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PubMed1989

Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation.

The clinical efficacy of intravenous amiodarone in terminating sustained ventricular tachycardia and in preventing recurrences of ventricular tachycardia and ventricular fibrillation was evaluated in 26 patients. All of them presented with organic heart disease accompanied by depressed left ventricular function. Intravenous amiodarone terminated spontaneous ventricular tachycardia in eight of 19 patients. Fifteen of the 26 patients had had at least one episode of ventricular tachycardia or ventricular fibrillation each day in the period immediately before the intravenous administration of amiodarone. Amiodarone controlled ventricular tachycardia or ventricular fibrillation in nine of these 15 patients; in three further cases it was successful when supplemented by additional administration of a previously ineffective antiarrhythmic drug and ventricular pacing. Two patients died despite these measures. In one, the amiodarone infusion had to be stopped because of an arrhythmogenic effect. Sustained deterioration of haemodynamic function or of pre-existing intraventricular conduction disturbances was never seen. Intravenous amiodarone was effective in terminating sustained ventricular tachycardia and in preventing frequent episodes of ventricular arrhythmia that were refractory to other antiarrhythmic drugs.

Amiodarone↗

PubMed1988

Behavioural and electrocortical changes induced by paraquat after injection in specific areas of the brain of the rat.

The behavioural and electrocortical effects of paraquat were studied after its administration into the substantia nigra, pars compacta, an area where dopamine-(DA) containing cell bodies are present, into the caudate nucleus, where DA-containing nerve endings of the DA nigro-striatal system project, into the locus coeruleus, an area containing noradrenaline cell-bodies and into the n. raphe dorsalis or into the n. raphe medianus, two nuclei containing serotonin (5-HT) cell bodies. The intraventricular administration of paraquat (10 and 50 micrograms) produced an intense pattern of behavioural stimulation and an increase in locomotor activity, circling and the wet-dog syndrome. This symptomatology was accompanied by desynchronization of the electrocorticogram (ECoG) and the appearance of bilateral high voltage epileptogenic spikes, culminating in clonic convulsions. The infusion of paraquat into the s. nigra produced contralateral head and neck deviation, behavioural and motor stimulation, these effects being observed also with smaller doses (1 and 5 micrograms), than those used intraventricularly. The ECoG activity was desynchronized and characterized by high voltage spike discharges. A similar behavioural, postural and ECoG pattern was also observed after infusion of paraquat into the caudate nucleus (10, 25 and 50 micrograms). In addition, paraquat, infused into the locus coeruleus or into the raphe nuclei (5 and 10 micrograms), produced circling, escape responses, jumping and clonic convulsions accompanied by ECoG desynchronization and epileptic phenomena. In conclusion, the present experiments showed that paraquat was able to produce central neurotoxicological effects which did not seem to be specific, at least for the doses used, for the DA nigro-striatal system.

Animals↗

PubMed1997

Possible roles of prostaglandins in the anteroventral third ventricular region in the hyperosmolality-evoked vasopressin secretion of conscious rats.

This study explored the roles of prostaglandins in the anteroventral third ventricular region, a cerebral osmoreceptor site, in the osmoregulation mechanism of vasopressin release. We injected (1 microliter) prostaglandin E2 (12.8 nmol) or meclofenamate (78.3 nmol), an inhibitor of prostaglandin biosynthesis, into the brain region or the lateral cerebral ventricle of conscious rats, examining their effects on plasma vasopressin and its controlling factors in the presence or absence of an osmotic stimulus. The injection of prostaglandin E2 into the anteroventral third ventricular region augmented plasma vasopressin and arterial pressure after 5 min and 15 min, without influencing plasma osmolality, sodium, potassium, or chloride. In contrast, intraventricular injection of prostaglandin E2 did not cause any significant effect on those variables. The i.v. infusion (0.1 ml.kg-1.min-1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin after 15 min and 30 min; this was accompanied by increased plasma osmolality, sodium, and chloride, and by unaltered or elevated arterial pressure. Meclofenamate given into the anteroventral third ventricular region 30 min before starting the hypertonic saline infusion abolished the osmotic vasopressin response without significantly changing the responses of the other variables. Histological analysis showed that the injection sites of meclofenamate in these rats were close to those of prostaglandin E2 in the anteroventral third ventricular region and included the organum vasculosum of the lamina terminalis and the surrounding area, the medial preoptic area, and periventricular and median preoptic nuclei. When injection cannulae for meclofenamate deviated from those areas incidentally or when the drug was expressly administered into the cerebral ventricle, the osmotic vasopressin response was not inhibited. Plasma vasopressin and the other variables observed during the i.v. infusion of isotonic saline (0.15 mol/l) were not affected significantly by meclofenamate administration into the anteroventral third ventricular region or the cerebral ventricle. On the basis of these results, we concluded that prostaglandins synthesized in and/or near the anteroventral third ventricular region might contribute to the facilitation of vasopressin release in the hyperosmotic state.

Animals↗

PubMed1995

Medical and surgical treatment in neurocysticercosis a magnetic resonance study of 161 cases.

In a prospective non-controlled study we have treated 161 consecutive cases of Active Neurocysticercosis (NCC) diagnosed by Magnetic Resonance (MR). Active NCC was classified in: (1) brain parenchymal cysts (85 cases); (2) ventricular cysts (24 cases); (3) subarachnoid cysts (46 cases); and (4) cysticercus racemose (6 cases). All patients had MR follow up 1 month after treatment. Twenty five patients had MR with gadopentetate dimeglumine (Gd) contrast enhancement. Cine MR was performed in one patient. Medical treatment with albendazole (ABZ) or Praziquantel (PZQ) was applied in 136 cases. Drug efficacy, assessed by disappearance of the lesion on MR, was 92.5% with ABZ and 60% with PZQ. Thirty patients were treated by surgery. Five patients of group I were treated surgically due either to refractory seizures or persistent abnormalities on MR. Ventricular cysts were removed in 20 cases; 4 cases with cysticercus racemose and one with subarachnoid spinal cyst were also treated by surgery. Two patients with 4th ventricle cysts received ABZ and ventricular shunt only. Two cases with intraventricular cysts (lateral ventricles) and two with racemose cysts were successfully treated with ABZ. The Gd infusion showed enhancement in cysts with adjacent inflammatory reaction or edema and in cases with meningeal inflammation. Cine MR was useful in the differential diagnosis with congenital arachnoid cyst. We conclude that (1) MR is sensitive in the diagnosis of active NCC and may be useful in evaluating degenerative changes in the parasite; (2) ABZ is highly effective in the treatment of parenchymal and subarachnoidal NCC; (3) Parenchymal lesions which remain with abnormal appearance on MR (Degenerative cysticerci or gliosis) and refractory seizures should be treated by surgery; (4) Cysticercus racemose without intracranial hypertension may be treated with ABZ; (5) Ventricular cysts are treated by surgical removal, however, ABZ and ventricular peritoneal shunt may also be an alternative approach.

Adolescent↗

PubMed1993

Sequential bilateral bundle branch block during dofetilide, a new class III antiarrhythmic agent, in a patient with atrial fibrillation.

INTRODUCTION: The mechanism of wide QRS complex tachycardias during dofetilide infusion was studied in a patient with atrial fibrillation. METHODS AND RESULTS: Endocardial recordings from the intraventricular conduction system showed that dofetilide caused "classic" aberrant conduction (Ashman phenomenon, typical QRS morphology) at high prematurity ratios (preceding interval = 1.78 x coupling interval--290), thus mimicking ventricular ectopy. In addition, there was frequent sequential bilateral bundle branch block, caused by a significant difference in preceding bundle-to-bundle intervals (mean difference +/- 1 SD: 74 +/- 26 msec). CONCLUSION: The present findings may prove helpful in the clinical assessment of wide QRS complex rhythms after dofetilide and possibly other "pure" Class III antiarrhythmics.

Adult↗

PubMed1981

Beneficial effects of adding propranolol to multidose potassium cardioplegia.

The use of propranolol with multidose potassium cardioplegia was studied in 32 in situ canine hearts subjected to 90 minutes of global ischemia at 15 degrees C and 60 minutes of reperfusion at 37 degrees C. All hearts received potassium (37 mEq/l) every 30 minutes during ischemia. There were four groups of equal size: group 1 received no propranolol, group 2 received low-dose propranolol and group 3 received high-dose propranolol. Group 4 received high-dose propranolol only with the initial potassium infusion. Myocardial CO2 (PmCO2) was monitored by mass spectrometry as an indicator of metabolic activity. An intraventricular balloon was used to measure isovolumic developed pressure, maximal dP/dt and end-diastolic pressure (EDP) before and after ischemia. During ischemia, peak PmCO2 was significantly higher in group 1 (45.6 +/- 2.8 mm Hg) than in groups 2, 3 and 4 (35.2 +/- 2.8 mm Hg, 33.4 +/- 2.8 mm Hg and 30.4 +/0 2.8 mm Hg, respectively) (p less than 0.05). There were no differences between the four groups in systolic ventricular function assessed by developed pressure and dP/dt. Hearts that received high-dose propranolol had significantly lower EDP after 60 minutes of reperfusion (group 3 13.3 +/- 1.5 mm Hg, group 4 10.4 +/0 1.5 mm Hg) compared with group 1 hearts (25.3 +/- 3.8 mm Hg, p less than 0.05). Hearts in groups 3 and 4 exhibited less ischemic injury as assessed by electron microscopy than hearts in groups 1 and 2. These data show that propranolol added to multidose potassium cardioplegia reduced metabolic activity during ischemia and improved ventricular compliance during reperfusion without depressing systolic function. Because left ventricular compliance and morphologic preservation were similar in groups 3 and 4, it appears that a single high dose of propranolol is sufficient and that subsequent doses do not further enhance the beneficial effects.

Animals↗

PubMed1977

Cardiovascular pharmacology of bepridil (1[3 isobutoxy 2 (benzylphenyl) amino] propyl pyrrolidine hydrochloride) a new potential anti-anginal compound.

In dogs intravenous bepridil (2.5 mg/kg) increased coronary sinus blood flow and PVO2. Arterial pressure was briefly lowered, and heart rate was slowed in animals with intact or denervated hearts, or after propranolol administration. Ventricular inotropism was reduced at higher doses. Bepridil (5 mg/kg i.v.) showed a partial antagonist activity on isoprenaline cardiovascular effects (or cardiac sympathetic stimulation effects) i.e. tachycardia, increase in left dP/dt max. and diastolic hypotension. The antitachycardia activity was particularly pronounced. It was found to be non-competitive. It was also found to be non-specific since glucagon, theophylline- and papaverine-induced tachycardia were also reduced. The continuous infusion of high doses of bepridil did not cause any disturbance in atrio-ventricular or intraventricular conduction. In rats, after 50 mg/kg/day p.o., bepridil did not alter myocardial noradrenaline levels.

Angina Pectoris↗

PubMed1981

Effects of acute central and peripheral administration of nicotine on ascending dopamine pathways in the male rat brain. Evidence for nicotine induced increases of dopamine turnover in various telencephalic dopamine nerve terminal systems.

The actions of intraventicular injections and intravenous infusions of nicotine were studied on dopamine stores and turnover in discrete areas of the forebrain of normal male rats. This was done by measuring the decline of the dopamine stores after tyrosine hydroxylase inhibition using alpha-methyl-tyrosine methyl ester (H44/68). The dopamine concentrations in the various telencephalic dopamine nerve terminal systems were measured using the Falck-Hillarp methodology involving quantitative microfluorimetry. The catecholamine concentrations in the anteromedial frontal cortex were measured biochemically using high pressure liquid chromatography combined with electrochemical detection. Intraventricular experiments. The dopamine levels in discrete areas of nuc. caudatus and nuc. accumbens were significantly reduced even with the lowest dose of nicotine (1 microgram/rat). Intraventricular injections of nicotine in a dose of 100 microgram/rat produced significant increases of dopamine turnover in various types of dopamine nerve terminal systems in the nuc. caudatus, nuc. accumbens and tuberculum olfactorium, and following a dose of 10 microgram/rat increases of dopamine turnover were observed in the medial part of the nuc. caudatus. Furthermore, nicotine (100 microgram/rat) significantly increased noradrenaline but not dopamine turnover within the anterofrontal cortex. Intravenous experiments. The dopamine levels were selectively reduced by nicotine (1000 microgram/kg) in the cholecystokinin positive and negative dopamine nerve terminal systems of the nuc. accumbens. On the other hand, dopamine levels in the anteromedial frontal cortex were increased after this dose of nicotine. Intravenous infusions of nicotine (10-1000 microgram/kg) produced dose-related increases of dopamine turnover in the various dopamine nerve terminal systems analysed in the telencephalon. These effects became significant with a dose of 1000 microgram/kg/h. The dopamine terminals in the nuc. caudatus showed a higher sensitivity to intravenous infusions of nicotine, being affected by 10-100 microgram/kg of nicotine. These findings suggest that relatively low dose of nicotine via an activation of central nicotine-like cholinergic receptors can reduce dopamine concentration and increase dopamine turnover in discrete limbic and striatal areas. These actions may in part represent the neurochemical basis for the rewarding actions of nicotine and for nicotine dependence in man.

Afferent Pathways↗

PubMed1992

Effects of intracerebral administration of neuropeptide-Y on secretion of luteinizing hormone in ovariectomized sheep.

Ovariectomized ewes received unilateral infusions of 20 micrograms neuropeptide-Y (NPY) at a total of 13 intracerebral sites. Episodic secretion of luteinizing hormone (LH) was transiently suppressed on more than one occasion by daily infusions at a total of five intracerebral sites. Four of the effective sites were located within the third ventricle (two sites) and the rostral and ventral part of a lateral ventricle (two sites). The precise neural site of action of exogenous NPY cannot be determined from intraventricular administration, but it indicates a neural rather than pituitary site of NPY action to inhibit LH-releasing hormone (LHRH) in sheep. The only tissue infusion site (ventromedial nucleus) at which NPY also suppressed LH/LHRH also supports a neural action on LHRH, but this single result is insufficient to establish the neural area at which NPY acted. It is known from other work that the production of endogenous NPY in neural tissue of underfed animals is increased, and if endogenous NPY exerts effects on LH/LHRH similar to the suppression presently observed following exogenous NPY this neuropeptide might serve as one neuroendocrine factor that suppresses reproduction in underfed animals.

Animals↗

PubMed1993

Calcium-mediated metabolic stimulation of neuroendocrine structures by intraventricular endothelin-1 in conscious rats.

We examined the hypothesis that the vascular- and brain-derived peptide, endothelin-1 (ET), would affect cerebral neuroendocrine structures when administered via the peripheral circulation or via a lateral cerebral ventricle (i.c.v.). ET was infused intravenously (14 nmol/min) or injected i.c.v. (9 pmol) in conscious rats in which local cerebral glucose metabolism was assessed by the quantitative autoradiographic [14C]deoxyglucose technique. Whereas intravenously infused ET was previously demonstrated to selectively stimulate metabolic activity in the pituitary intermediate and anterior lobes of conscious rats, it was without effect in 20 individual structures or subnuclei involved in neuroendocrine functions, including several circumventricular organs. Intraventricular ET, however, caused hypermetabolic responses in 9 neuroendocrine structures, including the pineal gland, subfornical organ, median eminence, the hypothalamic paraventricular and supraoptic nuclei, and other hypothalamic and preoptic structures. The metabolic stimulation resulting from central ET was abolished or attenuated regionally by i.c.v. pretreatment with the calcium L-channel inhibitor, nimodipine. The findings indicate that i.c.v. ET elicits a calcium-mediated hypermetabolic effect on several neuroendocrine structures in the forebrain involved in the regulation of fluid homeostasis, the cardiovascular system, and body temperature.

Animals↗

PubMed2006

Hyperglycemia is a risk factor for early death and morbidity in extremely low birth-weight infants.

OBJECTIVES: The objectives of this study were to determine the prevalence of hyperglycemia in extremely low birth-weight infants and to determine whether hyperglycemia increases the risk of early adverse outcomes (death or intraventricular hemorrhage of grade 3 or 4) and/or affects the length of hospital stay among survivors without intraventricular hemorrhage. METHODS: The charts of all extremely low birth-weight infants (n = 93) admitted to Texas Children's Hospital (Houston, TX) during 2001 were reviewed. The highest daily blood glucose concentrations, highest dopamine infusion rates, highest daily percentage of inspired oxygen, and mean blood sodium concentrations were averaged over the first week of life or before death or occurrence of grade 3 or 4 intraventricular hemorrhage. Among survivors without severe intraventricular hemorrhage, the time ratio for blood glucose concentrations of >150 mg/dL was calculated. RESULTS: More than 50% of the infants had persistent blood glucose concentrations of >150 mg/dL during their first week of life. Early adverse outcomes were associated with the average highest daily blood glucose concentration through interaction with the Clinical Risk Index for Babies score and with the average highest daily percentage of inspired oxygen. The length of hospital stay was associated with the time ratio for blood glucose concentrations of >150 mg/dL through interaction with birth weight and the average highest daily percentage of inspired oxygen. CONCLUSION: These data confirm the high prevalence of hyperglycemia among parenterally fed, extremely low birth-weight infants and show that high blood glucose concentrations increase the risk of early death and grade 3 or 4 intraventricular hemorrhage and the length of hospital stay among survivors without intraventricular hemorrhage, which suggests that prevention and treatment of hyperglycemia may improve the outcomes of extremely low birth-weight infants.

Age Factors↗

PubMed2006

Preventing vincristine administration errors: Does evidence support minibag infusions?

Although vincristine sulfate is indicated for IV use only, it has been inadvertently administered intrathecally. Accidental vincristine administration via the spinal route (intrathecally via a lumbar puncture or intraventricularly via an Ommaya reservoir) causes rapid sensory and motor dysfunction, usually followed by encephalopathy, coma, and death (Schulmeister, 2004). Autopsy findings include grossly edematous and congested brain and spinal cord tissue, with axonal degeneration and myelin loss of the spinal nerves (Kwack et al., 1999; Williams et al., 1983).

Adult↗

PubMed1985

Indolealkylamines and prolactin secretion. A structure-activity study in the central nervous system of the rat.

The present study was performed to examine the central effects of the indolealkylamine hallucinogens, 5-methoxy-N,N-dimethyltryptamine (MDMT), bufotenin and N, N-dimethyltryptamine (DMT), infused intracerebroventricularly (i.c.v.) into the lateral ventricle. They were found to have a stimulatory effect upon the secretion of prolactin. Their order of potency was compared. From a structure-activity point of view, MDMT is the most potent, followed by bufotenin, and then by DMT. Bufotenin, which does not readily cross the blood-brain barrier, caused a prolonged effect on the elevation of prolactin, with a suggestion of a biphasic effect at the maximum dose (0.02 M). N,N-dimethyltryptamine showed a clear dose-response relationship in the stimulation of the release of prolactin. The present results confirm those of previous investigators, who have demonstrated that these drugs cause the release of prolactin, with a possible biphasic effect. The present results suggest that, the response which was obtained was centrally mediated, and probably did not involve stimulation of peripheral receptors and the time course of action of indoles is different when infused centrally, compared to their time course when infused peripherally.

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↗

PubMed1971

Antinociceptive activity of morphine after injection of biogenic amines in the cerebral ventricles of the conscious rat.

1. A simple cannula and a cannula guide for making injections into the cerebral ventricles of conscious rats are described.2. Intraventricular injections of 5-hydroxytryptamine (5-HT) or of noradrenaline (NA) were without effect on the nociceptive threshold of rats.3. Intraventricular injection of 5-HT potentiated the antinociceptive effect of morphine. Reserpine pretreatment antagonized the antinociceptive effect of morphine; this effect was reversed by intraventricular injection of 5-HT.4. Intraventricular injection of NA attenuated the antinociceptive action of morphine but was without effect on the inhibition by reserpine of the antinociceptive effect of morphine.5. Subcutaneous injection or slow intravenous infusion of either 5-HT or NA (up to 300 mug/rat) were without significant effect on the antinociceptive effects of morphine.6. Intraperitoneal administration of dopa increased the nociceptive threshold above normal, but reduced the antinociceptive effect of morphine. Intraventricular injection of either dopa or dopamine had no antinociceptive effect but inhibited that of morphine.7. It is suggested that the antinociceptive effect of morphine may depend on the balance between the concentrations of 5-HT and NA in the brain.

Animals↗

PubMed1987

Cerebroventricular infusion of cholecystokinin (CCK-8) restores REM sleep in parachlorophenylalanine (PCPA)-pretreated cats.

Recently, some studies have shown that cholecystokinin (CCK-8) administered either intraventricularly or intraperitoneally has no effect on sleep. However, since in such studies CCK-8 was given at times when sleep predominates, in this study the effects of CCK-8 on sleep were determined in parachlorophenylalanine (PCPA) (400 mg/kg)-pretreated insomniac cats. Twenty-four hours after the second injection of PCPA one group of cats received 100 ng/100 microliter of CCK-8 and another group only 100 microliter of saline. A third group was studied only under the effects of PCPA. The results showed that CCK-8 was capable of restoring sleep in the otherwise insomniac cats and that this effect was restricted to REM sleep only. The observed REM sleep-promoting action of CCK-8 supports the notion that this polypeptide may be involved in REM sleep regulation.

Animals↗

PubMed1998

Neurotoxic potential of gadodiamide after injection into the lateral cerebral ventricle of rats.

PURPOSE: Results of a previous report showed that, if administered by intraventricular injection to access tissue normally protected by the blood-brain barrier, gadopentetate dimeglumine produced acute excitation, persistent ataxia, and widespread brain lesions in rats at 5-micromol/g brain but not at 3.8-micromol/g brain. The present study using gadodiamide was undertaken to see whether the effects were agent-specific. METHODS: Rats, surgically prepared with a lateral ventricular cannula, were administered a slow injection at 2 microL/min of gadodiamide into the lateral ventricle, and behavioral and neuropathologic changes were noted. RESULTS: Both gadodiamide and gadopentetate dimeglumine produced focal and generalized myoclonus over several hours. Gadodiamide did not produce the medium-term tremor or persistent ataxia seen after treatment with gadopentetate dimeglumine. Neuropathologic changes developed over 1 to 3 days and took three distinct forms: vacuolated thalamic lesions closely resembling those produced by gadopentetate dimeglumine; small but similar vacuolated symmetrical caudate lesions not produced by gadopentetate dimeglumine; and severe swelling and astrocytic hypertrophy and hyperplasia in the cerebellar vermis, again not produced by gadopentetate dimeglumine. Unlike gadopentetate dimeglumine, gadodiamide produced no spinal cord lesions. The cerebellar changes were seen at 1.25-micromol/g brain and above, behavioral changes at 2.5-micromol/g brain and above, and thalamic and caudate lesions at 10-micromol/g brain, the maximal dose used. Markedly reducing the rate of injecting the same volume over 28 hours prevented the acute excitation but did not reduce the severity of the morphologic effects. CONCLUSION: The acute excitatory effects of high intraventricular doses of gadopentetate dimeglumine and gadodiamide are similar and appear to be attributable to local action at the infusion site, but differences exist between the two agents in the character and topography of the distant morphologic changes. The cerebellum was the brain area most sensitive to gadodiamide in this experimental model. It is unlikely that gadodiamide would gain access to the brain at these tissue doses when used intravenously for conventional clinical imaging, but our experimental model suggested that it had some unexpectedly specific neuropathologic potential.

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↗