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PubMed1992

Intraventricular administration of substance P induces unattached Purkinje cell dendritic spines in rats.

Substance P was infused in the lateral ventricles of twenty Lewis rats for twenty days. The animals under the influence of the substance P demonstrated grooming of the head, the body and the forepaws. On the twentieth day the animals were sacrificed and the cerebellar cortex was processed for electron microscopy. The ultrastructural analysis revealed that although the granule cells, the parallel fibers and the systems of the afferent fibers were intact, numerous unattached Purkinje cell dendritic spines were seen embedded in the soma of the astrocytes, demonstrating postsynaptic differentiation. Numerous unattached spines of the secondary and tertiary dendritic branches of the Purkinje cells were also seen in the molecular layer surrounded by astrocytic sheath. Free unattached spines were also seen not surrounded by any astrocytic process, which did not demonstrate any postsynaptic specialization. The development of unattached Purkinje cell dendritic spines, in an otherwise intact cerebellar cortex, following the intraventricular administration of substance P, suggests that it may act as local growth factor, enforcing the preprogrammed-capability of the Purkinje cells in developing new synaptic surfaces.

Animals↗

PubMed1995

Intraventricular insulin and the level of maintained body weight in rats.

To determine whether central insulin administration lowers the level around which body weight is regulated, insulin (6 mU/day) or saline was infused into the third ventricles of four groups of rats. One insulin-infused and one saline-infused group were food-deprived for 3 days and were then returned to an ad lib feeding schedule. The other two groups were maintained on ad lib feeding throughout. Insulin-fused food-deprived rats. In ad lib fed rats, insulin caused a significant reduction of food intake and weight relative to saline-infused controls. When formerly food-deprived rats were returned to ad lib feeding, they gained weight, and this was significantly more pronounced in the saline-infused than the insulin-fused group. The body weights of the two insulin-infused groups converged on a value approximately 9% below the average of the two saline infused groups, with one group increasing its weight and the other decreasing its weight to achieve that weight. These findings suggest that the third-ventricular infusion of insulin does not incapacitate the rats and that they can alter their food intake either upward or downward to attain a new weight. The results are also consistent with the hypothesis that direct administration of insulin into the brain determines the level of weight maintained by the animal.

Animals↗

PubMed1980

CSF bicarbonate regulation in metabolic acidosis: role of HCO3- formation in CNS.

In metabolic acidosis, cerebrospinal fluid bicarbonate content (CSF [HCO3-]) falls in parallel with reductions in CSF CO2 tension (PCO2), and the fall is minimal with isocapnia. Regulation of CSF HCO3- was therefore investigated during 6 h of isocapnic metabolic acidosis in dogs. One group received intraventricular injections of acetazolamide to inhibit the centrally located carbonic anhydrase, essential in central nervous system (CNS) HCO3- formation, while the control group received intraventricular saline. Plasma [HCO3-] was reduced by 10 meq/l with iv infusion of 0.2 N HCl. CSF [HCO3-] fell in the control group from 22.8 to 17.7 meq/l at 6 h, whereas in the acetazolamide group it fell from 22.9 to 13.0 meq/l. Brain ammonia content was 1,286 +/- 153 microgram/100 g in the controls and 666.2 +/- 103 microgram/100 g in the acetazolamide-treated group at 6 h. Therefore, some reduction in CSF [HCO3-] occurred during 6 h of isocapnic metabolic acidosis along the chemical concentration gradient between CSF and blood, but further falls, in CSF [HCO3-] were minimized by de novo, carbonic anhydrase-dependent HCO3- formation within the CNS. Some of H+ formed were buffered by the increase in brain ammonia. These central mechanisms contribute to local CNS H+ homeostasis in metabolic acidosis.

Acetazolamide↗

PubMed1980

Depletion of central catecholamines alters amphetamine- and fenfluramine-induced taste aversions in the rat.

Conditioned taste aversions induced by pairing the consumption of saccharin with an amphetamine injection are attenuated in rats with depletion of central catecholamines caused by intraventricular administration of 6-hydroxydopamine (6-OHDA). The hypothesis that dopamine (DA) depletion is responsible for this effect was tested. The reduction in conditioning caused by intraventricular 6-OHDA could not be duplicated either with injections of 6-OHDA into the substantia nigra (Experiment 1) or with intraventricular 6-OHDA injections in animals pretreated with desmethylimipramine (Experiment 2). Both treatments, however, produced large depletions of telencephalic DA. 6-Hydroxydopa infusions caused a preferential loss of telencephalic norepinephrine (NE) but also failed to alter taste aversion learning. It is concluded that the effect of intraventricular 6-OHDA on amphetamine-induced aversions was the result of depletion of both NE and DA. In a third experiment the generality of the effect was examined by pairing saccharin consumption with injections of the amphetamine congener fenfluramine. Depletion of both NE and DA failed to alter fenfluramine-induced aversions. Infusion of 6-OHDA into the substantia nigra, however, retarded the extinction of such an aversion. Evidence is discussed for a peripheral site of action for fenfluramine in the conditioned aversion paradigm.

Animals↗

PubMed1972

Effects of catecholamines and adenosine derivatives given into the brain of fowls.

1. Adult fowls (Gallus domesticus) with cannulae chronically implanted into the IIIrd cerebral ventricle and various other sites of the brain received microinfusions or injections of catecholamines, adenosine, 3',5'-cyclic AMP or its dibutyryl derivative. The effects of these substances on behaviour, electrocortical activity and body temperature were studied.2. Behavioural and electrocortical sleep with fall in body temperature were obtained with intraventricular noradrenaline, alpha-methylnoradrenaline and isoprenaline; dopamine was ineffective. The doses required to elicit sleep were smaller than those affecting body temperature. Following mebanazine, the effects of noradrenaline were prolonged and doses of dopamine, previously ineffective, lowered body temperature and induced behavioural and electrocortical sleep.3. Noradrenaline, alpha-methylnoradrenaline, isoprenaline and dopamine infused into the hypothalamus induced sleep and lowered body temperature. Effective doses of noradrenaline, alpha-methylnoradrenaline and isoprenaline infused into the hypothalamus were one-twentieth to one-fifth those for intraventricular injection. Tachypnoea developed with isoprenaline and dopamine. Additionally with dopamine, there was deviation of the head to the contralateral side, together with repetitive jerking movements of the head. These effects were prolonged and intensified by mebanazine, whereas the involuntary movements with dopamine were greatly reduced by haloperidol.4. Involuntary movements, but without sleep, were induced by infusing dopamine into the paleostriatum augmentatum; noradrenaline infused into this site was ineffective.5. In three of five fowls pretreated with aminophylline, 3',5'-cyclic AMP infused into the hypothalamus induced behavioural and electrocortical sleep; without aminophylline pretreatment, 3',5'-cyclic AMP was ineffective. Adenosine infused into the hypothalamus, following pretreatment of fowls with aminophylline, consistently induced behavioural and electrocortical sleep. Dibutyryl cyclic AMP infused into the hypothalamus of intact fowls elicited behavioural arousal, followed by bursts of electrocortical spikes (6 Hz) over both cerebral hemispheres, spikes subsequently becoming regular at 1 Hz. Clonic limb and body movements occasionally accompanied the bursts of spike activity, infrequently developing into convulsions. In fowl encéphale isolé preparations, in which dibutyryl cyclic AMP was infused into the hypothalamus, spike activity was confined to the ipsilateral hemisphere.

Adenosine↗

PubMed1983

Human growth hormone and somatomedin C suppress the spontaneous release of growth hormone in unanesthetized rats.

To investigate the feedback control of GH secretion, we examined the effects of human GH (hGH) and somatomedin C (SmC) on spontaneous GH secretory surges in unanesthetized, freely moving rats. Under pentobarbital anesthesia a right atrial catheter and an intracerebroventricular cannula were placed 7-10 days before the experimentation. For iv studies, hGH (0.3 U/ml.h) was infused for 6 h after an iv loading dose (0.3 U) at the beginning of the experiments. For intraventricular injections, hGH (0.1 U/10 microliter) or SmC (500 ng/10 microliter) were injected into the lateral ventricle 2 h before the experiments. The equivalent dose of crystalline BSA diluted in the same vehicle solutions was administered to the same rat as a control on a separate day. Venous blood samples were collected every 20 min for 6 h. Intravenous and intraventricular administration of crystalline BSA did not affect the typical rat GH (rGH) surges which appeared about every 3 h and reached peak values of more than 300 ng/ml. The iv infusion of hGH significantly inhibited the amplitude of rGH surges compared to controls (planimetric areas under the secretory profile 752 +/- 172 vs. 1921 +/- 183, P less than 0.01, n = 6). rGH secretion was similarly inhibited by intraventricular hGH (701 +/- 127 vs. 2208 + 225, P less than 0.01, n = 6) and by intraventricular SmC (537 +/- 70 vs. 1503 +/- 114, P less than 0.01, n = 6). These findings suggest that both GH and SmC are active in the feedback regulation of rGH secretion.

Animals↗

PubMed1988

Myocardial reperfusion injury. Role of myocardial hypoxanthine and xanthine in free radical-mediated reperfusion injury.

The aim of this study was to differentiate myocardial reperfusion injury from that of ischemia. We assessed the role of the myocardial adenosine 5'-triphosphate (ATP) catabolites, hypoxanthine and xanthine, generated during ischemia and the early phase of reperfusion, in reperfusion injury by modulating adenosine transport and metabolism with specific metabolic inhibitors. This was followed by intracoronary infusion of exogenous hypoxanthine and xanthine. Twenty-four dogs instrumented with minor-axis piezoelectric crystals and intraventricular pressure transducers were subjected to 30 minutes of normothermic global myocardial ischemia and 60 minutes of reperfusion. In Group 1 (n = 7), normal saline was infused into the cardiopulmonary bypass reservior before ischemia and before reperfusion. Saline solution containing 25 microM p-nitrobenzylthioinosine (NBMPR) and 100 microM erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) was infused in Group 2 (n = 10) dogs. Group 3 (n = 7) dogs were treated exactly like those in Group 2 except, at the end of the ischemic period and immediately before releasing the cross-clamp, a solution of EHNA-NBMPR containing 100 microM hypoxanthine and 100 microM xanthine was infused into the aortic root. Left ventricular performance and myocardial adenine nucleotide pool intermediates were determined before and after ischemia. ATP was depleted by about 50% (p less than 0.05 vs. preischemia) in all groups after 30 minutes of ischemia. Inosine was the major ATP catabolite (9.29 +/- 1.2 nmol/mg protein) in Group 1, while adenosine (9.91 +/- 0.7 nmol/mg protein) was the major metabolite in EHNA-NBMPR-treated dogs (Groups 2 and 3). Hypoxanthine levels were fivefold more in Group 1 compared with Groups 2 and 3 (p less than 0.05). Left ventricular performance in Group 1 decreased from 76.8 +/- 7.6 to 42.9 +/- 9.8 and 52.3 +/- 8.4 dynes/cm2 x 10(3) (p less than 0.05), while myocardial ATP decreased from 30.9 +/- 2.2 to 17.2 +/- 1.0 and 16.5 +/- 1.0 nmol/mg protein during 30 and 60 minutes of reperfusion, respectively (p less than 0.05 vs. preischemia). Ventricular function in Group 2 dogs completely recovered within 30 minutes of reperfusion, and myocardial ATP recovered to the preischemic level at 60 minutes of reperfusion. In Group 3, left ventricular performance was depressed by 39% and 30% during 30 and 60 minutes of reperfusion (p less than 0.05), respectively, and myocardial ATP did not recover during reperfusion despite a significant intramyocardial adenosine accumulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenine↗

PubMed1997

Effects of verapamil in ventricular tachycardias. An experimental and clinical study.

To determine the effect of verapamil in ventricular tachycardias, we performed an experimental and clinical study. Experimental ventricular tachycardias (VT) were produced in dog hearts with minute aconitine crystals introduced into the periphery of a left ventricular area, damaged by intramural injection of 1.0-1.5 ml phenol. The response of these tachycardias to 0.2 mg/kg verapamil was analyzed. Verapamil was infused into the superior vena cava over 15-20 min. Leads II, aVL, intraventricular right and left unipolar records, as well as one of the superior vena cava, were registered under control conditions, in the presence of VT, and after application of verapamil. Recordings were obtained at constant intervals, waiting for the recovery of sinus rhythm (SR) and the posterior reappearance of tachycardia. Experiments were performed for 6 to 8 h under continuous infusion of Hartmann's solution. Throughout these periods, variations in systemic systolic pressure were recorded. From 75 animals submitted to this treatment, 30 (40%) recovered transiently the SR, whereas the drug exerted no antiarrhythmic effect in 19 (25%), and arterial systolic pressure fell importantly in 10 (13%) animals. In two more groups, of 15 dogs each, the VT response to verapamil was compared with the response to lidocaine and flecainide. Endovenous verapamil (5-10 mg) was administered to 10 patients, coursing with VT and having a structurally normal heart, after this arrhythmia was induced by electrical stimulation. The response to verapamil was satisfactory in nine patients (90%), in which VT originated in the septal and apical regions of the left ventricle. Verapamil seems to be effective in experimental and clinical ventricular tachycardias related to calcium-dependent potentials, in which the sustaining mechanism could either be triggered activity or reentry.

Aconitine↗

PubMed2006

Effect of intracerebroventricular continuous infusion of valproic acid versus single i.p. and i.c.v. injections in the amygdala kindling epilepsy model.

Two protocols were tested to assess anticonvulsant efficacy and drug concentrations after intracerebroventricular (i.c.v.) continuous valproic acid (VPA) infusion, as compared with acute injections in the kindling epilepsy model. Protocol 1: amygdala-kindled rats were injected via intraperitoneal (i.p.) and i.c.v. routes with varying doses of VPA and tested for seizure intensity, afterdischarge and seizure duration, ataxia and sedation. Concentrations of VPA were determined by immunofluorescence in the brain, plasma, cerebrospinal fluid (CSF) and liver in matching rats. Protocol 2: amygdala-kindled rats were implanted with osmotic minipumps containing a VPA solution in saline and connected to intraventricular catheters for 7 days. Seizure threshold, latency and duration, afterdischarge duration, ataxia and sedation were recorded daily before, during, and until 5 days after VPA infusion. In matching animals, CSF, brain, plasma and liver VPA concentration was determined. Acute i.c.v. VPA injection suppressed seizures with a remarkable ataxia and sedation. However, continuous i.c.v. infusion controlled generalised and even focal seizures without producing important side effects, high plasma levels or hepatic drug concentrations. In conclusion, continuous i.c.v. VPA infusion may protect against kindled seizures by minimising ataxia and sedation, and achieving suitable intracerebral, yet low plasma or hepatic drug concentrations, thus avoiding potential systemic toxicity.

Amygdala↗

PubMed1970

The effects of salicylate on temperature regulation in the rabbit.

1. A stable pyrexia has been produced in rabbits by intravenous injection of leucocyte pyrogen followed by a continuous infusion.2. Intravenous sodium salicylate, given 4 hr after the start of pyrogen infusion, induced rapid and progressive defervescence. The rate of fall of temperature was dose dependent.3. Intravenous injection of sodium salicylate had no effect on the temperature of afebrile rabbits.4. The intraventricular injection of small doses of sodium salicylate, given 4 hr after the start of a pyrogen infusion, caused a rapid, dose-dependent defervescence, but had no significant effect on the temperature of afebrile rabbits.5. Salicylates exert at least part of their antipyretic activity through an action on the central nervous system.

Animals↗

PubMed1987

Oligodendrogliomas of the lateral ventricle: computed tomography and angiography.

Computed tomographic (CT) and angiographic findings in four cases of oligodendroglioma of the lateral ventricle are reported. CT showed a midline nodular intraventricular mass containing punctate calcifications and cysts. The tumors were slightly to markedly enhanced after the infusion of contrast media. Angiography showed slightly increased vascularity in the mass, and displacement of subependymal veins near the tumor. Oligodendrogliomas of the lateral ventricle are rare but should be included in the differential diagnosis of intraventricular tumors near the foramen of Monro.

Adult↗

PubMed2001

Infusion of brain-derived neurotrophic factor into the lateral ventricle of the adult rat leads to new neurons in the parenchyma of the striatum, septum, thalamus, and hypothalamus.

The findings that brain-derived neurotrophic factor (BDNF) promotes in vitro the survival and/or differentiation of postnatal subventricular zone (SVZ) progenitor cells and increases in vivo the number of the newly generated neurons in the adult rostral migratory stream and olfactory bulb prompted us to investigate whether the infusion of BDNF influences the proliferation and/or differentiation of cells in other regions of the adult forebrain. We examined the distribution and phenotype of newly generated cells in the adult rat forebrain 16 d after intraventricular administration of BDNF in conjunction with the cell proliferation marker bromodeoxyuridine (BrdU) for 12 d. BDNF infusion resulted in numerous BrdU(+) cells, not only in the SVZ lining the infused lateral ventricle, but moreover, in specific parenchymal structures lining the lateral and third ventricles, including the striatum and septum, as well as the thalamus and hypothalamus, in which neurogenesis had never been demonstrated previously during adulthood. In each region, newly generated cells expressed the neuronal marker microtubule-associated protein-2, or neuron-specific tubulin, identified by the antibody TuJ1. The percentage of the newly generated cells expressing TuJ1 ranged from 27 to 42%, suggesting that the adult forebrain has a more profound capacity to produce neurons than recognized previously. The extent of cell proliferation after BDNF infusion was correlated with the level of expression of full-length TrkB, the high-affinity receptor for BDNF, despite the fact that the BrdU(+) cells were not themselves TrkB(+). Collectively, our results demonstrate that the adult brain parenchyma may recruit and/or generate new neurons, which could replace those lost as a result of injury or disease.

Animals↗

PubMed1993

Effects of neuropeptide Y on gonadotropin and prolactin release in normal, castrated or flutamide-treated male rats.

This study was carried out to clarify the central effects of neuropeptide Y (NPY) on gonadotropin and prolactin (PRL) release in the male rat and to evaluate the hypothesis that it may play a role in negative feedback regulation of gonadotropin secretion in the male. NPY (4 micrograms in 2 microliters 0.9% NaCl) or an equal volume of saline was microinjected into the third cerebral ventricle of conscious, unrestrained rats and its effects on plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH) and PRL concentrations, and the gonadotropin response to LH-releasing hormone (LHRH) were measured by radioimmunoassay in noncastrated, castrated (3 days before the experiment) rats or animals treated with flutamide, an androgen receptor blocker (10 mg/kg b.w. per day subcutaneously for 3 days). Blood samples were drawn periodically from a Silastic catheter in the external jugular vein just before and for 120 min after intraventricular injections. At 90 min after injection 25 ng of LHRH were infused intravenously and 3 additional blood samples were withdrawn at 10-min intervals after the injection. Normal male rats responded to NPY with a decrease in plasma LH concentrations at 60 min. Plasma LH was significantly lower at 120 min than values in the saline-injected controls. At that time there was a significant 2-fold augmentation of their response to LHRH. In contrast, NPY elevated plasma FSH significantly versus values in controls at 15 and 30 min after injection, but the FSH release in response to LHRH was not altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Vascular and contractile function and tissue metabolites after prolonged hypothermic ischaemia and reperfusion: comparison of single- versus multi-dose infusions with two cardioplegic solutions in blood-perfused neonatal pig hearts.

The effects of single- and multi-dose cardioplegia on post-ischaemic vascular function and contractile activity were compared in 69 blood-perfused neonatal pig hearts, as were the protective properties of two different cardioplegic solutions. Hearts (n = 6 or 9 per group) from neonatal (3-5 days old) pigs were excised, arrested with a 2 min infusion (at 15 degrees C) of St Thomas' Hospital cardioplegic solution number 1 (STH1) or number 2 (STH2), and then maintained in a state of hypothermic (15 degrees C) ischaemia for 6 or 8 h. Hearts in the multi-dose groups received cardioplegia every hour (2 min at 15 degrees C). At the end of ischaemia all hearts were reperfused (60 +/- 2 mmHg perfusion pressure) for 40 min with blood from a support pig. Systolic and diastolic functions were assessed with an intraventricular balloon, and endothelial and smooth muscle functions by measuring the response to infusions of defined concentrations of acetylcholine (8, 16 and 32 micrograms/min) and glyceryl trinitrate (40, 80 and 160 micrograms/min). Hearts (n = 9) not subjected to ischaemia were perfused for the same duration to act as aerobic controls. At the end of the perfusion period, hearts were frozen and taken for metabolite analysis. After 8 h ischaemia, the recovery of left ventricular developed pressure was greatest in the multi-dose STH1 and single-dose STH2 groups (113 +/- 6 and 117 +/- 6 mmHg, respectively, v 128 +/- 9 mmHg in aerobic controls, at an end-diastolic pressure of between 3 and 9 mmHg; P = N.S.) and the poorest in the single-dose STH1 group (92 +/- 5 mmHg; P < 0.05 v controls). The recovery of diastolic function was greatest in the multi-dose STH2 group and again poorest in the single-dose STH1 group (left ventricular end-diastolic pressure 1 +/- 2 and 30 +/- 10 mmHg, at a ventricular volume of 3.0 ml, v -1 +/- 1 mmHg in aerobic controls). Vascular responses to acetylcholine and glyceryl trinitrate and the myocardial high-energy phosphates content were better preserved in multi-dose groups and with STH2. Inter-group differences were less when the duration of ischaemia was reduced to 6 h. In conclusion, the neonatal pig heart was best preserved with multi-dose cardioplegia and STH2 was more efficacious than STH1. However, not all indices were optimally protected by multi-dose STH2. Thus, the best protection of systolic function was obtained with multidose STH1 and this was followed by single-dose STH2. Diastolic function was best preserved with multi-dose STH2 as were vascular function and high-energy phosphates.

Animals↗

PubMed2003

[Effect of different volumes of fluid resuscitation on hemorrhagic shock with pulmonary edema at high altitude in the unacclimated rat].

OBJECTIVE: To study the effects of different volumes of fluid resuscitation on hemorrhagic shock with pulmonary edema at high altitude in the unacclimated rat. METHODS: One hundred and twenty-six SD rats transported to Lasa, Tibet, 3 760 meters above the sea level, were anesthetized one week later with sodium pentobarbital (30 mg/kg, intraperitoneal). Hemorrhagic shock with pulmonary edema model was induced by hemorrhage (50 mm Hg for 1 hour, 1 mmHg=0.133 kPa) plus intravenous injection of oleic acid (50 microl/kg). Experiments were then conducted in two parts. Sixty-three rats in part I were equally divided into nine groups (n=7): normal control, hemorrhagic shock control, hemorrhagic shock with pulmonary edema (HSPE) without fluid infusion, HSPE plus infusing lactated Ringer's solution (LR) with 0.5-, 1-, 1.5-, 2- or 3- fold volume shed blood, and 1 volume of LR plus mannitol (10 ml/kg). Hemodynamic parameters including mean arterial blood pressure (MAP), left intraventricular systolic pressure (LVSP) and the maximal change rate of intraventricular pressure rise or decline (+/- dp/dt max) were observed at 15, 30, 60 and 120 minutes after infusion, blood gases were measured at 30 and 120 minutes after infusion and the water content of lung and brain was determined at 120 minutes after infusion. In part II, additional 63 rats were used to observe the effect of different volumes of fluid resuscitation on survival time of HSPE rats. RESULTS: 0.5 volume of LR infusion significantly improved MAP, LVSP and +/- dp/dt max, prolonged the survival time of HSPE animals (all P<0.01), while it did not increase the water content of lung and brain and had no marked influence on blood gases. One volume of LR infusion slightly improved hemodynamic parameters, prolonged the survival time and increased the water content of lung. More than 1 volume of LR infusion including 1.5-, 2- and 3- fold volume LR deteriorated the hemodynamic parameters and decreased the survival time of shocked animal, meanwhile they apparently increased the water content of lung. One volume of LR plus mannitol (10 ml/kg) infusion did not improve the hemodynamic parameters and blood gases; also it did not decrease the water content of lung. CONCLUSION: The tolerance to fluid infusion for the unacclimated animal subjected to hemorrhagic shock with pulmonary edema at high altitude is significantly decreased. 0.5-1 volume of LR infusion appears to be beneficial effect on resuscitation at high altitude, while over 1 volume of LR infusion would aggravate pulmonary edema and exacerbate fluid resuscitation effect.

Altitude↗

PubMed1985

Cardiovascular and catecholamine changes after administration of pancuronium in distressed neonates.

Heart rate, blood pressure, transcutaneous gases, and catecholamine changes following intravenous injection of pancuronium were evaluated in seven ill newborn infants (birth weight: 1,280 to 4,500 g; gestational age, 29 to 42 weeks). Each infant was monitored continuously for 30 minutes before and 50 minutes after infusion of the paralyzing agent. There were no significant changes in transcutaneous gases, whereas significant increases in heart rate; systolic, diastolic, and mean blood pressures; and blood norepinephrine and epinephrine levels were found. The increase in heart rate lasted for 30 minutes, and the increase in blood pressure persisted for 50 minutes after administration of the drug. Because of the potential relationship between increased blood pressure and intraventricular hemorrhage and myocardial dysfunction, heart rate and blood pressure must be monitored during infusion of pancuronium in distressed newborns. These data suggest that pancuronium stimulates sympathetic activity in distressed newborns.

Blood Pressure↗

PubMed2001

Delayed infusion of GDNF promotes recovery of motor function in the partial lesion model of Parkinson's disease.

Here we studied the effects of glial cell line-derived neurotrophic factor (GDNF) in a rat model that represents the symptomatic stages of Parkinson's disease. GDNF was infused starting 2 weeks after an intrastriatal 6-hydroxydopamine (6-OHDA) lesion in order to halt the ongoing degeneration of the nigrostriatal dopaminergic neurons. GDNF or vehicle was infused in the striatum or the lateral ventricle via an osmotic minipump over a total 4-week period (2-6 weeks postlesion). Motor function was evaluated by the stepping, paw reaching and drug-induced motor asymmetry tests before the pump infusion was initiated, and was repeated once during (5 weeks postlesion) and twice after the withdrawal of the minipumps (7 and 11 weeks postlesion). We found that within two weeks following the lesion approximately 40% of the nigral TH-positive neurons were lost. In the vehicle infusion groups there was an additional 20% cell loss between 2 and 12 weeks after the lesion. This latter cell loss occurred mainly in the caudal part of the SN whereas the cell loss in the rostral SN was almost complete within the first two weeks. Ventricular GDNF infusion completely blocked the late degenerating neurons in the caudal SN and had long lasting behavioural effects on the stepping test and amphetamine rotation, extending to 6 weeks after withdrawal of the factor. Striatal infusion affected the motor behaviour transiently during the infusion period but the motor performance of these animals returned to baseline upon cessation of the GDNF delivery, and the delayed nigral cell loss was marginally affected. We conclude that intraventricular GDNF can successfully block the already initiated degenerative process in the substantia nigra, and that the effects achieved via the striatal route, when GDNF is given acutely after the lesion, diminish as the fibre terminal degeneration proceeds.

Amphetamine↗

PubMed1993

Intraventricular morphine for intractable pain of advanced cancer.

Among the most difficult pain management problems are those associated with advanced head and neck cancer, and those in which pain is midline, bilateral, or diffuse. The authors report effective control of intractable pain in 52 patients by injection of small doses of morphine via an Ommaya or a Cordis reservoir into the lateral cerebral ventricle. The technique is safe and effective. The reservoir is usually inserted under local analgesia so the method of pain relief is available to patients in whom general anesthesia would be difficult or contraindicated. The doses of morphine required to maintain analgesia remain remarkably low. Tolerance reported by other authors has not been a problem when preoperative assessment of the patient has been thorough. Maximum survival time has been 75 wk and another patient has lived 65 wk. Complications included two colonized reservoirs, one dislodged ventricular catheter, three blocked catheters, and one postoperative meningitis. For patients with diffuse midline or bilateral pain, or intractable pain associated with advanced head and neck cancer, the use of intraventricular morphine should be considered when satisfactory pain relief is not achieved with oral morphine or continuous subcutaneous infusion.

Aged↗