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PubMed1993

Emergent aneurysm clipping without angiography in the moribund patient with intracerebral hemorrhage: the use of infusion computed tomography scans.

The authors report their experience with 25 patients (mean age, 44.3 +/- 12.1 years) with an intracerebral hematoma (ICH) from a ruptured aneurysm who were emergently operated on without angiography. Instead, preoperative high-resolution infusion computed tomography (CT) scans were used to identify the aneurysm causing the hemorrhage. In all patients, the preoperative Glasgow Coma Scale score was < 5 and brain stem compression was evident. ICH was present in the frontal or temporal lobe and was often associated with intraventricular hemorrhage (n = 17) and significant (> 1 cm) midline shift (n = 18). Infusion CT scans correctly identified the aneurysm in all patients (middle cerebral artery, 18; posterior communicating artery, 2; carotid bifurcation, 3; anterior communicating artery, 2). Partial evacuation of the hematoma guided by infusion CT scan was usually required first to clip the aneurysm definitively using standard microvascular techniques. Intraoperative rupture occurred twice, and temporary clips were used on four occasions. Lobectomy (n = 8), decompressive craniotomy (n = 15), and ventriculostomy (n = 8) were required to control cerebral swelling. All patients underwent postoperative angiography to confirm aneurysm obliteration. Eleven unruptured aneurysms were subsequently identified. Nine had been predicted by infusion scan. Twelve patients survived, eight of whom were only moderately disabled and were independent at 6-months' follow-up. Of the 13 patients who died, all except one died within 4 days of admission. The authors conclude that although angiographic verification before aneurysm surgery is preferable, in the moribund patient with intracerebral hemorrhage, infusion CT scanning provides sufficient information concerning vascular anatomy to allow rational emergency craniotomy and aneurysm clipping.

Adult↗

PubMedDate not supplied

[Protective effect of glucose-insulin-potassium solutions in myocardial damage caused by emetine].

This study was carried out on 170 dogs. Cardiotoxic effects of doses of 15 mg/kg of emetine hydrochloride were studied in 20 dogs. 20 mg/kg of emetine hydrochloride were administered intravenously over 60 min. to the remaining 150 animals. These dogs were distributed in groups of 25. One group received emetine alone. Phleboclyses with saline serum, glucose-insulin-potassium, glocose-insulin, glucose-potassium and glucose serum alone, respectively, were administered to the other 5 groups during the emetine infusion and cardial contraction and several electrograms were recorded. Mean systolic blood pressure was measured continuously in the femoral artery. Observations covered a 4 hour period. During the infusion of emetine alone, ventricular myocardial contraction and systemic arterial pressure decreased abruptly. Intra-atrial, atrio-ventricular and intraventricular conduction disorders, as weel as primary ventricular repolarization changes, were also observed. At the end of this infusion, the Q-T interval increased 25% and the heart rate decreased 26% of the control values. In the group also receiving glucose-insulin-potassium solution, the fall of the ventricular contraction amplitude was significantly less than in animals given emetine alone. Primary ventricular repolarization changes were less evident. The mortality rate reached only 4 per cent. In conclusion, the doses of emetine hydrochloride employed here have depressive cardiocirculatory effects. Glucose-insulin-potassium solution, administered simultaneously with emetine, seems to have a favorable metabolic effect against the emetine cardiotoxicity. This protective action of the G-I-K solution is superior to that obtained with each component, administered separately, and with saline serum.

Animals↗

PubMed1982

Pharmacokinetics of methotrexate following intravenous and intraventricular administration in acute lymphocytic leukemia and non-Hodgkin's lymphoma.

A pharmacokinetic study of methotrexate (MTX) administered by the intravenous (IV) and intraventricular (via an Ommaya reservoir) route was performed in 16 children, 13 with acute lymphocytic leukemia (ALL) and three with non-Hodgkin's lymphoma. Five children with ALL were treated "prophylactically" for presumed subclinical central nervous system (CNS) leukemia. The remaining 11 patients were treated for overt meningeal involvement. MTX was administered intravenously at a dose of either 500 mg/m2 or 1500 mg/m2 with one third by rapid intravenous infusion and two thirds intravenously over 24 hours with leucovorin rescue. Intraventricular MTX was given in some treatment courses at a dose of 12 mg/m2. At either 500 mg/m2 or 1500 mg/m2, when given only IV, MTX results in a 100 fold higher concentration in plasma compared to cerebrospinal fluid (CSF). The plasma levels are three times higher with the 1500 mg/m2 dose compared to the 500 mg/m2 dose. After intraventricular administration of MTX, patients with overt CNS leukemia retained MTX in the CSF significantly longer than patients treated prophylactically. This may be due to abnormal transport of MTX out of the CSF in patients with meningeal disease.

Adolescent↗

PubMed1989

Electrophysiologic effects of cocaine on the canine ventricle.

To evaluate the electrophysiologic effects of cocaine on the ventricle, 12 conscious dogs were studied before and after a bolus and infusion of cocaine titrated to maximum tolerance or to an increase in the mean blood pressure by at least 15%. Plasma cocaine levels, blood pressure, and surface and intracardiac electrograms were recorded. Programmed electrical stimulation was performed from the right ventricle at drive cycle lengths of 400 and 350 ms with introduction of up to three extrastimuli. The right ventricular effective refractory period decreased by 10% (p less than or equal to 0.01) and the mean blood pressure increased by 19% (p less than or equal to 0.01). No sustained spontaneous or induced ventricular arrhythmias were recorded after cocaine administration. There were no significant changes in pacing threshold, intraventricular conduction, heart rate, QRS or QTc intervals. The cocaine dose infused was 2.1 +/- 1.0 mg/kg; cocaine plasma levels were 1969 +/- 959 ng/ml immediately after the bolus and 508 +/- 234 ng/ml at the end of the study. It is concluded that in a presumably normal canine heart and at the doses given that cocaine decreases right ventricular effective refractory period, does not change intraventricular conduction, and does not result in sustained spontaneous or induced ventricular arrhythmias.

Animals↗

PubMed1989

Evidence that central 5-hydroxytryptaminergic neurones are involved in the anxiolytic activity of buspirone.

1. A two-compartment exploratory test was used to assess the role of central 5-hydroxytryptaminergic neurones in the anxiolytic activity of buspirone in rats. 2. Buspirone 0.1 mg kg-1, administered subcutaneously 15 min before testing, significantly increased black-white transitions (BWT) in control rats but had no effect in animals injected intracerebroventricularly one week before with 150 micrograms 5,7-dihydroxytryptamine (in 20 microliters). 3. Infusion of buspirone in the median raphe (but not in the dorsal raphe) significantly enhanced BWT, at doses from 1 micrograms to 10 micrograms (in 0.5 microliters). Buspirone 5 and 10 micrograms, but not 1 microgram, administered in the median raphe, significantly enhanced motor activity of rats during the first 10 min of testing in the activity cages. 4. The effect on BWT of 5 micrograms buspirone in the median raphe was completely antagonized in animals which had received either 5,7-dihydroxytryptamine intraventricularly, 150 micrograms (in 20 microliters), one week before or an infusion of 0.1 microgram (in 0.5 microliter) (-)-propranolol in the same area 5 min before. (-)-Propranolol infused in the median raphe did not modify the effect of buspirone on locomotion. 5. Infusion of 5 micrograms buspirone (in 0.5 microliter) in the median raphe significantly enhanced punished responses in a conflict test with no effect on unpunished responding. Buspirone infused in the dorsal raphe had no effect on punished or unpunished responding over a wide dose range. 6. The results indicate that at the relatively low dose used in the present study buspirone produces an anxiolytic effect by acting on central 5-hydroxytryptaminergic neurones. It is likely that activation of 5-hydroxytryptamine1A-receptors in the median raphe is involved.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1990

Corticotropin-releasing factor produces fear-enhancing and behavioral activating effects following infusion into the locus coeruleus.

The present series of experiments tested the hypothesis that the behavioral activating and anxiogenic effects produced by intraventricular administration of corticotropin-releasing factor (CRF) may be mediated by noradrenergic neurons in the brain-stem locus coeruleus (LC). Results showed that infusion of CRF into the LC (100 ng) significantly increased nonambulatory spontaneous motor activity measured in photocell cages; ambulatory (i.e., locomotor) activity was not altered. In the modified Porsolt swim test, which examines arousal and agitation in a stressful situation, significant behavioral activation (i.e., decreased floating) was seen following infusion of CRF (10 ng) into the LC; a 500 ng dose of CRF was necessary to produce similar effects following infusion into the lateral ventricle. The results of these 2 tests suggest that the behavioral activating effects of CRF in the LC may be related to arousing or stress-related effects, rather than to increased locomotor activity per se. Anxiogenic activity was assessed in animals placed in an open field containing a small, darkened compartment. Infusion or CRF into the LC (1-100 ng) significantly increased the time spent in the compartment and decreased the amount of time spent exploring the outside of the compartment or venturing into the inner squares of the open field, all indices of anxiogenic behavior. Biochemical studies showed that bilateral infusion of CRF into the LC produced significant increases in the concentration of the norepinephrine metabolite 3,4-dihydroxyphenylglycol in such forebrain projection areas of the LC as the amygdala and posterior hypothalamus. These data, taken together, suggest that CRF produces its behavioral activating and anxiogenic effects, at least in part, by increasing the activity of LC noradrenergic neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1998

Haemodynamic effects of a sixty minute infusion of dopamine hydrochloride in horses anaesthetised with halothane.

To describe the haemodynamic effects of a 60 min infusion of dopamine 4 microg/kg bwt/min during halothane anaesthesia, 7 mature Thoroughbred horses were studied. The infusion began 1 h after induction of anaesthesia by romifidine (100 microg/kg) and ketamine (2.2 mg/kg bwt). Throughout the period of dopamine infusion and for 30 min after its discontinuation, the horses were ventilated by intermittent positive pressure to maintain PaCO2 between 4.6-5.4 KPa. Inspired halothane concentration was adjusted to maintain an end tidal halothane concentration of 0.9%. Haemodynamic variables were measured using intracardiac strain gauge transducers sited in the left and right ventricle, aorta, and pulmonary artery. Left ventricular pressure was differentiated to obtain maximal rate of increase of intraventricular pressure (LVdp/dtmax). Transoesophageal Doppler echocardiography was performed to measure maximum aortic blood flow velocity (vmax) and acceleration (dv/dtmax), left ventricular velocity time integral (vTI) and cardiac output (CO), and left ventricular pre-ejection period (PEP) and ejection time (ET). Measurements were made during the 60 min infusion, and for 30 min after the infusion was discontinued. Infusion of dopamine 4 microg/kg/min significantly decreased mean aortic pressure, while left and right ventricular end-diastolic pressure and mean pulmonary artery pressure remained unchanged. There was a small, but significant, increase in heart rate during dopamine infusion. Maximum acceleration of aortic blood flow, CO and vTI were also significantly increased by dopamine infusion. Maximal rate of increase of intraventricular pressure (LVdp/dtmax) was significantly decreased 10 min after commencing infusion, but then returned to baseline for the remainder of the study. Left ventricular pre-ejection period (PEP) decreased during dopamine infusion whilst ejection time (ET) significantly increased. All measured variables except LVET had returned to baseline values within 30 min of discontinuing the infusion. This study demonstrated beneficial effects of dopamine infusion upon left ventricular systolic function. However, the therapeutic value of the drug is likely to be limited in clinical anaesthesia due to the simultaneous falls in arterial blood pressure which accompany its administration.

Anesthesia, Inhalation↗

PubMed2000

Umbilical artery catheters in the newborn: effects of heparin.

BACKGROUND: This section is under preparation and will be included in the next issue. OBJECTIVES: To determine whether the use of heparin in fluids infused through an umbilical arterial catheter in newborn infants influences the frequency of clinical ischemic events, catheter occlusion, aortic thrombosis, intraventricular hemorrhage, hypertension, death, or the duration of catheter usability. SEARCH STRATEGY: Randomized and quasi randomized controlled trials of umbilical catheterization use were obtained from the following sources: 1. Effective Care of the Newborn Infant, edited by JC Sinclair and MB Bracken. 2. Medline Search using Melvyl Medline Plus and the keyword headings 'Umbilic#', 'Catheter#' and subject heading 'Infant, Newborn' 3. Search of personal data files SELECTION CRITERIA: Randomized trials in newborn infants of any birthweight or gestation. Comparison of heparinised to non heparinised infusion fluids, including comparison of heparin in the infusate to heparin just in the flush solution. Clinically important end points such as catheter occlusion or aortic thrombosis. DATA COLLECTION AND ANALYSIS: There were five randomized controlled trials retrieved. All gave details of the incidence of catheter occlusion. Two also reported the incidence of aortic thrombosis. The intervention was reasonably consistent: heparin in the infusate at a concentration of 1 unit/mL was investigated in all trials except one which used a concentration of 0.25 units/mL. Studies generally included both term and preterm infants. MAIN RESULTS: Heparinization of the infusate decreases the incidence of catheter occlusion but does not affect the frequency of aortic thrombosis. Heparinization of the flush solution is not an adequate alternative. There does not appear to be an effect on frequency of intraventricular hemorrhage, death or clinical ischemic phenomena. REVIEWER'S CONCLUSIONS: Heparinization of the fluid infused through an umbilical arterial catheter decreases the likelihood of umbilical arterial catheters occluding. The lowest concentration tested so far (0.25 units/mL) has been shown to be effective. Heparinization of flushes without heparinizing the infusate is ineffective. The frequency of aortic thrombosis has not been shown to be affected; however, the confidence intervals for this effect are very wide. The frequency of intraventricular hemorrhage has not been shown to be affected by heparinization of the infusate, but again the confidence intervals are very wide and even a major increase in the incidence of grade 3 and 4 intraventricular hemorrhage would not have been detected.

Anticoagulants↗

PubMed2006

CP-154,526, a CRF type-1 receptor antagonist, attenuates the cue-and methamphetamine-induced reinstatement of extinguished methamphetamine-seeking behavior in rats.

RATIONALE: Previous studies from our laboratory and others have indicated a role for the hypothalamo-pituitary-adrenal (HPA) axis in the extinction/reinstatement animal model of cocaine relapse OBJECTIVE: This present study was designed to investigate the potential role for the HPA axis in the cue- and methamphetamine-induced reinstatement of extinguished methamphetamine-seeking behavior by determining the effects of ketoconazole and the corticotropin-releasing hormone (CRF) type 1 receptor antagonist, CP-154,526, on these behaviors. MATERIALS AND METHODS: Male Wistar rats were trained to self-administer methamphetamine (0.03 mg/kg/infusion). The delivery of methamphetamine was paired with the presentation of a tone and the illumination of a house light. Once stable responding was reached, the rats were placed into extinction. The effects of pretreatment with ketoconazole (25, 50, or 100 mg/kg, i.p.) or CP-154,526 (20 or 40 mg/kg, i.p.; 3 micro g, i.c.v) on cue-induced reinstatement were then evaluated. RESULTS: Cue-induced reinstatement was not significantly attenuated by pretreatment with peripherally administered CP-154,526 or by pretreatment with ketoconazole. However, centrally administered CP-154,526 (3 micro g, i.c.v.) significantly attenuated cue-induced reinstatement. In a separate group of rats, CP-154,526 (20 mg/kg, i.p.) attenuated methamphetamine-induced reinstatement (0.12 mg/kg priming infusion); whereas a higher dose (40 mg/kg) was necessary to attenuate reinstatement induced by a priming infusion of 0.24 mg/kg/infusion. Ketoconazole (50 mg/kg) did not affect reinstatement induced by a 0.12 mg/kg priming infusion and, therefore, was not tested at the higher methamphetamine priming dose. CONCLUSIONS: These data suggest an important role for CRF in the cue- and methamphetamine-induced reinstatement of extinguished methamphetamine-seeking behavior.

Amphetamine-Related Disorders↗

PubMed1991

Androgen-dependent vasopressinergic neurotransmission attenuates interleukin-1-induced sickness behavior.

Castrated male rats were found to be more sensitive than intact male rats to the depressing effects of recombinant human interleukin-1 beta (Il-1) on social exploration. This was the case whether Il-1 was injected acutely (1-5 micrograms/rat, i.p.) or continuously, via an implanted osmotic mini-pump (2 micrograms Il-1 per day). In this latter case, tolerance developed more rapidly to the behavioral effects of Il-1 than to its effects on body weight. Since there is evidence that extrahypothalamic arginine vasopressin (AVP) acts as an endogenous antipyretic in the brain and the local concentration of AVP is dependent on circulating androgens, we tested the hypothesis that the enhanced sensitivity of male rats to the behavioral effects of Il-1 was caused by a reduced brain concentration of vasopressin. Central injection of AVP (2.5 ng, i.c.v.) attenuated the behavioral effects of Il-1 (5 ng, i.c.v.) and this effect was more marked in castrated than in intact male rats. Conversely, central injection of an antagonist of the vasopressor receptors of AVP, dPTyr(Me)AVP (15 ng, i.c.v.) potentiated the behavioral effects of Il-1 (1 ng, i.c.v.) in intact but not in castrated male rats. These results are consistent with the possibility that androgen-dependent vasopressinergic neurons oppose the neural effects of Il-1.

Androgens↗

PubMed1984

Proglumide: selective antagonism of the rumination but not gastric motor effects induced by pentagastrin in sheep.

The effect of intravenous (IV) vs intracerebroventricular (ICV) administrations of pentagastrin on gastro-intestinal motility and rumination were investigated by electromyography in sheep; these effects were compared to those obtained after a previous IV or ICV injection of proglumide. When ICV administered at a dose of 20 ng X kg-1, pentagastrin did not significantly affect the frequency of reticular and abomasal spiking activity but elicited a 13 to 37 min period of rumination after a delay of 23 +/- 7 min. In contrast, when IV infused at a rate of 20 ng X kg-1 X h-1 during 20 min, pentagastrin inhibited significantly the frequency of reticular and abomasal contractions for 30 to 40 min but did not induce rumination. Proglumide ICV administered (0.8 mg X kg-1) abolished the rumination induced by central injection of pentagastrin whereas a 10 times higher dose administered systemically (8 mg X kg-1 IV) did not block these effects. Both of ICV and IV administrations of proglumide at respectively 0.8 and 8 mg X kg-1 were unable to antagonize the inhibitory effects of pentagastrin on reticulum and abomasum motility. It was concluded that (i) pentagastrin acts centrally to induce rumination and that (ii) proglumide selectively blocks these effects but not the pentagastrin induced gastro-intestinal hypomotility.

Abomasum↗

PubMed1998

Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) receptor antagonist attenuates lithium chloride-induced c-Fos induction in rat brainstem.

Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) and intraperitoneal (i.p.) injection of lithium chloride (LiCl) produce similar patterns of c-Fos induction in the rat brain. These similarities led us to assess the hypothesis that neuronal activity caused by i.p. injection of LiCl involves activation of central GLP-1 pathways. We therefore determined if third-ventricular (i3vt) infusion of a GLP-1 receptor antagonist would block LiCl-induced c-Fos expression in the brainstem. Relative to rats pretreated with i3vt infusion of vehicle, pretreatment with the potent GLP-1 receptor antagonist, des His1 Glu9 exendin-4 (10.0 microgram), significantly attenuated LiCl-induced (76 mg/kg; i.p.) c-Fos expression in several brainstem regions, including the area postrema, the nucleus of the solitary tract, and the lateral parabrachial nucleus. While central infusion of des His1 Glu9 exendin-4 also blocked GLP-1-induced (10.0 microgram) anorexia and c-Fos expression, the antagonist produced no independent effects on food intake or c-Fos expression. These results suggest that LiCl-induced c-Fos expression in the rat brainstem is mediated, at least in part, by GLP-1 receptor signaling.

Animals↗

PubMed1997

Deep cervical lymph flow following the infusion of mannitol in rabbits.

Jugular lymph flow of anesthetized rabbits in response to infusion of mannitol solutions differing in osmolarity were measured. Either an isotonic (310 mosmol), hypotonic (100 mosmol), or hypertonic (605 mosmol) mannitol solution was infused into either the internal carotid artery (ICA) or the right lateral ventricle (RLV). Lymph was collected continuously and measured over a 60 min preinfusion period, as well as during mannitol infusion and intermittent recovery periods. The mean peak flow rates of hypertonic infusion for the first 30 min via ICA and RLV were 2.2 +/- 0.4 (12% decrease) and 5.0 +/- 1.0 microliter/min (72% increase), over those of isotonic infusates which were 2.5 +/- 0.3 microliters/min (via ICA) and 2.9 +/- 0.5 microliters/min (via RLV), respectively. In contrast, lymph flow rates of hypotonic infusate for the first 30 min via ICA and RLV were 3.9 +/- 0.8 microliters/min and 2.3 +/- 0.4 microliters/min, respectively. A decrease both in intracranial pressure and in lymph flow following hypertonic mannitol infusion via ICA were observed. However, intracranial pressure and lymph formation were increased following hypertonic infusion via RLV. The results indicate that the changes in jugular lymph flow could be affected by the changing in osmolarity of mannitol infusate.

Animals↗

PubMedDate not supplied

Hyperglycemia and retinopathy of prematurity in very low birth weight infants.

OBJECTIVE: Retinopathy of prematurity (ROP) remains a leading cause of morbidity in the very low-birth-weight (VLBW) infant. This study investigates a possible association between serum/blood glucose and the development of ROP. METHODS: A retrospective case-control study of all infants born between 1992 and 1997 at the Johns Hopkins Hospital with birth weights less than 1000 g who developed Stage 3 or 4 ROP was conducted. Controls either had Stage 1 ROP or no eye disease and were matched 2:1 with ROP patients for gestational age, birth weight and year of birth. Odds ratios (ORs) of ROP were calculated for multiple exposures over the first month after birth, including oxygen concentration (FiO(2)), blood glucose levels, vitamin E, mean airway pressure and mean blood pressure. RESULTS: In a simple logistic regression analysis, we found an increased ROP risk for: (1) each 10 mg/dl increase of mean glucose (OR 1.96; 95% CI 1.13 to 3.42), (2) each 1% increase of mean FiO(2) (OR 1.06; 95% CI 1.004 to 1.13), (3) history of dopamine infusion (OR 5.4; 95% CI 1.16 to 25.2) and (4) intraventricular hemorrhage Grade 3 or 4 (OR 7.3; 95% CI 1.53 to 34.7). Using a multiple regression model, we found an increased ROP risk for each 10 mg/dl increase of mean glucose (OR 2.7; 95% CI 1.003 to 7.27). Each IU/kg/day of vitamin E supplementation reduced ROP risk (OR 0.37; 95% CI 0.16-0.86). CONCLUSION: In this study, we could demonstrate that glucose levels in the first month of life are associated with the development of ROP. Further studies have to determine if this association is causal or if hyperglycemia is just an expression of severity of illness.

Case-Control Studies↗

PubMed2000

Opposite effects of myocardial stretch and verapamil on the complexity of the ventricular fibrillatory pattern: an experimental study.

An experimental model is used to analyze the effects of ventricular stretching and verapamil on the activation patterns during VF. Ten Langendorff-perfused rabbit hearts were used to record VF activity with an epicardial multiple electrode before, during, and after stretching with an intraventricular balloon, under both control conditions and during verapamil (Vp) infusion (0.4-0.8 mumol). The analyzed parameters were dominant frequency (FrD) spectral analysis, the median (MN) of the VF intervals, and the type of activation maps during VF (I = one wavelet without block lines, II = two simultaneous wavelets with block lines, III = three or more wavelets with block lines). Stretch accelerates VF (FrD: 22.8 +/- 6.4 vs 15.2 +/- 1.0 Hz, P < 0.01; MN: 48 +/- 13 vs 68 +/- 6 ms, P < 0.01). On fitting the FrD time changes to an exponential model after applying and suppressing stretch, the time constants (stretch: 101.2 +/- 19.6 s; stretch suppression: 97.8 +/- 33.2 s) do not differ significantly. Stretching induces a significant variation in the complexity of the VF activation maps with type III increments and type I and II decrements (control: I = 17.5%, II = 50.5%, III = 32%; stretch: I = 7%, II = 36.5%, III = 56.5%, P < 0.001). Vp accelerates VF (FrD: 20.9 +/- 1.9 Hz, P < 0.001 vs control; MN: 50 +/- 5 ms, P < 0.001 vs control) and diminishes activation maps complexity (I = 25.5%, II = 60.5%, III = 14%, P < 0.001 vs control). On applying stretch during Vp perfusion, the fibrillatory process is not accelerated to any greater degree. However, type I and II map decrements and type III increments are recorded, though reaching percentages similar to control (I = 16.5%, II = 53%, III = 30.5%, NS vs control). The following conclusions were found: (1) myocardial stretching accelerates VF and increases the complexity of the VF activation pattern; (2) time changes in the FrD of VF during and upon suppressing stretch fit an exponential model with similar time constants; and (3) although stretching and verapamil accelerate the VF process, they exert opposite effects upon the complexity of the fibrillatory pattern.

Animals↗

PubMed1999

Prostaglandin E2 mediates activation of hypothalamic histamine by interleukin-1beta in rats.

The present study was designed to investigate the effects of peripheral interleukin-1beta (IL-1beta) on hypothalamic histamine (HA) systems. Intraperitoneal injection of IL-1beta increased the turnover rate of hypothalamic HA, which was assessed by accumulation of tele-methylhistamine after pargyline treatment. IL-1beta increased the activities of both histidine decarboxylase (HDC), an HA synthesizing enzyme, and HA-N-methyltransferase (HMT), an HA catabolizing enzyme. Pretreatment with indomethacin completely blocked the effects induced by IL-1beta on hypothalamic HA. Infusion of prostaglandin E2 (PGE2) into the third cerebroventricle increased the hypothalamic HA turnover rate, and simultaneously activated both HDC and HMT dose-dependently, but intravenous infusion of PGE2 had no effect on the dynamics of hypothalamic HA turnover. These results indicate that hypothalamic PGE2 activated by peripheral administration of IL-1beta, but not by peripheral PGE2, may enhance synthesis and release of hypothalamic HA by activation of HDC, and may facilitate degradation of extracellular histamine by activation of HMT.

Animals↗

PubMed1980

[Influence of sorbitol and mannitol on intracranial pressure (author's transl)].

The intracranial pressure was measured by an intraventricular catheter in 53 patients, in the course of 156 infusions of 40% Sorbitol and 72 infusions of 20% Mannitol. The amounts given and the rate of infusion were varied. The results show that the rate of the infusion is decisive in determining the fall in intracranial pressure, while the duration of the fall is dependent on the amount injected. After Sorbitol the influence on lowering the pressure was more marked and longer lasting than after injections of Mannitol. As a possible treatment for raised intracranial pressure one may conclude that small amounts given over a shorter time (50-80 ml/5 min) produce the most favourable effect.

Dose-Response Relationship, Drug↗

PubMed1994

Effects of pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) on prolactin, luteinizing hormone and growth hormone secretion in the ewe.

This study was undertaken to investigate the roles of PACAP and VIP in the control of pituitary hormone secretion in the ewe. The first experiment was designed to identify any direct effects at the level of the pituitary and was conducted during the luteal phase of a prostaglandin-synchronized oestrous cycle. PACAP (0.008, 0.04, 0.2 and 1.0 nmol/min) or VIP (0.06, 0.2, 0.6 and 1.8 nmol/min) was infused into the carotid artery over a 10 min period. Blood samples were taken before and after the infusions so that plasma PRL, LH and GH concentrations could be measured. Blood pressure was also monitored to determine if the doses used were biologically active. In no case was an effect on hormone secretion observed. In contrast, the highest dose of each peptide induced an increase in heart rate to almost three-fold the resting value. Although both peptides are active in vivo, this result suggests that neither peptide has a direct effect on hormone release from the pituitary of prostaglandin-synchronized ewes. In a second experiment, we investigated whether the peptides had central effects on hormone secretion. Intracerebroventricular (ICV) injection of PACAP or VIP at the dose 10 nmol was tested in ovariectomized ewes. After injection, PACAP suppressed PRL and GH secretion so that plasma hormone concentrations from 1-3 h after injection were significantly different from the control (P < 0.05 for PRL, P < 0.01 for GH). In addition, PACAP significantly reduced mean LH concentration (P < 0.05) and LH pulse frequency (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗