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PubMed1982

Central control of peripheral circulating somatostatin in dogs: effect of 2-deoxyglucose.

Circulating plasma somatostatin concentrations are known to fluctuate in response to nutrients and hormones. However, little is known about neural or central nervous system (CNS) control of somatostatin secretion. To test whether peripheral circulating somatostatin is influenced by a central stimulus, 2-deoxyglucose (37.5 mg/kg) was infused into a lateral cerebral ventricle of six conscious dogs over a period of 15 min. Plasma somatostatin levels rose from a base line of 105 +/- 6 pg/ml (mean +/- SE) to a peak of 154 +/- 10 pg/ml (P less than 0.005) at 30 min after the onset of the infusion. Somatostatin levels were still significantly elevated (P less than 0.025) at 60 min (119 +/- 6 pg/ml) and thereafter gradually returned toward base line. Plasma glucose and glucagon levels increased in response to intraventricular 2-deoxyglucose. Glucose concentrations rose from 105 +/- 5 mg/dl to peak at 203 +/- 16 mg/dl (P less than 0.005) at 80 min and remained elevated to 120 min. The concentration of plasma glucagon increased from 41 +/- 6 to 92 +/- 18 pg/ml at 60 min (P less than 0.05) and then declined. In marked contrast to intraventricular 2-deoxyglucose, similar concentrations of 2-deoxyglucose administered intravenously (n = 4) resulted in a slight fall in plasma somatostatin. Intraventricular saline did not result in a change in plasma somatostatin. It is concluded that peripheral circulating somatostatin may be susceptible to central nervous system control.

Animals↗
PubMedDate not supplied

[Effect of intravenous verapamil in experimental ventricular arrhythmia].

Experimental ventricular tachycardias (VT) were provoked in dog hearts with minute crystals of aconitine introduced into the periphery of an infarcted area, produced by intramural injection of 1-1.5 ml of phenol. The response of these tachycardias to verapamil was studied. Leads II, aVL, intraventricular right and left unipolar records, as well as one on the superior vena cava were registered under control conditions, with VT and after the injection of the antiarrhythmic agent. This injection was infused into superior vena cava over 15-20 minutes. Records were obtained with constant intervals, waiting for the recovery of sinus rhythm (SR) and the posterior reappearance of ventricular tachycardia. The experiments were performed 6 to 8 hs with continuous infusion of Hartmann's solutions. Throughout these periods, the variations of systemic systolic pressure were registered. Of the 75 dogs treated with 0.2 mg/kg of verapamil, SR was recovered transiently in 30 (40%), while it exerted no antiarrhytmic effect in 19 (25%). Arterial systolic pressure fell importantly in 10 animals (13%). In 3 other groups, of 15 dogs each, comparative administration of verapamil vs lidocaine (I), vs mexiletine (II) and vs propafenone (III), was tried. In Group I, verapamil reestablished transient SR in 73% and lidocaine in only 7%; in II, SR resulted from verapamil in 33% and from mexiletine in 7%; in III, SR reappeared in 21% with verapamil and in 28% with propafenone. The repeated positive effect of verapamil was found in 33% of 15 experiments. This drug is effective in certain experimental ventricular tachycardias, probably related to calcium-dependent potentials.

Animals↗
PubMed1991

Measurement of left ventricular contractility using transesophageal echocardiography in patients undergoing coronary artery bypass grafting. The Study of Perioperative Ischemia (SPI) Research Group.

Optimal assessment of left ventricular function requires the use of load-independent indices of myocardial contractility, which often are difficult to obtain in patients undergoing coronary artery bypass graft (CABG) surgery. We have investigated whether the relation between left ventricular end-systolic stress (ESS) (derived from high-fidelity intraventricular pressure measurements and transesophageal-derived wall thickness) and end-systolic area (ESA) (derived from transesophageal echocardiography [TEE]) could provide a load-independent index of left ventricular function. We studied seven men undergoing coronary revascularization. Multiple data points at varied loading conditions were generated for each patient by infusions of sodium nitroprusside and phenylephrine during the period immediately after induction of general anesthesia and preceding surgical incision. While peak systolic blood pressure was pharmacologically altered between 78 and 204 mm Hg, the correlations between ESS and ESA were excellent for all patients (range r = 0.90 to 0.99). Additionally, the slopes of these relations showed a close correlation to their respective baseline thermodilution cardiac indices (r = 0.85, p = 0.02). Appropriate shifts of the ESS/ESA relationships were documented during postextrasystolic potentiation. The authors conclude that the left ventricular ESS/ESA correlation, derived using TEE and intraventricular pressure measurements, may provide a load-independent index of left ventricular inotropic state in patients undergoing CABG surgery.

Aged↗
PubMed2003

Dobutamine-inducible left ventricular obstruction: head-up tilt and autonomic balance.

BACKGROUND: Dobutamine-inducible left ventricular obstruction lacks a sound clinical meaning. This phenomenon may be related to an abnormal response of the heart to the sympathetic stimulation, and head-up tilt would elicit intraventricular obstruction in patients known to develop it during dobutamine administration, through the synergistic effects of reduced preload, hypercontractility, and reflex increase in the cardiac sympathetic tone. METHODS: Twenty-one patients with normal coronaries and available dobutamine stress-echocardiography underwent 60 degrees -head-up tilt on echocardiographic and electrocardiographic monitoring in drug-free and nitroglycerin infusion (0.3 mcg/kg/min) protocols. Twelve patients had (group 1: 7 males, aged 61+/-7 years), and nine had not (group 2: 3 males, aged 60+/-9 years) developed left ventricular obstruction during dobutamine stress-echocardiography. Doppler echocardiographic measurements of left ventricular diameters, function and outflow tract flow velocity were performed; power heart rate variability was analysed on short electrocardiographic recordings (low/high frequency ratio); plasma catecholamines were determined at baseline and during the tilt manoeuvres. RESULTS: Intraventricular obstruction did not develop in group 1. There were baseline differences in ventricular dimensions and mitral early-to-late velocity ratio between group 1 and 2, but hemodynamic behaviour during either tilt manoeuvre was similar. Low/high frequency ratio, that was similar at baseline and similarly increased on head-up tilt, increased significantly less on nitroglycerin-tilt in group 1. No difference in plasma catecholamines was found. CONCLUSIONS: Reflex cardiovascular adaptive responses as those elicited by passive tilt are not involved in dynamic intraventricular obstruction in dobutamine-inducible obstruction patients, data indicating that left ventricular geometry and hypercontractility are not sufficient pathophysiological determinants.

Adaptation, Physiological↗
PubMed1973

The hypothermic effect of tetrodotoxin in the unanaesthetized cat.

1. The hypothermic effect on unanaesthetized cats of tetrodotoxin injected I.V. or into the lateral cerebral ventricle was examined.2. At an ambient temperature (T(a)) of 22 degrees C, tetrodotoxin given intraventricularly was over 400 times more potent in lowering body temperature (T(b)) than when given I.V. The magnitude of the hypothermia was dose-dependent for both routes. Decreases in T(b) as great as 6.8 degrees C were induced by infusions or multiple injections of tetrodotoxin into the ventricle.3. Tetrodotoxin also lowered T(b) at T(a) = 13, 30 or 35 degrees C. Tachypnoea, which lasted for longer durations and which became more intense the higher the T(a), accompanied development of hypothermia. Shivering was observed only during recovery from hypothermia at 13 degrees C.4. During the tetrodotoxin-induced hypothermia, animals were still able to regulate against environmental thermal stresses.5. EDTA disodium salt, leucocytic pyrogen and prostaglandin E(1) antagonized the hypothermic effect of tetrodotoxin when they were administered during recovery from tetrodotoxin.6. Activation of heat-loss mechanisms, and the absence of compensatory shivering during development of hypothermia after tetrodotoxin administration, plus lowering of T(b) by tetrodotoxin at T(a) above as well as below the thermoneutral temperature, indicate that lowering of the thermoregulatory set-point is the mechanism by which centrally or peripherally administered tetrodotoxin lowers T(b). Further evidence for set-point lowering after intraventricular administration of tetrodotoxin is provided by persistence of the ability to regulate against both heat and cold stresses during hypothermia. The possibility that the decrease in set-point could be due to the well known action of tetrodotoxin to block transient increases in membrane sodium ion conductance is discussed in terms of a recent hypothesis regarding ionic control of the thermoregulatory set-point.

Animals↗
PubMed1986

Acute and chronic effects of amiodarone on ventricular refractoriness, intraventricular conduction and ventricular tachycardia induction.

In eight patients, the right ventricular effective refractory period, rate-dependent changes in intraventricular conduction (as reflected by QRS duration during ventricular paced cycle lengths of 600 to 250 ms) and results of programmed ventricular stimulation were determined in the control state, 5 minutes after the intravenous infusion of 10 mg/kg body weight of amiodarone and after 2 months of treatment with oral amiodarone. The right ventricular effective refractory period was 230 +/- 30 ms (mean +/- SD) in the control study, 248 +/- 27 ms after intravenous amiodarone (p less than 0.001) and 296 +/- 26 ms after oral amiodarone (p less than 0.001). In the control state, QRS duration was constant at all paced cycle lengths. Intravenous amiodarone resulted in a rate-dependent prolongation of QRS duration. This rate-dependent prolongation was markedly accentuated by oral amiodarone in six patients who had an elevated serum level of reverse triiodothyronine (T3) after 2 months of oral treatment, but it was not more pronounced than the effects of intravenous amiodarone in two patients with a normal reverse T3 serum level after oral therapy. Both intravenous and oral amiodarone either suppressed or modified the induction of ventricular tachycardia by programmed stimulation in some patients, but in a discordant fashion. The relative effects of intravenous and oral amiodarone on ventricular refractoriness and conduction and on ventricular tachycardia induction did not correlate with serum amiodarone levels. Chronic amiodarone therapy results in a marked prolongation in ventricular refractoriness compared with the relatively small but significant increase that occurs after intravenous amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

Simultaneous response of myocardial contractility and a major proteolytic process to beta-adrenergic-receptor occupancy in the Langendorff isolated perfused rat heart.

The Langendorff isolated rat heart was adapted to the study of minute-to-minute percentage changes in bulk protein degradation by using non-recirculating perfusion. Hearts were perfused at 8 ml/min at 35 degrees C with Krebs-Henseleit buffer containing 11 mM-glucose, and only hearts with regular ventricular rhythm were employed. Proteins were labelled by infusion of [3H]leucine for 0.5 h in vitro. A complete amino acid mixture was then added at 3 times normal rat extracellular concentrations. After labelling, the re-incorporation of [3H]leucine was competitively inhibited by addition of either 4 mM-leucine or 20 microM-cycloheximide. The residual unincorporated radioactivity and the preferentially labelled rapid-turnover proteins were eliminated during a 3 h preliminary perfusion period. The basal rate of release of [3H]leucine and percentage changes were then determined at 1 min intervals, by using each heart as its own control. Leucine metabolism was inconsequential to results. Exchange of intracellular leucine pools with extracellular leucine and subsequent release in effluent perfusate was 95% complete within approx. 2 min. The basal rate of protein degradation was unchanged by electrical stimulation of the heart rate to 360 beats/min or cessation of contractile activity by membrane depolarization under 25 mM-KCl. Infusion of the beta-agonist isoprenaline at 5-500 nM caused a graded inhibition of myocardial protein degradation within 5-6 min, with a maximum inhibition of 30%. This inhibition was sustained for at least 1 h of drug administration and was reversed within 4-6 min of cessation of isoprenaline or simultaneous infusion of 1 microM of the beta-receptor antagonist propranolol. Minute-to-minute adrenergic proteolytic control was a simultaneous co-variable with beta-receptor-mediated inotropic changes in right-intraventricular systolic pressure. Stoppage of the heart in asystole by the Ca2+-channel blocker nifedipine (0.7 microM) delayed the onset, but did not cause sustained reversal, of adrenergic-inhibited degradation, indicating the absence of a direct obligatory mechanistic linkage between the events of the contraction-relaxation cycle and protein degradation in this preparation.

Animals↗
PubMed1992

Myocardial function in immature and mature sheep with pressure-overload hypertrophy.

The effect of pressure-overload left ventricular hypertrophy (LVH) on myocardial function is controversial. A major factor in the controversy may be the age at which the pressure overload was induced. The goal of this study was to determine whether the age at which the LVH was induced affected systolic myocardial function. We studied lambs (n = 8) and sheep (n = 7) with LVH induced by constricting the ascending aorta and their sham-operated controls (n = 7 and n = 7). This new, unsedated, ovine model of LVH was large enough to accommodate chronic surgical implantation of instrumentation and the induction of pressure-overload hypertrophy in both young and adult age groups. Solid-state intraventricular pressure transducers and sonomicrometer crystal were used to assess instantaneous left ventricular pressure and dimensions. Myocardial contractility was assessed with midwall shortening at common preload and afterload. Load alterations were induced by graded infusion of methoxamine. There was depressed myocardial function in adult sheep with LVH compared with adult controls. Lambs with and without LVH had normal left ventricular myocardial function, similar to adult controls. Similar results were obtained in studies after beta-adrenergic receptor blockade. We conclude that maturation decreases the ability of the myocardium to maintain normal contractility in the presence of pressure-overload hypertrophy.

Adrenergic beta-Antagonists↗
PubMed2005

Ventricular metastasis resulting in disseminated intravascular coagulation.

BACKGROUND: Disseminated Intravascular Coagulation (DIC) complicates up to 7% of malignancies, the commonest solid organ association being adenocarcinoma. Transitional Cell Carcinoma (TCC) has rarely been associated with DIC. CASE PRESENTATION: A 74-year-old woman with TCC bladder and DIC was found to have a cardiac lesion suspicious for metastatic disease. The DIC improved with infusion of plasma and administration of Vitamin K, however the cardiac lesion was deemed inoperable and chemotherapy inappropriate; given the patients functional status. We postulate that direct activation of the coagulation cascade by the intraventricular metastasis probably triggered the coagulopathy in this patient. CONCLUSION: Cardiac metastases should be considered in cancer patients with otherwise unexplained DIC. This may influence treatment choices.

Journal Article↗
PubMed2001

Comparative tolerability of pharmacological treatments for patent ductus arteriosus.

The ductus arteriosus is a vascular channel which, although vital to the fetal circulation, rapidly becomes unnecessary and even deleterious after birth. As such, it is 'preprogrammed' to constrict within the first few hours of life. In infants born prematurely this natural closure is often delayed and/or ineffective. In this review, we summarise the current knowledge of the delicately orchestrated control of normal ductal closure, with emphasis on the role of various biochemical mediators. The major focus of this review, however, is on pharmacological approaches designed to prevent and/or treat the persistently patent ductus arteriosus (PDA) which often fails to constrict spontaneously in the premature infant. The standard treatment regimen is based on the administration of 3 doses of the nonselective cyclo-oxygenase inhibitor, indomethacin. We begin by examining, from the vantage point of the ductus, the use of this indomethacin as a tocolytic. It seems that antenatal administration of indomethacin can cause transient, reversible ductus constriction which renders the post-treatment ductus resistant to subsequent closure, both natural and therapeutic. We then review some of the pros and cons associated with the prophylactic administration of indomethacin. Although prophylactic indomethacin is aimed primarily at preventing intraventricular haemorrhages in premature neonates, it does tend to reduce the risk of PDA as well. We then describe some novel therapeutic approaches to effect ductal closure with indomethacin, including the use of continuous infusions to minimise toxic vasoconstrictive phenomena and the use of prolonged maintenance dose to prevent PDA recurrences. Finally we discuss some of the newer agents described more recently which play a role in closing the persistently patent ductus over the next decade. Most prominent of these is ibuprofen which some studies have shown to have less undesirable vasoconstrictive adverse effects. Studies which compare the use of ibuprofen to indomethacin are summarised.

Cyclooxygenase Inhibitors↗
PubMedDate not supplied

[The action of intravenous flecainide in experimental ventricular arrhythmias].

Experimental ventricular tachycardias were provoked in dog hearts with minute crystals of aconitine introduced into the periphery of an infarcted area, produced by intramural injection of 1-1.5 ml of phenol near the apex of left ventricle. The response of these tachycardias (VT) to flecainide was studied. Leads II, aVL, intraventricular right and left unipolar records, as well as one on the superior vena cava (SVC) were registered under control conditions, with VT and after the injection of this antiarrhythmic agent. This injection was infused into SVC over 15-20 minutes. Records were obtained with constant intervals, waiting for the recovery of sinus rhythm (SR) and the posterior reappearance of ventricular tachycardia. The experiments were performed 6 to 8 hs with continuous infusion of Hartmann' solutions. Throughout these periods, the variations of systemic systolic pressure were registered. Of the 22 dogs receiving 4 mg/kg of flecainide, transient SR was observed in 12 (55%), while in 4 (18%) this medication had no effect. Heart block presented in 2 animals and a fall of arterial pressure in 4. Of another 25 dogs receiving 2.5 mg/kg of flecainide, similar to clinical doses, transient SR appeared in 11 (44%), while in 3 (12%) SR was not observed. In other 2 groups, each of 15 dogs, the repeated antiarrhythmic action of flecainide was present in 33% with 4 mg/kg and in 20% with 2.5 mg/kg. This medication had no effect in 20% of the former and in 40% of the latter. However the low dose did not produce undesirable effects. Furthermore these differences were no significant statistically. Flecainide is effective in certain experimental ventricular tachycardias probably related to sodium-dependent potentials.

Aconitine↗
PubMed1992

Involvement of pertussis toxin sensitive G-proteins in conditioned fear-potentiated startle: possible involvement of the amygdala.

The present study evaluated the effects of intraventricular or intracerebral administration of pertussis toxin on fear-potentiated startle (a measure of conditioned fear) and shock sensitization (a measure of unconditioned fear). In Experiment 1 all animals were unilaterally implanted with cannulae into the lateral ventricle 1 week prior to 2 days of fear conditioning (ten light-shock pairings on each of 2 days). Five days later, animals were infused with either 1 microgram pertussis toxin or saline and tested for fear-potentiated startle 24 h after infusion and tested for shock sensitization 26 or 50 h after infusion. Pertussis toxin blocked the ability of a light conditioned stimulus to facilitate startle but did not alter the ability of acute footshock to increase startle amplitude in the same animals. In Experiment 2 bilateral infusion of 1 microgram pertussis toxin into the basolateral nuclei of the amygdala, but not the interpositus nuclei of the cerebellum, also blocked fear-potentiated startle when animals were tested 6 h after infusion. These findings suggest a role for pertussis toxin sensitive G-proteins, perhaps within the amygdala, in the expression of conditioned but not unconditioned fear.

Acoustic Stimulation↗
PubMed2001

Selective behaviors altered in plasminogen-deficient mice are reconstituted with intracerebroventricular injection of plasminogen.

In vitro studies demonstrate a role for the plasminogen (Plg) system in neurological function and recently in vivo studies show a role of the Plg system in neurodegeneration after the injection of an excitotoxic agent. Differences in the development of neurological function, however, have not been demonstrated in the Plg-deficient (Plg-/-) mice compared to wild-type (WT) mice. The role of Plg system in neurological function may relate to remodeling which occurs in response to various environmental challenges. In this study, behaviors (open field, grooming, hind-leg gait, water maze, and acoustic startle reflex) were tested in the Plg-deficient and WT mice at 6-8 weeks of age. Grooming, a response to the stress of an open field or fur moistening, was increased in the Plg-/--deficient mice compared to WT mice, and the acoustic startle reflex (ASR) was markedly decreased in the Plg-/- mice. The reduced ASR in Plg-/- mice occurred in mice with a mixed C57BL:129 background or in mice with a C57BL background. Plg was required for the ASR, since a deficiency of the Plg activators, urokinase (uPA) or tissue Plg activator (tPA), did not cause a reduction in the ASR compared to their WT control. Infusion of Plg directly into the brain was effective in restoring the ASR in the Plg-/- mice, but had no effect on the ASR of WT mice. Peripheral bolus injections of Plg or infusion into the jugular vein were ineffective in restoring the ASR in the Plg-/- mice. These results indicate that Plg is required for the appropriate response to the environmental challenge of a sudden loud sound, and that the response can be restored in Plg-/- mice by directly infusing Plg into the brain.

Animals↗
PubMed1982

[Transfer of fosfomycin into the cerebrospinal fluid].

After the fosfomycin (FOM) infusion, its levels in serum and cerebrospinal fluid (CSF) were repeatedly measured in 8 cases without meningitis. 1. The peak concentration of FOM in CSF was 15.5 micrograms/ml with the average of 10.3 micrograms/ml and was reached at 240 minutes with the average of 210 minutes after the infusion. The biological half life time of FOM in CSF was 2 to 6.5 hours. 2. The peak concentration in CSF was compared with it in serum. The average ratio was 4.3 per cent. Each area under the curve (AUC) of FOM concentration in CSF and serum was calculated and average of their ratio was 9.0 per cent. 3. In a case with middle cerebral artery aneurysm, FOM transferred into CSF with ease. The lowest diffusion into the CSF was shown in 2 cases of meningioma. In 3 cases of hypertensive intracerebral hemorrhage with intraventricular perforation, FOM moderately transferred into CSF.

Adolescent↗
PubMed2003

Exploring the role of Tractocile in everyday clinical practice.

The purpose of this retrospective study is to evaluate the effects of atosiban (Tractocile available in Austria since February 2000) for routine treatment of women with threatened preterm delivery. The advantage of this drug compared to other tocolytic agents is its specific action on reproductive tissues without the accompanying severe side effects. Women (n = 208) were retrospectively evaluated. Diagnoses at admission were preterm labour (n = 117), preterm rupture of membranes (n = 65), incompetent cervix (n = 19) and vaginal bleeding (n = 7). Gestational age was between weeks 21 and 33 of pregnancy. Preterm labour was defined as >/=4 uterine contractions/30 min and cervical length <30 mm examined by vaginal ultrasound and/or detection of vaginal fetal fibronectin. Tocolytic effectiveness was determined as the number of women having a diagnosis of preterm labour who were still pregnant after 48 hours and after 7 days. The influence on the frequency of contractions before and 3-12 hours after the start of treatment was assessed. Maternal side effects, perinatal and neonatal morbidity and transfers to the NICU were also evaluated. The proportion of women who remained undelivered was 78.7% after 48 hours, and 64.3% after 7 days. Atosiban decreased the frequency of contractions from 5.4/30 min before treatment to 1.6 contractions/30 min after the start of treatment. At the initial bolus application, 20.2% of women presented drug-related side effects, such as nausea, vertigo and flush over a short period of 1-2 minutes. During infusion, side effects possibly related to atosiban could be detected in 6% of women. Mean length of stay was 11.8 days in the NICU and 30.9 days in intermediate care. Twenty-three children developed intraventricular haemorrhage (I-IV). In conclusion, atosiban is an effective tocolytic drug in the treatment of preterm labour and preterm rupture of the membranes. It has significantly less side effects due to its lack of cardiovascular activity.

Drug Evaluation↗
PubMed1989

[Meningioma of the lateral ventricle. 3 recent cases].

Three recent cases of intra-ventricular meningiomas are reported. The incidence of this tumor type is very low, since they account for only 0.2% of all intra-cranial neoplasms and 2% of all intra-cranial meningiomas in the adult. In our first 2 cases, the meningioma involved the right trigonal area. In our third patient, a 14 year-old girl, the tumor had involved the left occipital horn. It is usually assumed that their development is a result of meningothelial inclusion bodies normally present in the arachnoid of the tela choroidea. As mentioned in previous reports, their clinical presentation may be that of paroxysmal increased intra-cranial pressure and a mechanism of trapped ventricular horn has been advocated. However, under such circumstances, an intraventricular bleeding seems to be a more likely mechanism. Despite their rarety, intra-ventricular meningiomas are usually diagnosed on C.T. It typically shows a hyperdense mass, attached to the plexus and enhancing after contrast infusion. In one of our patients (obs. 2), the meningioma manifested on M.N.R. by a low signal intensity in T1 sequences and by a high signal in T2 sequences. In our third patient, the M.N.R. findings were indicative of a cystic lesion lying in the occipital horn, but not of a meningioma, the diagnosis of which was made on further microscopic examination. The angiographic evaluation remains useful to document preoperatively the arterial supply to the meningioma, which is mainly from the postero-lateral choroïdal arteries. At operation, anterior meningiomas lying near the foramen of Monro are easily exposed through a transfrontal approach and raise no technical problem.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗