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PubMed1976

Surgical indications in normotensive hydrocephalus. A retrospective analysis of the relations of some diagnostic findings to the results of surgical treatment.

Twenty two of fifty five patients initially suspected of suffering from normotensive hydrocephalus were surgically treated (CSF ventriculoatrial shunt). The results of surgery were related to the findings of the different diagnostic examinations (pneumoencephalography, isotope cisternography, transfer fron CSF to blood of isotope labelled serum albumin, constant infusion manometric test, long lasting intraventricular pressure recording). 1.Pneumoencephalography, intraventricular pressure recording, and, above all, isotope cisternography provided the most reliable data for diagnosis and surgical prognosis. 2. The combined use of pneumoencephalography and isotope cisternography was sufficient for a correct diagnosis and surgical prognosis in about 50% of the patients examined. 3. When the diagnostic information given by the combined results of the two above examinations was not sufficient, intraventricular pressure recording proved to be the most useful examination to supplement it. 4. The relation of the results of the study of transfer of istope labelled serum albumin from CSF to blood and of the constant infusion manometric test to the surgical outcome was uncertain.

Adult↗
PubMed1984

Mechanisms underlying the pressor responses to acute and chronic intraventricular administration of carbachol in the rat.

Infusions of carbachol into the posterior region of the 3rd ventricle of rats for 7 days produced a sustained elevation of blood pressure and heart rate at doses of 0.6 and 1.2 microgram/hr, but only transient rises in blood pressure were obtained at 2.4 microgram/hr. Carbachol, at 0.6 microgram/hr, increased water consumption. At 1.2 microgram/hr, the dipsogenic effect was observed in 50% of the animals and at 2.4 microgram/hr there was no significant change in drinking. Plasma vasopressin levels, measured by radioimmunoassay, were increased by 19-fold 3 min after acute i.c.v. administration of carbachol (0.5 microgram/rat). However, in rats infused with carbachol for 2 or 5 days, the vasopressin levels were not significantly different from controls. The pressor responses to acute and chronic administration of carbachol could be ascribed to the stimulation of periventricular muscarinic receptors because the effects were blocked by atropine, but not by hexamethonium. In carbachol-infused animals, the pressor responsiveness to i.v. norepinephrine and vasopressin were unchanged. From studies using phentolamine, chlorisondamine and a specific vasopressin vasopressor antagonist, it could be inferred that the pressor responses to acute i.c.v. injections of carbachol were due to increased sympathetic activity and vasopressin release. However, the sustained hypertension produced by chronic infusion of carbachol was due primarily to increased sympathetic activity and not to increased plasma levels of vasopressin.

Animals↗
PubMed1985

Role of natriuretic factor in central nervous system (CNS)-induced natriuresis.

The presence of a natriuretic factor in the plasma of rats in which a 350 mM Na (high Na) artificial cerebrospinal fluid (CSF) was infused into the lateral ventricle was tested. Blood was obtained from control rats and rats which received an infusion of high Na CSF intraventricular (IVT) for 15 min. The plasma was incubated for 30 min at room temperature, acidified, placed in a boiling-water bath, and then centrifuged. The plasma supernate was assayed for natriuretic activity in pentobarbital anesthetized bioassay rats. Sodium excretion increased 6.5 +/- 1.1 mueq/kg X min in rats which received an infusion of a control saline solution, 13.3 +/- 3.2 mueq/kg X min in rats which received infusion of control plasma supernates, and 32.1 +/- 8.3 mueq/kg X min in those rats which received plasma supernates from rats infused with high Na CSF IVT. Blood pressure was unchanged in all groups. The increment in sodium excretion elicited by plasma supernate from the high Na IVT group was significantly greater than that elicited by either control saline solution or control plasma extracts. Therefore, it is concluded that a heat-stable and nonpressor natriuretic factor is present in the plasma of rats infused IVT with high Na CSF.

Animals↗
PubMed1986

Norepinephrine inhibition of pulsatile LH release: receptor specificity.

Infusion of norepinephrine (NE) into the third ventricle of ovariectomized (OVX) adult rats inhibits pulsatile luteinizing hormone (LH) secretion. This study examines the effects of pretreatment with specific alpha- and beta-adrenergic blockers on the subsequent NE-induced suppression of LH release. Unanesthetized long-term OVX rats were injected ip or iv with phenoxybenzamine (alpha-adrenergic receptor blocker), propranolol (beta-adrenergic blocker), or an equal volume of saline (as controls). Approximately 1-1.5 h later, the animals were given an intraventricular (ivt) administration of NE. Infusion of acidified saline into the third ventricle of OVX rats failed to affect the pulsatile pattern of LH release characteristic of these animals. After ivt of NE, the control rats showed a significant decrease in mean blood LH level of ca. 30%. Pretreatment of OVX rat with propranolol either ivt or ip failed to affect pulsatile LH release. Subsequent ivt infusion of NE either at 1 h or 15 min after propranolol treatment also caused a 28-30% decrease in the mean LH levels and suppressed pulsatile discharge of LH, an effect that lasted for approximately 45-50 min. In sharp contrast to the saline and propranolol-treated groups, rats pretreated with phenoxybenzamine had sporadic or no LH pulses during the 70-min postphenoxybenzamine period and had significantly lower mean LH levels when compared with control animals (P less than 0.05). Moreover, a drop in mean blood LH levels after NE infusion was not observed in the rats pretreated with phenoxybenzamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.

Acetazolamide↗
PubMed1992

Dynamic intraventricular obstruction during dobutamine stress echocardiography. A new observation.

BACKGROUND: The implications of hypotension occurring during dobutamine stress echocardiography have not been elucidated. We observed in some patients that hyperdynamic left ventricular function developed during dobutamine stress echocardiography and hypothesized that intracavitary obstruction was occurring and might account for hypotension in some patients. METHODS AND RESULTS: Fifty-seven consecutive patients undergoing dobutamine stress echocardiography underwent pulsed-wave and continuous-wave Doppler examination of the left ventricular cavity at rest and at peak dobutamine infusion. The development of an intraventricular gradient with dobutamine stress was defined as a late-peaking left ventricular Doppler velocity profile that exceeded basal velocity by at least 1 m/sec. During dobutamine stress testing, left ventricular outflow velocity or intracavitary velocity increased in all patients. Obstruction occurred in 12 patients (21%, group 1). Group 2 was the remaining 45 patients. Peak velocities in group 1 ranged from 2.0 to 5.0 m/sec (mean, 3.5 m/sec), and the mean increase from velocity at rest was 2.3 m/sec. The mean change in systolic blood pressure was significantly lower in patients in group 1 (-15 versus 4 mm Hg, p = 0.02). When the 18 patients with an ischemic response to stress testing (evidenced by new or worsening wall motion abnormalities) were excluded from analysis, systolic blood pressure response was still significantly different for the two groups (-19 versus 2 mm Hg, p = 0.03). CONCLUSIONS: Dynamic left ventricular obstruction is a new observation; it may develop frequently in patients undergoing dobutamine stress echocardiography. Obstruction rather than ischemia may explain a decrease in blood pressure during dobutamine stress echocardiography.

Aged↗
PubMed1975

Contractile and electrophysiological responses to progressive digitalis toxicity.

Contractile force and intraventricular conduction during progressive ouabain infusion were examined in 15 dogs using a Walton-Brodie strain gauge arch and sequential atrial and bundle of His pacing. This permitted: (1) contractile force determination; (2) overdrive of arrhythmias; (3) maintenance of normal contraction sequences; (4) 'normal' ventricular depolarization; (5) rate control; (6) conduction measurements of the H-V interval (His-Purkinje conduction), QRS (intramyocardial conduction), and H-S interval (total intraventricular conduction). Contractile force increased 21.2 plus or minus 4.3% at the onset of toxicity. After toxicity, there was a significant further increase (P smaller than 0.01) to 50.1 plus or minus 12.4%. However, immediately before ventricular fibrillation, a 43.8 plus or minus 8.2% decrease occurred (P smaller than 0.01). H-V time showed no change (from 30 plus or minus 2.7 to 31.5 plus or minus 2.4 ms) at the onset of toxicity but after toxicity, it lengthened to 40.5 plus or minus 3.1 ms (P smaller than 0.05). QRS did show significant prolongation (69.5% plus or minus 5.3 to 79.5 plus or minus 6.9 ms; P smaller than 0.05) at the onset of toxicity, but this was more marked (79.5 plus or minus 6.9 to 130.5 plus or minus 8.1 ms; Pplus or minus 0.01) after toxicity. H-S time was significantly prolonged (99.5 plus or minus 6.2 to 111.0 plus or minus 8.9 ms) before (P smaller than 0.02) and after (P smaller than 0.01) toxicity (111.0 plus or minus 8.9 to 171.1 plus or minus 10.6 ms). During toxicity there is progressive increase in contractile force with continued ouabain infusion Progressive prolongation of intramyocardial conduction occurs in nontoxic and toxic doses, but His-Purkinje conduction is prolonged only in supratoxic doses.

Animals↗
PubMed1985

Rate-dependent effects of procainamide on His-Purkinje conduction in man.

Microelectrode studies in isolated cardiac tissues have shown that the depressant effect of several antiarrhythmic drugs on the maximal upstroke velocity of the cardiac action potential is rate-dependent. To determine whether this effect of antiarrhythmic drugs is seen in humans, 14 patients undergoing atrial pacing at several rates were prospectively studied before and after the infusion of procainamide (15 mg/kg). The HV interval (His-Purkinje conduction rate) and the QRS duration (intraventricular conduction rate) were measured. Before procainamide infusion, atrial pacing did not significantly prolong the maximal HV interval (from 54 +/- 15 to 58 +/- 13 ms). After procainamide infusion (mean serum level 10.0 +/- 3 micrograms/ml) atrial pacing at an average of 5 pacing rates significantly prolonged the HV interval (from 67 +/- 18 to 80 +/- 20 ms, p less than 0.001). The extent of HV prolongation with atrial pacing after procainamide infusion was independent of the HV interval at rest before procainamide. The duration of the QRS complex also tended to prolong with atrial pacing after procainamide infusion, but this prolongation was not statistically significant. Thus, procainamide produces a rate-dependent depressant effect on His-Purkinje and intraventricular conduction, confirming observations made in isolated tissue preparations.

Adult↗
PubMed1995

Determination of intracellular calcium in vivo via fluorine-19 nuclear magnetic resonance spectroscopy.

Fluorine-19-nuclear magnetic resonance (19F-NMR) spectroscopic detection of the NMR-active Ca2+ indicator 5-fluoro-1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (5F-BAPTA) is one method for measuring cytosolic free Ca2+ concentration ([Ca2+]i) and has been used previously to measure [Ca2+]i in isolated cells and perfused organs. The aim of the present investigation was to demonstrate the feasibility of determining [Ca2+]i in vivo and in situ using 19F-NMR and 5F-BAPTA. Experiments were performed on male Sprague-Dawley rats with a surface-coil antenna employed for NMR interrogation. The Ca2+ indicator, 5F-BAPTA, was infused either intravenously (kidney, spleen) or intraventricularly (brain) as a 100 mg/ml solution of the cell-permeant acetoxymethyl ester (5F-BAPTA-AM) in dimethyl sulfoxide. Rats tolerated intravenous infusion without evident change in mean arterial blood pressure. In all tissues examined, kidney, spleen, and brain, [Ca2+]i was approximately 200 nM. To our knowledge, these results represent the first in vivo and in situ determinations of [Ca2+]i employing 19F-NMR.

Animals↗
PubMed1977

Distribution and degradation of [3H]methotrexate after intravenous and cerebral intraventricular injection in primates.

Four hr after either a single injection or continuous infusion of methotrexate (MTX) plus purified [3',5',9(n)-3H]MTX in cynomolgus or rhesus monkeys, 80 to 98% of the 3H radioactivity present in the plasma was found not to represent intact MTX. The percentage of 3H-containing MTX products in the urine after 4 hr was considerably less, although more variable. This variability seemed to be related to variability in the amount of the total dose excreted. Non-MTX products were also found in selected tissues and the percentage of intact MTX found 4 hr after i.v. injection varied from 2 to 26%. The percentage of intact MTX was routinely measured by comparing the values obtained using the dihydrofolate reductase assay with values based on the specific activity of [3',5',9(n)-3H]MTX. Results obtained by diethylaminoethyl column chromatography on a few samples, however, showed good agreement with results from the reductase assay. [3',5',9(n)-3H]MTX products appeared in peaks eluting from the diethylaminoethyl column both earlier and later than the MTX peak, with the earlier peaks being present in only small amounts in the urine. After continuous i.v. infusion, only 2% or less of the radioactivity found in the cerebrospinal fluid after 4 hr represented intact MTX, with the remaining radioactivity eluting much earlier than MTX. In contrast, after direct injection into the left lateral ventricel, all the 3H radioactivity in both cerebrospinal fluid and brain tissue represented intact MTX for up to 4 hr after injection. The appearance of MTX products in the plasma and selected tissues of these primates a short time after i.v. injection is compared to other work in experimental animals and man and suggests a greater metabolism of MTX than was previously suspected.

Animals↗
PubMed1997

GDNF is a trophic factor for adult rat corticospinal neurons and promotes their long-term survival after axotomy in vivo.

Glial cell line-derived neurotrophic factor (GDNF) is a trophic factor for several neuronal populations involved in motor control. The present study evaluates the trophic actions of GDNF on corticospinal neurons, an important central nervous system motor projection into the spinal cord. Death of spinal motoneurons and corticospinal neurons is observed in the neurodegenerative disease amyotrophic lateral sclerosis. Axotomy of adult rat corticospinal neurons at internal capsule levels induces half of them to die, and the surviving population displays severe atrophy. To examine the trophic effects of GDNF on corticospinal neurons, Fast Blue-labelled corticospinal neurons were stereotaxically axotomized at internal capsule levels and GDNF was infused intracortically to lesioned corticospinal neurons at total doses of 2, 4, 10, 20, 40, 100 and 300 microg for 7 days. GDNF prevented axotomy-induced death of corticospinal neurons at doses between 2 and 40 microg and abolished or attenuated their atrophy at all doses examined. In addition, treatment with 8 microg GDNF for the first 2 weeks after axotomy resulted in the long-term survival of corticospinal neurons for 42 days. With regard to the development of treatment strategies for upper motoneuron degeneration in amyotrophic lateral sclerosis, application of GDNF via the cerebrospinal fluid may be more relevant than intracortical delivery as its diffusion within the brain parenchyma is limited. Intraventricular as well as intracisternal infusion of GDNF (300 microg over 7 days) completely prevented corticospinal neuron death. These results show that GDNF promotes the long-term survival of corticospinal neurons and has a positive effect on their size in vivo. Furthermore, the survival-promoting effect of GDNF on corticospinal neurons after delivery via cerebrospinal fluid has important clinical implications for potential treatment of the upper motoneuron degeneration seen in amyotrophic lateral sclerosis.

Animals↗
PubMed1984

Comparison of ventricular steady-state infusion with bolus infusion and pressure recording for differentiating between arrested and non-arrested hydrocephalus.

In 6 years 26 adult patients with chronic communicating or non-communicating hydrocephalus underwent ventricular fluid pressure (VFP) recording, including intraventricular steady-state and bolus infusion tests. Patients were treated with a shunt when steady-state infusion yielded a csf outflow resistance (Rcsfs) greater than 10 mm Hg/ml/min; the success rate was 83%. The main purpose of the study was to compare Rcsfs with outflow resistance obtained by bolus infusions (Rcsfb), pressure-volume index (PVI) and VFP. Rcsfs was higher than Rcsfb, particularly when resistance was high and the degree of disturbance of csf dynamics was reflected by Rcsfs better than by Rcsfb. The PVI showed a roughly inverse relationship with the Rcsfs but was not helpful in differentiating arrested from non-arrested hydrocephalus. Rcsfs and VFP correlated better than expected. A high Rcsfs was associated with an elevated VFP and a normal Rcsfs with a normal VFP. VFP only varied when Rcsfs exhibited a mild to moderate increase. It is concluded that steady-state infusion remains the most reliable method for the prediction of the result of shunting. We recommend shunting when Rcsfs is greater than 10 mm Hg/ml/min. Bolus infusions provide valuable data on brain elastance and additional information on csf outflow resistance. VFP recording is certainly worthwhile because infusion tests can be omitted when VFP is clearly elevated and useful information is obtained when Rcsf is borderline.

Adolescent↗
PubMed1979

Effects of intraventricular and intra-aquaductal 6-hydroxydopamine on monoamine containing neurons of the fowl paleostriatum, diencephalon and mesencephalon.

The effects of a single intraventricular or intra-aquaductal infusion of 6-hydroxydopamine (6-OHDA) on monoamine fluorescence in the paleostriatum augmentatum, diencephalon and mesencephalon were studied. Present experiments have enable us to better characterize the distribution of catecholaminegic axons in the paleostriatum augmentatum, preoptic area, hypothalamus, median eminence, periventricular areas as well as of cell-bodies and axons exbiting green fluorescence in the n. mesencephalicus properties and other mesencephalic nuclei.

Animals↗
PubMed1989

Intraventricular or epidural injection of morphine for severe pain.

Intraventricular or epidural injection of morphine through implantable infusion devices was used for severe pain in 50 patients with advanced cancer, arachnoiditis, or spinal injury. Intraventricular catheter was inserted for injection of morphine in 21 patients, 29 were treated through epidural infusion. For the evaluation of results the multimodal evoked potential (MEP) has been obtained before and after each treatment. 80% of the patients experienced good results. No significant side effects have been noted in patients with either epidural or intraventricular injection of morphine. These may be excellent methods for pain control in well selected patients.

Adult↗
PubMed1981

Sodium appetite in sheep induced by cerebral ventricular infusion of angiotensin: comparison with sodium deficiency.

Intraventricular administration of supraphysiological amounts of renin, nerve growth factor preparation, or angiotensin II greatly increased the consumption of water and hypertonic sodium bicarbonate solution by sheep. These effects were antagonized by intraventricular administration of drugs that prevent the formation of angiotensin II or block its receptors. The fact that these angiotensin-blocking drugs did not change the sodium intake of sodium-deficient sheep challenges the idea that central angiotensin action is involved in sodium appetite due to a deficiency.

Angiotensin II↗
PubMed1989

Nerve growth factor (NGF) reverses axotomy-induced decreases in choline acetyltransferase, NGF receptor and size of medial septum cholinergic neurons.

Intraventricular nerve growth factor (NGF) infusion in the adult rat can prevent and also, if delayed, reverse the disappearance of most of the axotomized medial septum cholinergic neurons immunostained for choline acetyltransferase (ChAT). We have utilized the delayed NGF treatment protocol to (i) extend to 3 months the delay time between axotomy and NGF treatment, (ii) define the time course of their recovery, (iii) determine that immunostaining for the (lower affinity) NGF receptor (NGFR) parallels loss and reversal of the ChAT marker, and (iv) evaluate changes in cholinergic somal size following axotomy and subsequent NGF treatment. While NGF treatments starting only 7 days after the fimbria-fornix transection (axotomy) almost entirely restored the number of both ChAT- and NGFR-positive medial septum neurons, longer delayed (2-3 weeks) treatment brought about recovery from the baseline of 20-25% to only about 70% of the control numbers. This limited recoverability, however, persisted even after a 95 day delay period. In all cases examined maximal recoveries were achieved within 3-7 days of NGF treatment. Neuronal size analyses provided evidence for an axotomy-induced atrophy. NGF treatments, started with 1 or 2 week delays, not only reversed fully the average somal size loss but also induced an actual hypertrophy of several of those neurons. These results provide additional evidence that at least half of the apparent loss of cholinergic medial septum neurons upon axotomy is due to a loss of markers such as the transmitter-related enzyme ChAT and NGFR rather than to actual neuronal cell death. These results also show that NGF exerts a genuine trophic influence by regulating the size of its target neurons as well as their content of several proteins.

Animals↗
PubMed1976

Pharmacological study of cefazolin during intermittent and continuous infusion: a crossover investigation in humans.

Levels of cefazolin were determined in plasma, urine, bile, and cerebrospinal fluid in humans after a bolus intravenous injection and during a controlled, continuous intravenous infusion. All the patients were studied in a steady-state and crossover fashion. In plasma, the mean peak level after bolus injection (1.5 g) studied in 12 patients was 206.5 mug/ml; during continuous infusion (6 g daily), the mean level remained stable at 52.6 mug/ml. With bolus injection and continuous infusion, respectively, 89.7 and 86.3% of the administered dose of cefazolin were excreted in the urine of nine patients over the 6-h period considered. The levels of cefazolin in common bile duct bile were studied in six cholecystectomized patients. In bile collected during the two 3-h periods of the experiment, the mean concentration of the drug in the bile after bolus injection was 66.9 and 22.0 mug/ml, respectively; during continuous infusion, the corresponding biliary levels were 50.7 and 51.3 mug/ml, respectively. In four neurosurgical patients with an intraventricular catheter, neither bolus injection nor continuous infusion resulted in a demonstrable concentration of cefazolin in the cerebrospinal fluid. The continuous intravenous administration of cefazolin might have some advantage over the intravenous bolus intermittent injections. In plasma, the area under the curve is greater with continuous infusion than with bolus injection. In bile, the levels of cefazolin are more sustained with continuous infusion than with bolus injection. This approach to intravenous administration of cefazolin deserves more pharmacological and clinical trials.

Bile↗