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Results for “Infusions, Intraventricular”

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PubMed1986

The influence of central infusions on drinking due to peripheral osmotic stimuli in the pigeon (Columba livia).

The drinking responses of pigeons infused simultaneously IV (0.334 ml/min) and ICV (2 microliters/min) for 15 min with various osmotic solutions were observed during, and for 60 min after, the combined infusions. Drinking in response to IV infusion of 0.5 M NaCl or 1.0 M sucrose was unaffected by simultaneous ICV infusion of 0.15 M NaCl, enhanced by ICV 0.3 M NaCl, inhibited during the infusion of water ICV and attenuated by ICV infusion of 0.9 M sucrose. Drinking in response to IV infusion of 1.0 M NaCl or 1.5 M sucrose, two solutions that would have greatly increased CSF sodium concentration, was only slightly affected by simultaneous ICV infusions of NaCl, sucrose or water. These results show that drinking following IV administration of osmotic stimuli can be affected by ICV infusions that may have further increased or decreased CSF sodium concentration thereby suggesting that CSF sodium concentration may play a "permissive role" in osmotically induced drinking.

Animals↗

PubMed1986

D-glucose suppression of eating after intra-third ventricle infusion in rat.

To clarify the hypophagic action of D-glucose, meal size, postprandial intermeal interval and eating rate were analyzed after infusion of glucose into the third cerebroventricle. The effects of glucose structure modification on feeding modulation were examined by comparing the effects of glucose to those of its epimers, D-mannose, D-allose and D-galactose. Glucose, infused in doses of 6 to 24 mumol, dose relatedly reduced meal size, but did not change other meal parameters. The minimum dose of glucose to induce feeding suppression was between three and 6 mumol. The epimers, at doses of 24 mumol, did not affect food intake or body weight. Drinking patterns and ambulatory activity were not changed by glucose infusion. These findings were consistent with neuronal activity observed in the ventromedial hypothalamic nucleus.

Animals↗

PubMed1998

Cannabinoid effects in basal ganglia in a rat model of Parkinson's disease.

Cannabinoid receptors in the brain are highly concentrated in the basal ganglia, which is in accordance with their well known effects on motor behavior. In this study, rats with 6-hydroxydopamine lesions of the nigrostriatal pathway were implanted with cannulae in the striatum, globus pallidus and substantia nigra. The effect of unilateral infusion of the potent cannabinoid agonist CP55,940 on turning behavior was studied for each structure. Lesioned animals responded to intrapallidal and intrastriatal administration of the cannabinoid in a manner that was similar to that of unlesioned animals. However, lesioned animals showed greater contralateral turning in response to the cannabinoid infusions in the substantia nigra than unlesioned animals.

Animals↗

PubMed2005

Hypothalamic expression of NPY mRNA, vasopressin mRNA and CRF mRNA in response to food restriction and central administration of the orexigenic peptide GHRP-6.

In this study, we examined the effects of restricted feeding and of central administration of an orexigenic ghrelin agonist GHRP-6 on peptide mRNA expression in the hypothalamus. We compared rats fed ad libitum with rats that were allowed food for only 2?h every day, and treated with a continuous chronic i.c.v. infusion of GHRP-6 or vehicle. Ad libitum fed rats exposed to GHRP-6 increased their food intake and body weight over 6 days, but, at the end of this period, neuropeptide Y mRNA expression in the arcuate nucleus was not different to that in control rats. By contrast, expression of neuropeptide Y mRNA in the arcuate nucleus was elevated in food-restricted rats, consistent with the interpretation that increased expression reflects increased hunger. However, neuropeptide Y mRNA expression was no greater in food-restricted rats infused with GHRP-6 than in food-restricted rats infused with vehicle; thus if the drive to eat was stronger in rats infused with GHRP-6, this was not reflected by higher levels of neuropeptide Y mRNA expression. Expression of vasopressin mRNA and corticotrophin releasing factor (CRF) mRNA in the paraventricular nucleus (PVN) was not changed by food restriction. GHRP-6 infusion increased CRF mRNA expression in ad libitum rats only.

Animals↗

PubMed2001

Sleep-promoting activity of prolactin-releasing peptide (PrRP) in the rat.

The present study examines whether or not prolactin-releasing peptide (PrRP) infused intracerebroventricularly (i.c.v.) affects sleep and the release of prolactin (PRL) and growth hormone (GH) in rats. At a dose of 0.1 nmol, PrRP promoted rapid-eye-movement (REM) sleep, whereas 1.0 nmol increased both non-REM and REM sleep and 10.0 nmol enhanced only non-REM sleep. During the i.c.v. infusion of PrRP with 0.1 nmol, levels of plasma PRL were elevated, but GH levels were significantly decreased. Since it is reported that PrRP fails to induce PRL release from the male pituitary, the stimulatory effects of PrRP on PRL release observed here seem to be indirect. However, PRL stimulated by i.c.v.-infused PrRP could take part in the REM sleep-promoting activity of PrRP.

Animals↗

PubMed1992

Differential baroreceptor reflex modulation by centrally infused angiotensin peptides.

The present study was designed to investigate the effect of intracerebroventricular (icv) and intravenous (iv) infusion of angiotensin (ANG)-(1-7), ANG III, and ANG II on the baroreceptor control of heart rate (BHR) in conscious rats. Reflex changes in HR were elicited by bolus iv injection of either phenylephrine or sodium nitroprusside before and within 1 and 3 h of icv infusion of ANG II (n = 10), ANG III (n = 9), ANG-(1-7) (n = 9), or saline (n = 9) at a rate of 3 nmol.7.5 microliter-1.h-1. In another group of animals (n = 23), iv infusion of the same amount of ANG peptides was carried out at a rate of 0.7 ml/h. The average ratio of changes in HR in beats per minute and changes in mean arterial pressure (MAP, mmHg) was used as an index of BHR sensitivity. ANG II and ANG III produced a significant increase in the basal levels of MAP, but only during the first hour of infusion (iv or icv). No significant changes in baseline HR were observed. ANG-(1-7) and saline infusion did not change basal levels of HR or MAP (iv or icv). ANG II (iv and icv) and ANG III (icv) caused a significant decrease in the BHR sensitivity for reflex bradycardia. In contrast, icv infusion of ANG-(1-7) induced a significant increase in BHR sensitivity for reflex bradycardia (-3.0 +/- 0.3, 1 h, and -2.8 +/- 0.1 beats.min-1.mmHg-1, 3 h vs. -2.1 +/- 0.2 beats.min-1.mmHg-1, before infusion).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗

PubMed1994

Comparison of fos-like immunoreactivity induced in rat brain by central injection of angiotensin II and carbachol.

Rats were given intracerebroventricular injections of either angiotensin II (ANG II) or the cholinomimetic carbachol. Some rats received cotreatment with ANG II antagonists selective for either angiotensin receptor AT1 (losartan) or AT2 (PD-123319, CGP-42112A). One hour later, the rats were killed and the brains processed for immunocytochemical detection of Fos-like immunoreactivity (FLI). ANG II treatment induced strong FLI in the anterior subfornical organ (SFO), median preoptic nucleus (MnPO), organum vasculosum laminae terminalis (OVLT), and supraoptic and paraventricular hypothalamic nuclei (SON, PVH). The AT1 antagonist abolished FLI in all regions normally stimulated by ANG II. The AT2 antagonist PD-123319 reduced FLI in SON and PVH, but CGP-42112A was less effective. Carbachol induced strong FLI in SON, PVH, and MnPO and only moderate FLI in SFO and OVLT. The AT1 antagonist prevented carbachol-induced FLI in the MnPO only. The distributions of FLI are compared between these central dipsogens and with that previously reported after peripheral infusion of ANG II, and their implications for mapping central thirst pathways are discussed.

Angiotensin II↗

PubMed1998

Effects of chronic central infusion of oxytocin on the response of the magnocellular neuroendocrine system to osmotic stimulation.

The effect of continuous intracerebroventricular (i.c.v.) infusion of oxytocin (OT) on the release of OT and vasopressin (VP) following osmotic stimulation was studied in ovariectomized rats treated peripherally with gonadal steroids to simulate late gestation/lactation. Artificial cerebrospinal fluid (CSF) with or without OT (2 ng/microg) was infused (0.5 microl/h) i.c.v. continuously for 7 days along with sequential peripheral administration of progesterone (2 mg/kg i.m.) for 4 days, then 17-beta-estradiol (200 microg/kg i.m.) for 2 days. Following 7 days of OT infusion, isotonic (0.15 mol/l NaCl) or hypertonic (1.5 mol/l NaCl) saline was injected (15 ml/kg s.c.); the animals were decapitated 1 h later. Animals infused centrally with OT had higher basal levels of OT in plasma (p < 0.01 vs. CSF). While osmotic stimulation increased plasma levels of both OT and VP (0.15 mol/l NaCl < 1.5 mol/l NaCl; p < 0.01), only circulating VP was enhanced further (p < 0.01) in animals infused with OT compared with those receiving CSF. These changes in hormone levels could not be explained by differences in neural lobe stores of OT or VP or by alterations in daily water intake during the infusion period. Thus, chronic i.c.v. infusion of OT stimulates basal release of OT and increases the response of the VP system to osmotic stimulation.

Animals↗

PubMed1980

Intracerebroventricular 2-DG causes feeding in the absence of other signs of glucoprivation.

Intracerebroventricular (ICV) infusions of 2-deoxy-D-glucose (2-DG) elicited hyperglycemia and increased feeding at short latencies. If access to food was prevented for 6 h post-2-DG infusion, when blood glucose levels were normal and brain 2-DG concentrations were virtually zero, the rats still ate significantly more food than they did 6 h after control infusions. These data indicate that activation of brain glucoreceptors may mediate increased feeding even after other signs of cerebral glucoprivation have disappeared.

Animals↗

PubMed1993

Phosphodiesterase III inhibitors: long-term risks and short-term benefits.

Heart failure is now viewed as a disorder of the circulation, not merely the heart, which becomes manifest only when certain compensatory mechanisms break down. After treatment with diuretics, the two main strategies in treating heart failure involve decreasing the work of the heart by vasodilatation or increasing ventricular contractility by positive inotropic agents. It is now apparent, however, that the resulting hemodynamic benefit need not equate with long-term clinical improvement or increased longevity; indeed, the reverse can be true. Inhibitors of phosphodiesterase III, which is specific for the breakdown of cyclic adenosine monophosphate (cAMP), produce useful hemodynamic effects following intravenous and oral dosing, but have not fulfilled their initial promise in the chronic oral treatment of heart failure patients. The reason for reduced survival in the long-term studies of milrinone is not clear, but cardiac arrhythmias, possibly resulting from the increased intracellular levels of cAMP, may be responsible. However, intravenous usage may not suffer from the same limitations as chronic oral dosing. Short-term intravenous administration produces the expected beneficial hemodynamic effects of positive inotropism and vasodilatation. Though infusions of milrinone have been shown to enhance atrioventricular conduction in some, but not all, studies, there appears to be no significant increase in ventricular premature contractions, or ventricular or sustained tachyarrhythmias. Because milrinone does not have a significant adverse effect on His-Purkinje conduction, its use should be well tolerated in patients with intraventricular conduction disturbances. However, accurate assessment of the mortality risk and benefit of short-term intravenous treatment remains to be made in sufficiently powerful prospective, randomized controlled studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output, Low↗

PubMedDate not supplied

Time dependent partial loss of the effects of isoproterenol on function and energy metabolism of isolated rat hearts.

In isolated perfused rat hearts (medium: Krebs-Ringer solution containing about 15% bovine red cells) the following parameters were estimated: heart rate (F), left intraventricular peak pressure (P), dP/dt, oxygen consumption (VO2); myocardial tissue content of glycogen, ATP, ADP, AMP, cAMP, phosphocreatin (PC) and inorganic phosphate (Pi). Isoproterenol (ISO) was administered to the non circulating system in the concentration range of 5 x 10(-10) to 5 x 10(-5) M for 4 min and 1 hour respectively by infusion into the perfusate close to the aortic canula. After administration period of 4 min dependent on the concentration of ISO, P, dP/dt, VO2 and the content of cAMP are increased. The ratios of PC/Pi and ATP/ADP as well as glycogen content are reduced. For an administration period of 1 hour at a level of 5 x 10(-9) M the effects of isoproterenol are maintained. At ISO concentration higher than 5 x 10(-9) M the effects on mechanical parameters and VO2 fall to the level of those values which are produced at 5 x 10(-9) M ISO. In contrast, high energy phosphates and glycogen content remain reduced while that of cAMP is elevated.

Adenine Nucleotides↗

PubMed1983

Chronic infusion of angiotensin II into the olfactory bulb elicits an increase in water intake.

Chronic infusion of angiotensin II (ANG II) into the olfactory bulb (OB) elicited a moderate dipsogenesis which occurred only during the dark phase, essentially doubling the water-to-food intake ratio. Removal of the food from the ANG II-OB group reduced water consumption to the level of the saline-infused/food-deprived controls. These experiments suggest that ANG II may interact with the OB to alter the normal water/food relationship.

Angiotensin II↗

PubMed1982

Infusions of chemicals into the brain and the development of sustained elevations of blood pressure in the rat.

Osmotic minipumps were used to infuse carbachol chloride (1.23 micrograms/hr), echothiophate iodide (0.5 microgram/hr), histamine dihydrochloride (10 micrograms/hr), prostaglandin E2 (1.0 microgram/hr) and thyrotropin-releasing hormone (0.5 and 5.0 micrograms/hr) solutions into the cerebral ventricles of unanesthetized rats and blood pressure was measured by the tail-cuff method. Histamine dihydrochloride, prostaglandin E2 and thyrotropin-releasing hormone produced an initial rise in blood pressure, but were not effective in producing sustained elevations in blood pressure. Carbachol infusions elevated blood pressure throughout the 7-day infusion period when results were compared to saline-infused animals. Infusions of echothiophate iodide, an anticholinesterase agent, produced an initial rise in blood pressure but these pressor effects were not sustained. In animals infused with echothiophate for 7 days, the pressor response to a challenge dose of echothiophate was diminished.

Animals↗

PubMed1984

The antagonistic action of 6-aminomethyl-3-methyl-4H,1,2, 4-benzothiadiazine-1,1-dioxide (TAG) on the prolactin-releasing action of taurine.

The action of the putative taurine antagonist 6-aminomethyl-3-methyl-4H-1, 2,4-benzothiadiazine-1,1 dioxide (TAG) was examined on the prolactin-releasing action of taurine. The study utilized unanesthetized male rats with indwelling jugular and cerebroventricular cannulas. The intracerebroventricular (I.C.V.) infusion of taurine (0.5 mumole) elicited an increase in prolactin (PRL) secretion elevating plasma levels significantly by 10 min. The I.C.V. infusion of TAG (0.01 mumole) did not alter baseline plasma PRL levels. When a combined I.C.V. infusion of taurine and TAG was given the PRL levels normally induced by taurine were significantly reduced. Neither taurine nor the antagonist TAG altered pituitary secretion of luteinizing hormone.

Animals↗

PubMed1994

Infusion of a pineal gland-derived antigonadotropic decapeptide into the lateral ventricle depresses prolactin levels in male rats.

The primary structure of a pineal gland-derived antigonadotropic decapeptide (AGD) was determined recently, and a synthetic analog prepared by solid state methods. Adult male Harlan SD rats were maintained under controlled photoperiods. Each was fitted stereotaxically with a stainless steel cannula for infusion into a right lateral ventricle. Each cannula was attached to a subcutaneous osmotic minipump filled either with artificial cerebrospinal fluid (CSF) or the AGD in CSF (0.5 micrograms/microliters). Additional Tygon microbore cannulae were inserted through the femoral artery and placed in the abdominal aorta for blood sampling and the determination of prolactin (PRL) levels by radioimmunoassay. CSF (1.0 microliter/hr) or the AGD (0.5 microgram/hr) was infused into the right lateral ventricle over a period of seven days. Circulating PRL concentrations were significantly depressed by AGD infusion both in the morning and late afternoon; adenohypophysial concentrations were concomitantly elevated on infusion day seven. These results confirm previous observations of inhibitory effects of the AGD on PRL secretion, and further support its postulated central mechanism of action.

Adrenal Glands↗

PubMed1984

Chronic cerebroventricular infusion of hypertonic sodium chloride in rats reduces hypothalamic sympatho-inhibition and elevates blood pressure.

To determine whether or not salt loading restricted to the brain would elevate blood pressure, chronically implanted osmotic minipumps were used to infuse hypertonic sodium chloride solutions made in artificial cerebrospinal fluid into a jugular vein intravenously or the third cerebral ventricle, intracerebroventricularly, for 11 days in awake rats. During intracerebroventricular infusion of hypertonic sodium chloride, tail-cuff systolic pressures began to rise on day 4 and were significantly elevated by day 9. In contrast, infusions of either artificial cerebrospinal fluid alone, intracerebroventricularly, or hypertonic sodium chloride, intravenously, were ineffective. Confirming the blood pressure elevation thereby detected, systolic and mean pressures recorded directly from indwelling aortic catheters after the same rats had been anesthetized with urethane on day 11, were also significantly higher following intracerebroventricular infusion of hypertonic sodium chloride than after infusion of artificial cerebrospinal fluid alone. Magnitude of depressor and sympatho-inhibitory responses elicited by graded electrical stimulation of the anterior hypothalamus invariably increased with the current strength used for stimulation. At all current strengths used for hypothalamic stimulation, depressor responses as well as attendant decreases in sympathetic neural firing, were smaller in rats that had been infused intracerebroventricularly with hypertonic sodium chloride than in any of the controls. Inhibition seemed specific for the anterior hypothalamus because pressor responses to stimulation of the ventromedial hypothalamus were the same whether or not the intracerebroventricular infusion contained hypertonic sodium chloride. An explanation based on diminished cardiovascular sensitivity also appeared unlikely, since depressor responses to intravenously injected histamine were almost equal in both groups. Our results are compatible with the interpretation that hypertonic sodium chloride infused chronically into the 3rd ventricle acts by reducing anterior hypothalamic inhibition of sympathetic vasomotor tone, and that this, in turn, then elevates blood pressure.

Animals↗

PubMed1984

Baroreflex impairment precedes hypertension during chronic cerebroventricular infusion of hypertonic sodium chloride in rats.

Osmotic minipumps were implanted chronically for continuous 11-d infusion of hypertonic sodium chloride (NaCl) into the third cerebral ventricle (ICV) of awake rats to determine whether baroreflex sensitivity would be altered. Systolic and mean pressures, recorded from aortic catheters on day 11 while the rats were anesthetized with alpha-chloralose, were significantly higher in rats infused with artificial cerebrospinal fluid (CSF) containing hypertonic NaCl than in controls similarly infused with artificial CSF alone. Reflex changes in heart rate produced by subsequent intravenous infusions of either phenylephrine or sodium nitroprusside were inhibited, but reflex changes in renal nerve activity were unaltered. Magnitude of reflex bradycardia during pressor responses to phenylephrine, as well as of reflex tachycardia during depressor responses to sodium nitroprusside, was consistently smaller in NaCl-infused than in control rats. By contrast, group differences in attendant renal nerve firing were not significant. After sinoaortic denervation, drug-induced blood pressure effects persisted, but reflex responses in heart rate and renal nerve firing were abolished or markedly diminished. Peripheral effects produced by hypertonic NaCl leakage from the infusion site were considered unlikely because after 11 d of ICV infusion, sodium concentration, though appreciably elevated in CSF samples collected from the cisterna magna, was unaffected in corresponding serum samples. When cardiovascular responses to phenylephrine were recorded while chronic ICV infusions were in progress, awake rats receiving hypertonic NaCl were still normotensive on day 2 yet reflex bradycardia was already attenuated. In showing that baroreflex impairment preceded the development of hypertension, our results suggest that by depressing the anterior hypothalamus, chronic ICV infusion of hypertonic NaCl reduces sympatho-inhibition, and the ensuing baroreflex impairment then elevates blood pressure. However, other mechanisms could also be involved.

Animals↗

PubMed1997

Intraventricular dexmedetomidine decreases cerebral blood flow during normoxia and hypoxia in dogs.

We tested the hypothesis that a centrally administered alpha 2-receptor agonist could alter the cerebrovascular response to hypoxia, without evidence of systemic absorption of the drug. Beagle dogs were anesthetized with 1.4% isoflurane and exposed to hypoxic hypoxia (Pao2 approximately 22 mm Hg) before and after ventricular-cisternal perfusion with mock cerebrospinal fluid (CSF group, n = 5) or dexmedetomidine (100 micrograms/mL; total dose 300 micrograms; DEX group, n = 6). Cerebral perfusion pressure, Paco2 and arterial oxygen content were controlled and regional cerebral blood flow (CBF; microspheres) and global cerebral metabolic rate for oxygen consumption (CMRO2) were measured. In another group (n = 5), drug distribution under the experimental conditions was assessed by 3H-clonidine administered by ventricular-cisternal perfusion. In the mock CSF group, flow to the cerebral hemispheres increased during hypoxia under baseline conditions and after CSF infusion: 66 +/- 8 to 170 +/- 15 mL.min-1.100 g-1 (265% +/- 24% of baseline value), 83 +/- 9 to 154 +/- 14 mL.min-1.100 g-1 (201% +/- 54% of post-CSF infusion value). DEX decreased normoxic flow in the cerebral hemispheres from 76 +/- 6 to 44 +/- 4 ml.min-1.100 g-1 with decreases in other regions of similar magnitude. After DEX, the absolute flow in all regions during hypoxia was 52%-55% of that prior to DEX (P < 0.05). However, because DEX also decreased normoxic CBF, the percent increase in flow during hypoxia was similar before and after DEX. CMRO2 was not affected by hypoxia prior to DEX. However, after DEX, hypoxia caused a marked reduction in cerebral oxygen delivery (5.2 +/- 1.0 vs 13.7 +/- 2.3 ml.min-1.100 g-1 for the CSF group) and CMRO2 (2.5 +/- 0.6 vs 3.9 +/- 0.6 ml.min-1.100 g-1). Regional accumulation of intraventricularly administered 3H-clonidine was greatest in periventricular brain structures (e.g., caudate nucleus, dorsal brainstem), and the concentration in the cerebral cortex was approximately 1% of the concentration in the ipsilateral caudate nucleus. We conclude that centrally administered DEX reduces CBF during normoxia and prevents adequate oxygen delivery during hypoxia. The mechanism of DEX-induced CBF reduction is not metabolically mediated, since CMRO2 is maintained at control values during normoxia despite the significant blood flow reduction. We believe that the reduction in CMRO2 during hypoxia in DEX-treated dogs is the result of a reduction of oxygen delivery rather than the underlying mechanism for the observed reduction in CBF during hypoxia.

Adrenergic alpha-Agonists↗