Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Injections, Intraventricular”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed1983

Relationship between catalase activity and uptake of elemental mercury by rat brain.

Uptake of mercury by brain after intravenous injection of elemental mercury was investigated in the rat. Catalase activity was inhibited by aminotriazole either by intraperitoneal injections affecting catalase in most tissues of the animal or by intraventricular injections affecting catalase in the brain selectively. Uptake of elemental mercury by rat brain was not influenced by intraperitoneal administration of aminotriazole resulting in 50% inhibition of brain catalase. However, when the inhibitor was injected intraventricularly in concentrations to give a 50% inhibition of brain catalase, it was shown that the mercury uptake by the brain was significantly decreased. In the latter case when only brain catalase was inhibited and the supply of elemental mercury to brain was maintained, mercury uptake by brain was proportional to the activity of catalase in brain tissue and to the injected amount of elemental mercury. Contrary to the intraventricular injection of aminotriazole, in animals receiving aminotriazole intraperitoneally prior to elemental mercury injection, we suggest that the lower activity of brain catalase is compensated by an increased supply of elemental mercury caused by the generally lower oxidation rate in the animal. This view is supported by the finding that mercury uptake by liver increased due to aminotriazole intraperitoneally although activity of catalase was depressed.

Amitrole↗
PubMed1991

Feedback of follicle-stimulating hormone to inhibit luteinizing hormone and stimulate follicle-stimulating hormone release in ovariectomized rats.

Injection of ovine follicle-stimulating hormone (o-FSH) into the third cerebral ventricle significantly suppressed plasma luteinizing hormone (LH) release in conscious, unrestrained ovariectomized rats. Intraventricular injection of o-FSH (0.5 microgram) significantly lowered the plasma levels of LH by 70 min and decreased pulse frequency, whereas the pulsatile release of FSH was unchanged during the 180-min duration of the experiment. In a 12-hour experiment, the suppression of LH release reached the maximum within 3 h (p less than 0.001), followed by a return of plasma LH level to initial values 6-8 h after intraventricular injection of o-FSH at doses of 0.5, 4 and 8 micrograms. Plasma levels of FSH were not significantly changed by the low dose of o-FSH (0.5 microgram), but there was a delayed elevation of plasma FSH during the 8-12 h after intraventricular injection of o-FSH at higher doses (4 and 8 micrograms). On the other hand, plasma prolactin was unchanged after intraventricular injection of o-FSH. Since the pituitary responsiveness to synthetic LH-releasing hormone (LHRH) was unimpaired at the end of the sampling and incubation with o-FSH suppressed the release of LHRH from median eminence terminals, these data indicate that FSH acts intrahypothalamically to suppress LHRH release. The late elevation of plasma FSH may be the result of enhanced release of FSH-releasing factor or of a delayed, direct effect of the hormone on the gonadotropes to increase release of FSH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Differential actions of intrathecal naloxone on blocking the tail-flick inhibition induced by intraventricular beta-endorphin and morphine in rats.

In the present study, it is proposed that the opioids applied to supraspinal brain sites produced their analgesic effects by the activation of different descending pain inhibitory systems. The blockade of the spinal endorphinergic system by intrathecal naloxone on the production of tail-flick inhibition induced by intraventricular beta-endorphin and morphine was then studied. Intraventricular injection of beta-endorphin and morphine produced an inhibition of the tail-flick response to the heat stimulus in rats. Intrathecal injection of naloxone at doses of 0.4 to 40 micrograms caused a dose-related blockade of the inhibition of the tail-flick response induced by intraventricular injection of beta-endorphin, and a high dose of naloxone (40 micrograms) completely blocked the tail-flick inhibition induced by intraventricular beta-endorphin (16 micrograms). On the other hand, intrathecal naloxone (12-120 micrograms) had only a very weak effect on the tail-flick inhibition induced by intraventricular morphine (40 micrograms). Intraventricular injection of naloxone at doses of 1.2 to 12 micrograms equally antagonized in a dose-dependent manner the tail-flick inhibition induced by intraventricular beta-endorphin and morphine. The results indicate that a spinal naloxone-sensitive endorphinergic system is involved in the production of beta-endorphin but not morphine-induced tail-flick inhibition, and suggest that intraventricular beta-endorphin and morphine elicit their pharmacological actions via the activation of different descending pain inhibitory systems; descending epsilon and mu systems for beta-endorphin and morphine, respectively, are proposed.

Analgesia↗
PubMed1985

Ultrashort-loop positive feedback of corticotropin (ACTH)-releasing factor to enhance ACTH release in stress.

Previous experiments have shown that intraventricular injection of ovine corticotropin (ACTH)-releasing factor (oCRF) in doses too low to elevate plasma ACTH by direct action on the pituitary does not lower plasma ACTH, suggesting that the peptide lacks a negative ultrashort-loop feedback action to suppress its own release under resting conditions. The present study was performed to determine whether oCRF has any action to alter CRF release in stress. The peptide was injected into the third ventricle or external jugular vein of freely moving ovariectomized female rats 5 min prior to application of ether stress. When oCRF was injected into the third ventricle in doses of 500 pg (0.1 pmol) or less, there was no significant alteration in plasma ACTH prior to ether stress; however, there was a significantly enhanced increase in plasma ACTH 2 and 5 min after ether stress applied 5 min after intraventricular injection of oCRF at doses of 50 (0.01 pmol) or 150 pg (0.03 pmol). These results suggest that the peptide acts on structures adjacent to the third ventricle to augment stress-induced CRF release. To rule out the possibility that the sensitivity of the pituitary itself to CRF increases dramatically following stress, 10 or 100 ng of oCRF was injected i.v. These doses produced a significant dose-related increase in plasma ACTH at 2, 5, or 15 min. In other groups receiving the same doses of oCRF and ether stressed 5 min later, plasma ACTH was significantly higher 2 or 5 min after ether stress when compared with plasma ACTH in ether-stressed saline-injected animals. However, in contrast with the results of intraventricular injection of oCRF, the release of ACTH was no greater than that obtained by summing the independent effects of exogenous oCRF and the CRF released by stress. We conclude that CRF may have a positive ultrashort-loop feedback action to enhance stress-induced ACTH release and that this enhancement is not due to increased sensitivity of anterior pituitary corticotrophs to CRF.

Adrenocorticotropic Hormone↗
PubMed1981

Drainage of cerebral interstitial fluid into deep cervical lymph of the rabbit.

Lymph from the jugular lymph trunks of anesthetized rabbits has been continuously collected and radioiodinated albumin (RISA) therein estimated after microinjection of 1 microliter of 131I-albumin into the caudate nucleus, after single intraventricular injections, and during intraventricular infusions. Comparison of lymph at 7 and 25 h after intracerebral microinjection with efflux of radioactivity from whole brain suggests that about 50% of cleared radioactivity goes through lymph. Concentrations, normalized to cerebrospinal fluid (CSF), were much higher in lymph and retropharyngeal nodes after brain injection than after CSF injection or infusion. Also after brain injection, lymph and nodes contained more activity on injected side in contrast to lack of laterality after CSF administration. Calculation suggests that less than 30% of RISA cleared from brain can do so via a pool of well-mixed CSF. Analysis of tissues is compatible with much RISA draining by bulk flow via cerebral perivascular spaces plus passage from subarachnoid space of olfactory lobes into submucous spaces of nose and thus to lymph.

Animals↗
PubMed1977

Perseveration and rotational behavior elicited by d-amphetamine in a Y-maze exploratory task: differential effects of intraperitoneal and unilateral intraventricular administration.

Mice received either intraperitoneal (1.0, 3.0, 5.0, or 15.0 mg/kg) or unilateral intraventricular injection (50.0, 100.0 or 200.0 microgram) of d-amphetamine. Both routes of injection produced circling behavior in a dose-related fashion when animals were tested in a circular alley-way. In contrast, performance in a free running Y-maze alternation task was differentially affected by the route of administration. Whereas intraperitoneal injection induced perseveration (i.e., animals consecutively visited only two arms of the maze), intraventricular injection augmented alternation behavior normally seen in saline-treated mice. It was suggested that Y-maze performance following intraventricular d-amphetamine injection reflects response perseveration, whereas systemic d-amphetamine treatment produced stimulus perseveration (repetition of location rather than direction). Moreover d-amphetamine-induced circling produced by intraperitoneal administration probably is an artifact of drug-induced stimulus perseveration as opposed to motor biases observed following intraventricular injections.

Animals↗
PubMed1979

Central and peripheral effects of bradykinin and prostaglandin E2 on blood pressure in conscious rats.

Bradykinin or prostaglandin E2 (PGE2), when injected intravenously, decreased blood pressure of conscious rats in a dose-dependent manner, while intracerebroventricular injections of bradykinin or PGE2 caused a dose-dependent increase in blood pressure. SQ 14,225, an inhibitor of angiotensin converting enzyme, potentiated the central pressor or peripheral depressor effect of bradykinin. Indomethacin, an inhibitor of prostaglandin synthesis, almost completely inhibited the central pressor effect of bradykinin when injected intraventricularly. Indomenthacin, when injected intravenously, failed to inhibit the peripheral depressor effect of bradykinin, whereas it significantly attenuated the peripheral depressor effect of bradykinin when the angiotensin converting enzyme was inhibited with SQ 14,225. These results suggest that the central pressor effect of bradykinin is mainly mediated by the synthesis of prostaglandins in the central nervous system, while only a small fraction of peripheral depressor effect of bradykinin is, at least in conscious rats, mediated by the synthesis of prostaglandins in the systemic circulation.

Animals↗
PubMed1992

Analgesic effects of intraventricular and intrathecal injection of morphine and ketocyclazocine in the infant rat.

Little is known of the neural bases of analgesia in immature animals. This experiment examined the effects of intracerebroventricular (i.c.v.) and intrathecal (i.t.) administration of morphine or ketocyclazocine in tests of antinociception in rats aged 3 to 14 days of age. Analgesia tests were conducted using both thermal and mechanical (pressure) noxious stimuli applied to the forepaw, hindpaw or tail. In the 3-day-old morphine-injected i.c.v. produced analgesia in the forepaws when either the mechanical or thermal noxious stimulus was used. There was no effect when the hindpaw or tail was tested. At 10 days of age, when the mechanical stimulus was used, morphine was analgesic in tests on all three appendages but was only effective in the forepaw when the thermal stimulus was used. Morphine was fully effective in all tests with both stimuli at 14 days of age. Ketocyclazocine had no consistent effect when given i.c.v. When injected i.t., morphine produced analgesia in the forepaws in the thermal test at 4 days of age and in all appendages by 10 days. When the mechanical test was used, morphine was effective in all appendages at all ages tested. Ketocyclazocine was analgesic at all appendages for the mechanical stimulus at all ages but was only transiently effective in the thermal test. The results demonstrate differential development of analgesia mediated at different levels of the neural axis and are consistent with the development of descending inhibitory that may mediate analgesia induced by i.c.v. injections of morphine. Neural mechanisms that are involved in the analgesic effects of these drugs against the two types of stimuli are also developmentally distinct.

Analgesics↗
PubMedDate not supplied

Effect of substance P on thyrotropin secretion from the pituitary gland in the rat.

The role of substance P (SP) on thyrotropin (TSH) secretion was investigated in ovariectomized (OVX) female, estrogen-primed OVX, and normal male rats. Third ventricular administration of SP induced a significant increase in plasma TSH levels when compared to control animals in E-primed OVX rats (p less than 0.001). The plasma TSH levels increased in a dose-related manner and reached maximum levels at 10 min after injection. In contrast, intraventricularly injected SP failed to alter plasma TSH levels in both OVX rats and normal male rats. Intravenous administration of SP dramatically stimulated TSH release in E-primed OVX rats (p less than 0.001), whereas SP had no effect on the release of TSH when injected in OVX rats and normal male rats. To investigate any direct action of SP on TSH release from the anterior pituitary gland, synthetic SP was incubated with dispersed anterior pituitary cells harvested from E-primed OVX rats and normal male rats. SP, in the dose range between 10(-8) M and 10(-6) M, failed to alter the release of TSH into the culture medium in vitro. These findings indicate that SP has a stimulatory role in the control of TSH release by an action on the hypothalamus but only in estrogen-primed rats.

Animals↗
PubMed1988

Hypoxanthine transport and metabolism in the central nervous system.

The mechanisms by which hypoxanthine, the principal purine in plasma and CSF, enters and leaves rabbit brain, choroid plexus, and CSF were investigated in the isolated choroid plexus in vitro and by injecting [14C]hypoxanthine intraventricularly and [3H]hypoxanthine intravenously. The isolated choroid plexus accumulated and extensively metabolized [14C]hypoxanthine; however, 14C was readily released from choroid plexus principally as [14C]-hypoxanthine. After infusion of [3H]hypoxanthine intravenously, [3H]hypoxanthine entered CSF and brain slowly and was converted in brain to nucleotides. Fewer than 5% of the acid-soluble purine nucleotides in brain entered rabbit brain from plasma hypoxanthine (and inosine) per 24 h. After intraventricular injection of [14C]hypoxanthine, the [14C]hypoxanthine was cleared from the CSF into the blood or accumulated by brain and largely converted into 14C-nucleotides. Little [14C]xanthine and no [14C]uric acid or allantoin were formed. These studies show that brain, unlike most other tissues, rapidly recycles hypoxanthine and converts it into purine nucleotides, and not unsalvageable purines.

Animals↗
PubMed1977

Respiratory and circulatory effects of saxitoxin in the cerebrospinal fluid.

1 In cats anaesthetized with pentobarbitone, saxitoxin and, on a few occasions, tetrodotoxin were injected into a lateral cerebral ventricle or into the subarachnoid space of the lower brain stem. Observations were made on frequency and tidal volume of breathing, on CO(2) responsiveness and on electrical responsiveness of the respiratory centre. Effects on the blood pressure were observed simultaneously.2 A single large dose of toxin, e.g., 250 ng, produced within minutes apneustic breathing and a rise in blood pressure which were converted rapidly to respiratory failure and hypotension. In contrast, repeated small doses, e.g., 25 ng, yielded only progressive slowing of the respiration together with circulatory hypotension. Bulbar depression was produced as effectively by subarachnoid injection as by intraventricular injection of the toxins. Onset of action was detectable within seconds.3 Slowing of the respiration occurred independently of change in tidal volume and whether or not the vagus nerves were cut. The reduction in breathing frequency is attributed to direct toxin-induced depression of the central respiratory oscillator.4 Steady-state measurements of tidal volume at controlled levels of alveolar CO(2) pressure in intermediate stages of respiratory depression showed that the toxins produced an increase in CO(2) stimulation threshold as well as a reduction in gain of CO(2) responsiveness, whether or not the vagus nerves were cut. Carotid arterial chemoreceptor reactivity to O(2) was demonstrable when central sensitivity to CO(2) was depressed. These effects are attributed to a direct influence of the toxins upon the brainstem CO(2)-tidal volume controller.5 Responsiveness of the medullary inspiratory centre to electrical stimulation persisted after the failure of spontaneous breathing was caused by the toxins. Conversely, restitution of electrical responsiveness preceded the reappearance of spontaneous respiratory activity in the recovery phase of toxic depression. Circulatory effects paralleled the changes in respiratory behaviour.6 On the basis of the relatively prompt and discrete alterations in the central respiratory and circulatory control mechanisms produced by saxitoxin and tetrodotoxin placed in the cerebrospinal fluid, it is concluded that the agents rapidly penetrated to deep target loci in the lower brain stem.

Animals↗
PubMed1990

Physiologically significant inhibitory hypothalamic action of substance P on prolactin release in the male rat.

To evaluate a possible physiological role of endogenous substance P (SP) in the control of prolactin (PRL) release, conscious adult male rats were given injections of a specific antiserum against SP (anti-SP) into the third ventricle (3 microliters) or intravenously (0.5 ml). Third-ventricular injection of anti-SP induced a significant increase in plasma PRL levels when compared to values in control animals injected with normal rabbit serum (p less than 0.02). Plasma PRL concentrations were significantly elevated within 2 h after injection of antiserum and remained elevated for the 4-hour duration of the experiment. In contrast, injections of large doses of anti-SP intravenously had no effect on plasma PRL levels. In order to confirm the effect of SP itself, synthetic SP was injected intravenously and intraventricularly. Opposite effects of SP on PRL release were observed after intravenous and intraventricular injections of low or high doses of the peptide. A lower dose of SP (10 ng, 7.42 pmol) injected into the third ventricle suppressed the release of PRL (p less than 0.01), whereas higher doses (1 microgram, 0.74 nmol, or 5 micrograms, 3.71 nmol) had a stimulatory effect on PRL release (p less than 0.01). Similarly, a low dose of SP (0.1 microgram, 0.07 nmol) injected intravenously lowered plasma PRL (p less than 0.05). Large doses of intravenous SP (50 micrograms, 37.1 nmol) dramatically stimulated PRL release (p less than 0.001). To evaluate a possible direct action of SP on PRL release from the anterior pituitary, the peptide was incubated with dispersed anterior pituitary cells for 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Uridine transport and metabolism in the central nervous system.

The mechanisms by which uridine enters and leaves brain, choroid plexus, and cerebrospinal fluid (CSF) were investigated in the isolated choroid plexus in vitro and by injecting [3H]uridine intravenously and intraventricularly. Consistent with its postulated role in transporting uridine from blood into CSF, the isolated rabbit choroid plexus concentrated uridine with 10 microM uridine in the medium. [3H]Uridine, with and without unlabeled uridine, was infused at a constant rate into conscious adult rabbits. At 180 min, [3H]uridine entered CSF, choroid plexus, and brain more rapidly than mannitol. In brain, approximately 60-80% of the nonvolatile radioactivity was [3H]uridine phosphates. The addition of 2.1 mmol/kg of unlabeled uridine to the infusion syringe decreased the relative entry of [3H]uridine into brain by approximately 75% due mainly to the decreased formation of [3H]uridine phosphates and increased formation of [3H]uracil. Two hours after the intraventricular injection of [3H]uridine, [3H]uridine was cleared from CSF more rapidly than mannitol, in part to brain, where approximately 75% of the [3H]uridine was converted to [3H]uridine phosphates. The intraventricular injection of 42 mumol unlabeled uridine with the [3H]uridine decreased the phosphorylation of [3H]uridine in brain significantly and also decreased the clearance of [3H]uridine from the CSF. From blood, uridine enters CSF and the extracellular space of brain. Uridine then can enter brain cells, be phosphorylated to uridine phosphates, and subsequently incorporated into RNA or be catabolized to uracil.

Animals↗
PubMed1997

[Effects of intraventricular and epicardial application of adenosine on electrical activity of medullary PGL neurons].

The effects of intraventricular injection and epicardial application of adenosine on spontaneous electrical activity of nucleus paragigantocellularis lateralis (PGL) neurons in rostral ventrolateral medulla (RVLM) were examined in 35 anesthetized rats with sinoaortic denervation and vagotomy. The results obtained were as follows: (1) The spontaneous discharge of 121 PGL neurons (mean discharge rate: 22.5 +/- 1.9 spikes/s) were recorded in 35 rats. (2) In response to intraventricular injection of adenosine (0.5 mumol/kg), mean arterial pressure (MAP) was initially increased by 1.7 +/- 0.2 kPa(P < 0.001) and subsequently decreased by 4.6 +/- 0.5 kPa(P < 0.001), while the heart rate (HR) was decreased by 126.5 +/- 12.3 bpm (P < 0.001). Of 35 PGL spontaneous discharge units responsive to intraventricular injection of adenosine, 30 showed an average increase from 21.9 +/- 2.6 to 29.2 +/- 3.4 spikes/s (P < 0.001), 3 with no change, while 2 with a decrease. (3) Following epicardial application of 20 mmol/L adenosine, the BP and HR were not significantly changed, while the spontaneous discharge of 22 PGL neurons were increased from 18.8 +/- 1.9 to 26.9 +/- 2.8 spikes/s (P < 0.001), and that of 3 neurons was not changed. (4) The excitatory response of PGL neurons to intraventricular injection or epicardial application of adenosine was completely inhibited by pretreatment with selective adenosine A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX, 500 micrograms/kg). (5) Following epicardial application of phenol or bilateral stellate ganglionectomy, adenosine failed to affect the activity of PGL neurons. The results obtained indicate that adenosine may stimulate cardiac sympathetic afferents through adenosine A1-receptor, thereby resulting in the activation of PGL neurons.

Action Potentials↗
PubMed1984

Inhibition of brain protein synthesis suppresses the release of prostaglandin E2 in febrile rabbits.

In rabbits the third cerebral ventricle was perfused using a push-pull cannula. Prostaglandin E2 concentration in the perfusate was measured by radioimmunoassay. Prostaglandin concentration rose during fever induced by an intraventricular injection of endogenous pyrogen. Both fever and the increased prostaglandin concentration were suppressed by the intraventricular injection of 100 micrograms of the protein synthesis inhibitor, anisomycin. A possible interpretation of the findings is that anisomycin inhibits the formation of phospholipase A2. If this is true, the implication is that phospholipase A2 has a rapid turnover in brain.

Animals↗
PubMed1998

Absence of antinociceptive tolerance to improgan, a cimetidine analog, in rats.

Improgan, an analog of the histamine receptor antagonist cimetidine, produces highly effective analgesia following intraventricular injection. The present study examined changes in the antinociceptive effects of improgan following once daily intraventricular injections. Improgan (100-150 microg) produced near maximal antinociception 10 and 30 min after daily administration on all 4 test days, whereas comparable morphine treatments (50 microg) induced considerable tolerance. Thus, improgan produced highly effective analgesia without the development of tolerance.

Analgesics, Non-Narcotic↗