumoral infusion of a novel targeted toxin, TP-38.

Brain Neoplasms↗

PubMed2002

Effect of intravenous propranolol on left ventricular apical ballooning without coronary artery stenosis (ampulla cardiomyopathy): three cases.

The precise etiological basis of transient left ventricular apical ballooning without coronary artery stenosis (ampulla or so-called 'takotsubo' cardiomyopathy) remains unknown, so the present study examined the acute effects of intravenous propranolol (2-4 mg) in 3 female patients (age range, 61-76 years) with the condition. Although one patient who did not have any intraventricular pressure gradients showed no improvement in the electrocardiographic and left ventricular wall motion abnormalities, the other 2 patients, who had significant intraventricular pressure gradients, did show improvement. Dynamic intraventricular obstruction might play a role in maintaining apical ballooning, at least, in patients exhibiting an intraventricular pressure gradient.

Adrenergic beta-Antagonists↗

PubMed2000

Comparison of the electropharmacological effects of verapamil and propranolol in the halothane-anesthetized in vivo canine model under monophasic action potential monitoring.

The cardiovascular profile of verapamil was assessed in the halothane-anesthetized canine model and compared with that of propranolol. Verapamil was infused at the rates of 1, 3 and 10 microg x kg(-1) x min(-1) (n=6), whereas propranolol was administered at a fixed rate of 10 microg x kg(-1) x min(-1) (n=6). Each infusion was performed over 30 min, and the parameters were assessed for 20-30 min after the start of each infusion. Verapamil in a dose of 10 microg x kg(-1) x min(-1) significantly suppressed atrio-ventricular (AV) node conduction and slightly decreased the mean blood pressure, but no significant change was detected in the left ventricular end-diastolic pressure, maximum upstroke velocity of the left ventricular pressure, sinus automaticity, double product, cardiac output, intraventricular conduction, and ventricular repolarization phase and refractoriness. Propranolol suppressed AV node conduction to an extent similar to that of verapamil, but it also inhibited intraventricular conduction, sinus automaticity and ventricular contraction, increased the ventricular refractoriness, and decreased the double product and cardiac output, without any significant change in the other variables measured. These results suggest that verapamil can selectively affect the AV node, and that the greater part of the suppressive action of propranolol on the multiple cardiovascular performance is through a beta-blocking action and direct membrane effect, although the halothane inhalation itself might have modified each of the drug's effects. The abbreviation of the relative refractory period of the ventricle by propranolol may show its potential utility for re-entry type ventricular tachycardia.

Action Potentials↗

PubMed1985

[Intravenous cibenzoline in the treatment of ventricular and supraventricular arrhythmias].

The efficacy of intravenous cibenzoline in the treatment of supraventricular and ventricular arrhythmias was demonstrated in a French trial of 212 patients including 40 in the acute phase of myocardial infarction. The minimal therapeutic plasma concentration was about 0.3 microgram/ml: this was obtained by a loading dose of 1 mg/kg relayed by a perfusion of 8 mg/kg/24 hours. The clinical tolerance was satisfactory in 96.2% of cases when the contra-indications were respected (severe cardiac failure, intraventricular conduction defects and non-paced 2nd and 3rd degree atrioventricular block). Local tolerance was excellent in all cases.

Anti-Arrhythmia Agents↗