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PubMed2005

Evidence of roles of central alpha1-adrenoceptors and epinephrine in orexin A-induced hyperactivity in mice.

Previous studies have shown that central alpha1-adrenoceptor activity is necessary, acutely, for gross behavioral activity in response to novel surroundings and various psychostimulants. The present experiment tested whether it is also necessary for the hyperactivity produced by the peptide, orexin A, which is present in several central monoaminergic nuclei. Mice, pretreated intraventricularly with the alpha1-antagonist, terazosin, or the alpha2-antagonist, atipamezole, were given orexin A, intraventricularly (i.v.t.), and videotaped for gross movement and locomotion in the home cage between 30 and 60 min post-infusion. The alpha1-antagonist was found to produce a significant dose-dependent decrease of orexin A-induced activity, which was first seen at the 3 nmol dose and was near total at 30 nmol. The alpha2-antagonist, at 10 nmol, had no effect on the orexin A response. Pharmacological inhibition of the synthesis of epinephrine, a potential neurotransmitter at central motoric alpha1-adrenoceptors, with 2,3-dichloro-alpha-methylbenzylamine also significantly attenuated orexin A-induced hyperactivity. It is concluded that central alpha1-adrenoceptor activity, presumably caused by epinephrine release, is necessary for the gross behavioral activation produced by orexin A.

Adrenergic alpha-Antagonists↗
PubMed1989

Effects of crystalloid and colloid infusions on intracranial pressure and computerized electroencephalographic data in dogs with vasogenic brain edema.

This experiment was designed to study the effects of intravascular volume expansion with crystalloid and colloid agents on intracranial pressure (ICP) and computerized electroencephalographic (EEG) data in dogs with cerebral vasogenic edema. A liquid nitrogen cold lesion was produced in the right parietal lobes of 30 anesthetized mongrel dogs. ICP data from an intraventricular catheter, hemodynamic data, and EEG power data were recorded continuously during the course of the experiment. Six hours after creation of the liquid nitrogen cold lesion, each dog was infused with one of the following treatments: 1) no treatment (control); 2) 5% dextrose in water (D5W) (30 ml/kg/h); 3) 0.9% NaCl (30 ml/kg/h); 4) hetastarch (10 ml/kg/h); and 5) hetastarch (30 ml/kg/h). The animals were treated for 2 hours, killed, and the brains examined and measured for water content. During the D5W infusion, ICP increased significantly (141%) but the EEG power data did not change. During the normal saline infusion, ICP increased significantly (91%) and the EEG power data showed marked deterioration. Both hetastarch infusions produced no change in ICP and demonstrated an improvement in the EEG power data (P less than 0.001). These data suggest that crystalloid infusions may have profound deleterious effects in the presence of brain edema, but colloids do not, and should be considered in the fluid management of patients with cerebral edema.

Animals↗
PubMed2005

Randomised controlled trial evaluating effects of morphine on plasma adrenaline/noradrenaline concentrations in newborns.

OBJECTIVES: To determine the effects of continuous morphine infusion in ventilated newborns on plasma concentrations of adrenaline (epinephrine) and noradrenaline (norepinephrine) and their relation to clinical outcome. DESIGN: Blinded, randomised, placebo controlled trial. SETTING: Level III neonatal intensive care units in two centres. PATIENTS: A total of 126 ventilated neonates (inclusion criteria: postnatal age <3 days, duration of ventilation <8 hours, indwelling arterial catheter for clinical purposes; exclusion criteria: severe asphyxia, severe intraventricular haemorrhage, major congenital anomalies, neuromuscular blockers). INTERVENTIONS: Plasma adrenaline and noradrenaline concentrations were determined in patients during blinded morphine (n = 60) and placebo (n = 66) infusion (100 microg/kg plus 10 microg/kg/h). RESULTS: Plasma concentrations at baseline (nmol/l with interquartile range in parentheses) were comparable in infants treated with morphine (adrenaline, 0.22 (0.31); noradrenaline, 2.52 (2.99)) or placebo (adrenaline, 0.29 (0.46); noradrenaline, 2.44 (3.14)). During infusion, median adrenaline concentrations were 0.12 (0.28) and 0.18 (0.35) and median noradrenaline concentrations were 2.8 (3.7) and 3.8 (4.0) for the morphine and placebo treated infants respectively. Multivariate analyses showed that noradrenaline (p = 0.029), but not adrenaline (p = 0.18), concentrations were significantly lower in the morphine group than the placebo group. Furthermore, noradrenaline concentrations were related to the length of stay in the neonatal intensive care unit. CONCLUSIONS: Continuous morphine infusion significantly decreased plasma noradrenaline concentrations in ventilated newborns compared with placebo treatment. The results of this study support the idea that routine morphine administration decreases stress responses in ventilated neonates.

Analgesics, Opioid↗
PubMed1995

Differential regulation of seizure activity in the hippocampus of male and female rats.

OBJECTIVE: The aim of the current study was to directly examine and compare the susceptibility to N-methyl-D-aspartate-induced seizures in male versus female rats. We also sought to compare the anticonvulsant effects of magnesium sulfate in these two groups. STUDY DESIGN: Eighteen female and 10 male rats were stereotaxically implanted with a chronic bipolar recording electrode in the hippocampus and an injection cannula in the lateral cerebral ventricle. After 1 week rats randomly received an intravenous injection of 90 mg/kg magnesium sulfate or saline solution control. Fifteen minutes after the infusion rats were given the convulsant N-methyl-D-aspartate at a dose of 5 micrograms/microliters by direct intraventricular injection. Electrical seizure activity was thereafter assessed for 20 minutes. All data were analyzed by the Mann-Whitney U test and Student t test. RESULTS: In saline solution-treated rats receiving the convulsant N-methyl-D-aspartate, females had significantly lower total duration (p < 0.01) and total number of seizures (p < 0.05) compared with the male rats. The initial seizure was not affected by gender. In the female animals magnesium sulfate significantly reduced first seizure duration (p < 0.01) compared with saline solution controls. In males magnesium sulfate reduced both total duration (p < 0.05) and total seizure number (p < 0.05) compared with saline solution-treated animals. CONCLUSION: N-methyl-D-aspartate-induced seizure activity is more severe in males versus female rats. Magnesium sulfate's effect on N-methyl-D-aspartate-induced seizures is also dependent on gender. We speculate that seizure regulation may be hormonally influenced.

Animals↗
PubMed1996

Effects of cardioplegia on vascular function and the "no-reflow" phenomenon after ischemia and reperfusion: studies in the isolated blood-perfused rat heart.

The ability of cardioplegia to protect against cardiac contractile dysfunction caused by ischemia and reperfusion is well established. The effects of cardioplegia on vascular injury and the no-reflow phenomenon, however, remain controversial. We used the blood-perfused rat heart to study the effect of St. Thomas' Hospital cardioplegic solution on postischemic endothelium-dependent and endothelium-independent vascular function, the extent of the no-reflow phenomenon, and the temporal relationship between postischemic vascular and contractile function. Isolated rat hearts (16 per group) perfused with blood from a support rat at 60 mm Hg were subjected to 10, 20, 30 or 40 minutes of global ischemia and 40 minutes of reperfusion at 37 degrees C. Eight hearts in each group also received cardioplegia (45 mm Hg for 2 minutes) before ischemia. Left ventricular developed pressure was measured with an intraventricular balloon. At the end of reperfusion, a bolus of 250 micrograms nitro-L-arginine methyl ester was infused to assess endothelium dependent vascular function. After a 20-minute washout, 25 micrograms sodium nitroprusside was infused to assess endothelium-independent vascular function. Fluorescein (1 ml, 1% weight/volume) was then infused to assess no-reflow; this involved freezing the hearts, cutting them into transverse sections (10 x 1 mm), video recording the sections under ultraviolet light, digitizing the images, and analyzing density of fluorescence. No-reflow was defined as a flow of less than 5%. Compared with nonischemic control responses, endothelium-independent vascular function was significantly decreased only after 30 and 40 minutes of ischemia (48.1% +/- 3.8% and 24.3% +/- 7.4%, p < 0.05), but it was significantly protected by cardioplegia (66.6% +/- 3.9% and 64.5% +/- 5.2%, p < 0.05). A significant reduction in endothelium-dependent vascular function was observed after 40 minutes of ischemia (-31.8% +/- 6.6% vs -50.4% +/- 1.6% in control hearts, p < 0.05), and again this was improved by cardioplegia (-45.0% +/- 3.4%, p < 0.05 vs ischemic group). Areas of no reflow were present after 30 and 40 minutes of ischemia (11.9% +/- 6.8% and 33.4% +/- 14.1% of left ventricular mass), and at each time period they were significantly decreased by cardioplegia (0.7% +/- 0.4% and 3.8% +/- 1.6%, p < 0.05). Postischemic contractile dysfunction was observed before any vascular alteration was apparent. After only 20 minutes of ischemia, the postischemic recovery of left ventricular developed pressure fell to 56.7% +/- 4.0%, but both endothelium-dependent vascular function and endothelium-independent vascular function were unaffected. In conclusion, vascular alterations are apparent only after prolonged periods of ischemia, longer than those required to observe contractile dysfunction, and cardioplegia protects against postischemic endothelium-dependent and endothelium-independent vascular dysfunction and reduces the extent of the no-reflow phenomenon.

Animals↗
PubMed2000

Experimental study of intermittent crossclamping with fibrillation and myocardial protection: reduced injury from shorter cumulative ischemia or intrinsic protective effect?

OBJECTIVE: During coronary artery revascularization, some surgeons favor intermittent crossclamping with ventricular fibrillation in preference to cardioplegic ischemic arrest for myocardial protection. It is unclear, however, whether intermittent crossclamping with fibrillation is equally protective or whether ischemic injury is reduced as a consequence of shorter cumulative ischemia. METHODS: We used isolated, Langendorff-perfused rat hearts, measured preischemic function (left ventricular developed pressure) with an intraventricular balloon, and then subjected the hearts to either (1) 40 minutes of global ischemia, (2) a 2-minute infusion of cardioplegic solution and 40 minutes of ischemia, (3) multidose (every 10 minutes) infusions of cardioplegic solution during 40 minutes of ischemia, (4) continuous ventricular fibrillation during 40 minutes of ischemia, (5) intermittent (4 x 10 minutes) ischemia with 10 minutes of reperfusion, (6) intermittent (4 x 10 minutes) ischemia preceded by intermittent cardioplegia, (7) intermittent (4 x 10 minutes) ischemia with ventricular fibrillation, (8) continuous (40 minutes) ventricular fibrillation during coronary perfusion, or (9) intermittent (4 x 10 minutes) ventricular fibrillation (with perfusion). All protocols were followed by 60 minutes of reperfusion. RESULTS: After 60 minutes of reperfusion, the percentage recovery of left ventricular developed pressure for groups 1 through 9 was as follows: 32% +/- 2%, 57% +/- 6%, 82% +/- 3%, 19% +/- 3%, 73% +/- 3%, 70% +/- 3%, 78% +/- 4%, 55% +/- 2%, and 57% +/- 3%, respectively. No significant differences were identified among groups 3, 5, and 7, but the percentage recovery of developed pressure in group 3 was significantly higher than that in group 6; the degree of recovery in groups 3 and 5 to 7 was significantly (P <.05) higher than in groups 1, 2, 4, 8, and 9. Early recovery was significantly (P <.05) more rapid in groups 3 and 5 to 9, reaching a plateau (of 55%-80%) by 10 minutes of reperfusion; in groups 1, 2, and 4, the recovery plateau occurred after 50 minutes. Left ventricular end-diastolic pressure was elevated in groups 1, 2, and 4 but was almost unchanged from baseline in the other groups. CONCLUSIONS: A similar level of myocardial protection was achieved with multidose (intermittent) cardioplegia or intermittent crossclamping (with or without fibrillation), indicating that intrinsic preservation by intermittent crossclamping with fibrillation does not exacerbate ischemic injury.

Animals↗
PubMed2001

Hypotension and functional left ventricular obstruction during dobutamine stress echocardiography--two case reports.

Although hypotension during dobutamine stress echocardiography has been reported, the mechanism of this response is still controversial. In two patients, a 72-year-old woman and 64-year-old man, with exercise-induced ST-T change, continuous-wave Doppler examination of the left ventricular cavity was performed at baseline and peak dobutamine infusion. No echocardiographic abnormalities at rest or angiographic coronary lesions were observed in either patient. The intracavitary pressure gradient at peak dosage of dobutamine for both patients was 121 mm Hg and 100 mm Hg, and was reproducibly confirmed by cardiac catheterization. During dobutamine infusion, echocardiography or left ventriculography revealed that papillary muscle motion was dramatically augmented by dobutamine and mid-left ventricular obstruction was produced at the systolic phase. Although blood pressure response improved following beta-blocker treatment, intracavitary pressure gradient during dobutamine infusion remained the same. A hypotensive response during dobutamine stress echocardiography may be produced by the development of dynamic intraventricular obstruction and a vasodepression reflex. The exercise-induced electrocardiographic changes may have been related to the systolic pressure augmentation in the mid-to-apical left ventricular cavity.

Aged↗
PubMed1993

Effect of ajmaline on sustained ventricular tachycardia induced by programmed electrical stimulation in conscious dogs after myocardial infarction.

As yet the antiarrhythmic efficacy of ajmaline with regard to suppressing the induction of sustained ventricular tachycardia after myocardial infarction has not been determined. Therefore, programmed electrical stimulation was performed in 8 conscious, chronically instrumented mongrel dogs 8-20 days after a 4-hour occlusion of the left anterior descending coronary artery. At baseline all animals responded with sustained ventricular tachycardia. Thereafter, ajmaline was administered at two consecutive i.v. doses: a bolus of 0.7 mg kg-1 followed by infusion of 2 mg kg-1 h-1 and infusion of 4 mg kg-1 h-1. The induction of sustained ventricular tachycardia was prevented in 2/8 animals by 2 mg kg-1 h-1 ajmaline and in 1/8 animals by 4 mg kg-1 h-1 ajmaline. During sinus rhythm only 4 mg kg-1 h-1 ajmaline significantly increased QRS-duration and intraventricular activation times, but during rapid right ventricular pacing (cycle length = 330 ms) both doses of ajmaline increased QRS duration and intraventricular conduction times. 4 mg kg-1 h-1 ajmaline also increased the cycle length of induced sustained ventricular tachycardia. In 3 animals induction of sustained ventricular tachycardia during infusion of 4 mg kg-1 h-1 ajmaline was achieved by introduction of less extrastimuli than at baseline. Furthermore the coupling intervals of extrastimuli that induced sustained ventricular tachycardia were substantially prolonged by this dose. Inhomogeneity of conduction between left ventricular normal zone and left ventricular infarct zone was significantly increased by 4 mg kg-1 h-1 ajmaline during rapid right ventricular pacing, but not during sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Ajmaline↗
PubMed1987

A comparison of cocaine and its metabolite norcocaine: effects on locomotor activity.

Intraventricular and intraperitoneal administration of cocaine and its metabolite norcocaine were studied in adult male rats. Norcocaine (10-100 micrograms) had no behavioral activity following central infusion but proved to be toxic at high doses (50-100 mg/kg) when given peripherally. Cocaine at high doses (100 micrograms), produced possible hypoactivity after central injections but produced significant hyperactivity after peripheral administration (20 mg/kg).

Animals↗
PubMed1979

Simple cannula for repeated intracerebral drug administration in rats.

A simply constructed cannulation system for chronic implantation in rats is described. The guide cannula, stylet and injection cannula are all made from stainless steel tubing, require litte time to construct, and are designed for minimum brain damage and atraumatic infusion into unanesthetized rats.

Animals↗
PubMed1977

Timing of intraventricular haemorrhage.

The detection of the onset of intraventricular haemorrhage (IVH) during life is a necessary preliminary to understanding the cause of this condition. In 10 infants of very low birthweight treated with serial transfusions of adult blood the proportions of transfused cells circulating after each transfusion were compared with the proportion of transfused cells found in the intraventricular clot at necropsy. This allowed the timing of IVH to be restricted retrospectively to the period between consecutive blood transfusions. In addition, the proportional changes of transfused cells produced by infusion of a known red cell mass allow changes in the babies' original red cell mass to be followed during life. A fall in this value occurred in 8 infants dying with IVH and was taken to indicate haemorrhage. Comparison of the two methods in 9 infants suggested that, while in some cases intraventricular bleeding occurs rapidly, in others it takes place over a period of time. The interval between birth and the onset of haemorrhage was directly proportional to the gestational age of the infant.

Blood Transfusion↗
PubMedDate not supplied

Calcitonin--C.N.S. action to control the pattern of intestinal motility in rats.

Synthetic calcitonin injected into the lateral ventricles (ICV) of rats at picomolar concentration restores the "fasted' motility pattern of the small intestine in fed rats at doses as low as 0.083 picomoles. This effect which appeared in less than 5 min and persisted at least 2 hours for 0.83 picomole, was blocked by a previous intraventricular administration of 10 micrograms/ of calcium gluconate. At 0.83 picomole ICV, calcitonin also suppressed the disruption of the "fasted' pattern induced by intravenous infusion of Pentagastrin (6 micrograms.kg-1.h-1) but not that induced by insulin (0.5 U.kg-1). These findings support the hypothesis that calcitonin acts centrally to control the pattern of intestinal motility by inhibiting the digestive influences responsible for the "fed' pattern. All of these peripheral influences are mediated by a Ca++ sensitive central structure.

Animals↗
PubMed1983

Pharmacokinetics of intraventricular administration.

The widespread use of neurosurgical devices for intraventricular drug delivery has led to an escalation in the number of CSF pharmacokinetic studies. When experimental data for ventricular CSF concentration vs. time are normalized for dose and plotted for drugs with a wide range of physical properties, there is a remarkably narrow range. Simulations from a distributed model for the central nervous system suggest that the narrow range of observed CSF half-times following bolus administration is a consequence of physiologic limits upon rate of drug removal from CSF. Whereas bulk flow of CSF establishes minimum rate of drug washout, diffusion through brain tissue and subsequent removal by capillaries establishes a maximum rate of drug egress which is only seven times the minimum rate. Predictions of CSF concentration vs. time can be made based upon the capillary exchange rate for a particular drug, which could be estimated or calculated from CSF concentration measurements following systemic administration. Simulations are also presented of steady-state CSF concentrations during continuous ventricular infusions.

Animals↗
PubMed1992

Effect of endothelin on production of cerebrospinal fluid in rabbits.

BACKGROUND AND PURPOSE: Endothelin is a potent vasoconstrictor in several tissues, including the choroid plexus. The goal of this study was to determine whether endothelin affects the production of cerebrospinal fluid. METHODS: Ventriculocisternal perfusion was used to measure the production of cerebrospinal fluid in anesthetized rabbits. Changes in production of cerebrospinal fluid were examined in response to vehicle, intravenous endothelin (alone and in the presence of indomethacin), and intraventricular endothelin. RESULTS: Under control conditions, the reduction in production of cerebrospinal fluid in response to endothelin administered intravenously was only modestly greater than that during infusion of vehicle. Because endothelin releases cyclooxygenase products that attenuate the direct effects of endothelin in several tissues, effects of endothelin on the production of cerebrospinal fluid were also examined after inhibition of cyclooxygenase. Production of cerebrospinal fluid in response to 1 micrograms/kg i.v. endothelin was reduced more in animals treated with indomethacin than in untreated animals (-34 +/- 7% [mean +/- SEM] versus -14 +/- 6%, p less than 0.05). Thus, effects of endothelin on the production of cerebrospinal fluid are attenuated by cyclooxygenase products. Finally, responses to intraventricular endothelin were examined. Intraventricular endothelin produced a modest, but significant, reduction in the production of cerebrospinal fluid. CONCLUSIONS: In summary, endothelin may play a role in regulation of the brain fluid balance by affecting the rate of production of cerebrospinal fluid, and this effect is modulated by cyclooxygenase products.

Animals↗
PubMedDate not supplied

Correlated cholinomimetic-stimulated beta-endorphin and prolactin release in humans.

Previous studies, both in animals and humans, have demonstrated that the intravenous or intraventricular administration of endogenous opioids and opiates produce dose dependent increases in plasma concentrations of prolactin. Notably, in humans, intravenous infusion of centrally active cholinomimetic drugs, such as physostigmine or arecoline, may produce significant increases in plasma concentrations of prolactin and beta-endorphin immunoreactivity. In three separate studies, conducted collaboratively between the National Institute of Mental Health and the University of California at San Diego, physostigmine and arecoline associated increases in plasma concentrations of beta-endorphin immunoreactivity were highly correlated with increases in plasma prolactin concentrations. These results are of interest because centrally active cholinomimetic drugs have been variously reported either to have no effect, to increase, or to inhibit anterior pituitary prolactin release. We propose that cholinergic stimulation of hypothalamic beta-endorphin may represent an interesting example of peptidergic modulation of primary neurochemical effects on hypothalamic-pituitary hormonal regulation.

Endorphins↗
PubMed1984

Repetitive measurements of intracranial pressure in awake rabbits.

Previous measurements of the intracranial pressure in experimental animals suffer from acute and subacute effects of cannulation. In order to obtain reliable, repetitive or continuous values, we measured the intracranial pressures in awake rabbits with a new permanent adjustable ventricular cannula that included a separate entrance to the subarachnoid space. The mean intraventricular pressure ten days after the operation was 5.2 +/- 1.1 mmHg (SD) (70 animals). Manipulation of the cannula system and infusion of artificial cerebrospinal fluid did not damage the blood-brain barrier (indicated by extravasation of Evans Blue). The intracranial pressure was constant for as long as 6 months and as many as 22 separate measurements and infusions. The cerebrospinal fluid cells and protein content did not change in animals with permanent cannulae and in animals perfused with 2-4 ml artificial cerebrospinal fluid. In 30 animals the ventricular cannula functioned for 10-180 (median 65) days and the subarachnoid entrance for 11-23 (median 16) days.

Animals↗
PubMed1978

Left and right ventricular dimensions during ventricular fibrillation in the dog.

Ventricular dimensions by surface echocardiography and intraventricular pressures were monitored in 27 dogs before and during ventricular fibrillation (VF) induced by coronary embolization (nine dogs), potassium infusion (nine dogs) and calcium infusion (nine dogs). Left ventricular diameter (LVD) fell by an average of 10.3 mm during the first 30 s after the onset of VF induced by ischemia or potassium and remained smaller than the prefibrillation end-diastolic LVD during the ensuing 10 min. LVD fell during calcium infusion, and after the onset of VF it remained only slightly larger than the preinfusion end-systolic LVD. Right ventricular (RV) diameter increased progressively for the first 2 min during VF an average of 15.9 mm. The failure of LV size to increase during VF was explained by a pressure gradient inhibiting LV filling during the early phase of VF. Despite progressive RV filling, pressure in the more compliant RV remained lower than in the LV, which exhibited reduced compliance during VF. Therefore, cardiac dilation during VF appears to be confined to the RV, and inhibition to LV filling is an important feature of the syndrome.

Animals↗