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PubMed1992

[Left intraventricular gradients measured by Doppler echocardiography at rest, during exercise and during isoproterenol test in hypertrophic cardiomyopathy].

Doppler echocardiography has been shown to be an accurate method of assessing left ventricular outflow obstruction in hypertrophic cardiomyopathy (HCM). One of the characteristics of this pressure gradient is its variability and, therefore, we measured this parameter during dynamic exercise testing in 33 patients. The results were compared with those recorded during isoproterenol infusion, the reference stress test for patients with HCM. Submaximal exercise in the recumbent position is usually well tolerated and resulted in a 43% increase in heart rate and a 47% increase in pressure gradient. There was a significant correlation between resting and exercise outflow obstruction (r = 0.90; p = 0.001). Moreover, exercise echo revealed obstruction in 26% of patients without resting pressure gradients (latent obstruction). The interpretation of results obtained with isoproterenol infusion is more difficult: this test resulted in an important increase in the left ventricular pressure gradient (231%) and "revealed" obstruction in 84% of cases. Therefore, we believe that exercise is more physiological and better tolerated than isoproterenol stress infusion and should be adopted as the investigation of choice in HCM even without obstruction at rest. If it is not possible to perform the exercise or no outflow tract obstruction can be demonstrated, an isoproterenol infusion may be used but this is not always well tolerated and the results should be interpreted with caution.

Cardiomyopathy, Hypertrophic↗
PubMed1996

Endogenous adenosine increases O2 utilisation efficiency in isoprenaline-stimulated canine myocardium.

OBJECTIVE: We have previously demonstrated that myocardium is capable of down-regulating its O2 requirements and thus avoiding ischaemia when O2 supply is limited. The present study tested the hypothesis that endogenous adenosine produced this protective response when O2 supply was decreased by moderate coronary hypoperfusion or moderate coronary hypoxaemia. METHODS: In anaesthetised dogs, hearts were exposed by left thoracotomy and instrumented for measuring intraventricular pressure and regional myocardial segment length. The left anterior descending coronary artery was isolated, cannulated, and extracorporeally perfused. Coronary O2 supply was moderately reduced by lowering coronary perfusion pressure from 100 to 60 mmHg or by lowering coronary arterial O2 content by 50%. Hearts were treated with intracoronary infusions of adenosine, adenosine deaminase to degrade endogenous adenosine or with erythro-9-(2-hydroxy-3-nonyl)-adenine x HCl (EHNA) to inhibit adenosine degradation by endogenous adenosine deaminase, during beta-adrenergic stimulation with isoprenaline. Cardiac power in the left anterior descending perfusion territory was indexed by the product of heart rate x left ventricular peak systolic pressure x percent systolic segment shortening. O2 utilisation efficiency was taken as the ratio of power index/myocardial O2 consumption. RESULTS: Prior to a reduction in O2 supply, isoprenaline did not alter O2 utilisation efficiency. Intracoronary adenosine increased O2 utilisation efficiency during isoprenaline stimulation by 23% (P < 0.05). EHNA slightly increased O2 utilisation efficiency during isoprenaline stimulation (10%; P < 0.05); adenosine deaminase was without effect. When coronary perfusion pressure was decreased, adenosine deaminase sharply lowered cardiac power and O2 utilisation efficiency during isoprenaline stimulation, whereas EHNA augmented isoprenaline-enhanced power and increased efficiency. During hypoxaemia, adenosine deaminase lowered regional power but not efficiency during isoprenaline infusion; EHNA did not affect power but lowered O2 consumption and increased efficiency. Myocardial lactate extraction and contractile function during isoprenaline stimulation were not attenuated by reduced O2 supply, indicating that myocardial ischaemia did not occur under these conditions. CONCLUSION: Endogenous adenosine increases myocardial O2 utilisation efficiency during beta-adrenergic stimulation, and thus helps avert ischaemia when myocardial O2 supply is reduced.

Adenine↗
PubMedDate not supplied

The electrophysiologic effects of nicardipine hydrochloride in man.

Nicardipine hydrochloride is an investigational antianginal calcium channel blocking agent with potent vasodilating properties. To study its acute electrophysiological effects in man, 12 patients (mean age 66, range 58-84), 6 with normal conduction and 6 with bifascicular block were evaluated. Each subject underwent electrophysiologic studies before and after a bolus and an intravenous infusion of nicardipine titrated to lower the mean blood pressure by at least 10%. The actual drop in mean blood pressure was 17% (p less than .01). The mean bolus was 2.2 +/- 1.2 mg (mean +/- standard deviation). The infusion rate was .21 +/- .06 mg/min. The drop in mean blood pressure was associated with an increase in heart rate of 13% (p less than .01). Maximum sinus node recovery time and sinoatrial conduction time decreased (p less than .01). The QT interval decreased (p less than .01), although the corrected QT remained unchanged. There was a tendency for a decrease in the atrioventricular nodal effective refractory period, functional refractory period, paced atrioventricular and ventriculoatrial conduction times. Intra-atrial, intraventricular and infranodal conduction times did not change. The administration of intravenous nicardipine produces hemodynamic effects consistent with arteriolar vasodilatation and a reflex sympathetic increase in heart rate. Except for the changes in sinus node function, the lack of marked electrophysiologic effects with intravenous nicardipine suggests that reflex sympathetic activity masks its direct slow channel blocking electrophysiologic effects in man.

Aged↗
PubMed1989

Limited neocortical devascularizing lesions causing deficits in memory retention and choline acetyltransferase activity--effects of the monosialoganglioside GM1.

In mature rats with unilateral cortical lesions, choline acetyltransferase activity was found to decrease by 40% in the ipsilateral nucleus basalis magnocellularis, compared with control animals. Intraventricular administration of the monosialoganglioside GM1 (5 mg/kg per day), via minipumps, over a period of 14 days prevented this fall in choline acetyltransferase activity. The activity of this enzyme in the sham operated subjects was not significantly different from that in the unoperated group. This biochemical data is in full agreement with regards to the protective action of monosialoganglioside GM1 on forebrain cholinergic neurons. In this study the behavioral effects of these cortical lesions were investigated for the first time. Results show that these lesions, with their associated retrograde neuronal degenerative effects, altered a variety of sensorimotor and memory-based behaviors. In particular, the limited unilateral devascularization of the neocortex increased baseline locomotor activity above control; affected motor coordination; impaired passive avoidance retention and reacquisition; and decreased the retention of learnt Morris water-maze information. Infusion of the monosialoganglioside into the ventricles, whilst having no effect on the increased motor activity or motor coordination deficit, did enhance the reacquisition of information in both memory-related tasks.

Animals↗
PubMed1980

Inhibition of lordotic behavior in female rats following intracerebral infusion of anticholinergic agents.

Cholinergic antagonists were bilaterally infused into forebrain areas of ovariectomized female rats brought into sexual receptivity by administration of estrogen and progesterone. Infusion of hemicholinium-3 (HG-3, 5 or 7.5 micrograms/cannula), an acetylcholine synthesis inhibitor believed to interfere with choline uptake, decreased the incidence of lordotic behavior displayed by females. This inhibition was prevented by infusion of choline chloride (120 micrograms/cannula) along with HC-3. Atropine sulfate, an acetylcholine receptor blocker, also reduced lordotic behavior in females following intracerebral infusion (20 micrograms/cannula). These results lend support to the suggestion that lordotic behavior is facilitated by central cholinergic activity.

Animals↗
PubMed1997

ICV beta-hydroxybutyrate: effects on food intake, body composition, and body weight in rats.

This study examined the effect of long-term intracerebroventricular (ICV) infusion of beta-hydroxybutyrate (beta HB) on food intake, diet selection, body weight, and body composition in rats. Female rats were divided into 2 groups and implanted with a 28-day osmotic pump connected to a lateral cerebroventricular cannula. One group was infused with artificial cerebrospinal fluid (aCSF) and the other with beta HB for 28 days. The rats had free access to both a high-fat/low-carbohydrate and a low-fat/high-carbohydrate diet (isocaloric) for the 28-day infusion period. The group infused with beta HB had a significantly lower body weight gain during the infusion period. Cumulative food intake increased in the same manner in both groups. Fat pad weights and carcass lipid content were significantly higher in beta HB rats, despite the equivalent caloric intake in both groups and the decreased body weight. Our observations are in accord with earlier studies indicating that beta HB infused ICV reduces body weight, but not necessarily food intake. Increased adiposity in association with decreased body weight change in beta HB-infused rats strongly suggests that energy is being partitioned to fat deposition at the expense of lean tissue growth when ketone bodies are infused into the cerebroventricles.

3-Hydroxybutyric Acid↗
PubMed2002

Glutamate infusion coupled with hypoxia has a neuroprotective effect in the rat.

Traumatic brain injury leads to a rise in glutamate, interference with oxygen supply and secondary neuronal death in the region surrounding the primary lesion. In the present experiments we have examined the effect of combining glutamate infusion with hypoxia on both brain metabolism and neuronal death. We have used microdialysis in unanaesthetised rats with a novel dual assay for glucose and lactate to monitor the temporal relation of changes in these metabolites resulting from infusion of 100 mM glutamate alone or combined with a reduction of inspired oxygen to 8%. In a parallel series of experiments we have compared the size of neuronal lesions under the same experimental conditions. We have used MAP2 antibody staining to measure the size of the neuronal lesion. Our results demonstrate that a 30 min glutamate infusion causes an immediate increase in neuronal glucose utilisation and a rise in lactate production. When hypoxia is added during the last 15 min of glutamate infusion there is a small rise in glucose and a large additional increase in lactate. The size of the neuronal lesions produced by infusion of 100 mM glutamate is reduced by the addition of hypoxia.

Animals↗
PubMed1986

Saralasin blocks the effect of angiotensin II and extracellular fluid saline expansion on the Na-K-ATPase inhibitor release in rats.

A low molecular weight substance which behaves like ouabain as inhibitor of brain membrane Na-K-ATPase and 3H-ouabain binding was found in plasma after saline expansion of extracellular fluid or angiotensin II infusion into the third brain ventricle in the rat. Intracerebroventricular infusion of angiotensin II antagonist, saralasin, blocks the increase of the Na-K-ATPase inhibitor produced by infusion of angiotensin II into the third ventricle or extracellular fluid saline expansion.

Angiotensin II↗
PubMed1982

Inhibition of acetylcholine turnover rate in rat hippocampus and cortex by intraventricular injection of adenosine analogs.

The effects of i.c.v. administration of adenosine receptor agonists and antagonists on the turnover rate of acetylcholine (TRACh) in various areas of the rat brain were examined in an effort to better understand the role of adenosine as a neuromodulator or cotransmittr. TRACh was determined by gas chromatographic-mass fragmentographic analysis of the rate of deuterium incorporation into ACh and choline during a constant rate infusion of deuterated phosphorylcholine. The i.c.v. administration of the adenosine receptor agonist, 2-chloroadenosine (2-CIAdo), in a dose of 82 nmol failed to change the ACh or choline content of any of the brain areas examined. This dose of 2-CIAdo elicited significant reductions in the TRACh in both the hippocampus and frontal cortex, but not in the striatum. The extent of the TRACh reduction was 67 and 36% in hippocampus and cortex, respectively. This inhibition of TRACh elicited by 2-CIAdo was antagonized by pretreatment (i.c.v.) with theophylline (278 nmol), suggesting that an activation of adenosine receptors is operative in the action of 2-CIAdo. Further support for a participation of adenosine receptors in the action of 2-CIAdo was obtained by comparing the effects of the L- and D-isomers of phenylisopropyladenosine (PIA) on TRACh. The i.c.v. administration of L-PIA (65 nmol) elicited a 79% reduction in the TRACh in the hippocampus, whereas D-PIA (65 nmol i.c.v.) had no significant effect on hippocampal TRACh. This finding supports the view that these effects on TRACh may be mediated by adenosine A1 receptors, but not by A2 receptors, because the former, but not the latter, display marked stereoselectivity toward PIA. It also was demonstrated that intraseptal injections of L-PIA or theophylline failed to reduce the TRACh in the hippocampus, suggesting that adenosine receptors located in the septum are not operative in mediating the i.c.v. action of PIA.

2-Chloroadenosine↗
PubMed1994

Induction of interleukin-1 in various brain regions after peripheral and central injections of lipopolysaccharide.

The presence of bioactive interleukin-1 (IL-1) in various brain regions (cerebellum, cortex, brainstem, diencephalon or hippocampus) after either intraperitoneal (i.p.) or intraventricular (i.c.v.) injection of lipopolysaccharide (LPS) was studied in the rat. To detect IL-1, extracellular fluid and cell lysate were fractionated by gel exclusion chromatography and fractions tested for thymocyte stimulation; presence of IL-1 was confirmed by blockade of stimulation by addition to the assay of a monoclonal antibody (mAb) to IL-1 receptor. When LPS was infused i.c.v., IL-1 was detected in the brainstem and diencephalon 2 h after injection, and in all the brain regions except cerebellum 6 h after injection; IL-1 was not detected in the plasma of these animals. When LPS was injected i.p., IL-1 was detected in the plasma but not in the brain 2 h after the injection, and in all brain regions but not in the plasma 6 h after the injection. In all of these cases, IL-1 was found in extracellular fluid; in some cases (cortex, cerebellum) cell lysate of the region did not produce detectable bioactivity, thereby indicating that IL-1 in these brain regions is processed to active peptide during release, as has been reported in the periphery. In those cases where bioactivity was detected in cell lysate (brainstem, diencephalon), bioactivity was not blocked by IL-1 receptor mAb, indicating presence of a non-IL-1 stimulating factor. These results further support the idea that IL-1 is secreted by cells in the brain, and indicate that it is found in the extracellular fluid of many brain regions following an appropriate stimulus in the periphery as well as in the brain.

Animals↗
PubMed2006

Comparison of two gene transfer models for the attenuation of myocardial ischemia-reperfusion injury following preservation for cardiac transplantation.

OBJECTIVE: Two models of ex vivo gene transfer were compared by examining the protective effect of adenovirus-mediated transfection of a free radical scavenger superoxide dismutase (SOD) during experimental ischemia-reperfusion mimicking preservation for cardiac transplantation. METHODS: Donor rat hearts (n=6 per group) were infused (subgroups IA and IB) or continually perfused (subgroups IIA and IIB) with solution containing adenoviral vector carrying beta-galactosidase (subgroups IA and IIA) or Mn-SOD (subgroups IB and IIB) over 5s with 1h storage and 15 min, at 4 degrees C, respectively. Hearts were then implanted heterotopically into the abdomen of recipient rats. Four days later, transplanted hearts were collected, connected to Langendorff perfusion apparatus and subjected to 6h of ischemia followed by 1h of reperfusion. Cardiac function was evaluated using intraventricular balloon at the beginning of Langendorff perfusion and following ischemia-reperfusion. RESULTS: Blue staining from hydrolyses of X-gal by beta-galactosidase was confirmed in AdLacZ transduced hearts. Immunoreactivity with anti-human Mn-SOD antibody then staining was positive in AdMnSOD-transduced hearts. Percent recovery of preischemic left ventricular developed pressure (LVDP) increased from 55.9+/-3.1% to 67.3+/-6.2% (P=0.048) and from 58.0+/-8.0% to 78.9+/-6.0% (P<0.001) in subgroups IA, IB, IIA and IIB, respectively. The difference in LVDP recovery between treatment groups of the two transfection methods (IB vs IIB) was significant (P=0.044). CONCLUSION: Adenoviral Mn-SOD ex vivo delivery using continuous myocardial perfusion is superior to bolus infusion in the attenuation of myocardial ischemia-reperfusion injury.

Adenoviridae↗
PubMed2003

Intracerebral oxytocin modulates sleep-wake behaviour in male rats.

Oxytocin released within the brain under basal conditions and in response to stress is differentially involved in the regulation of the hypothalamo-pituitary-adrenal (HPA) axis. Because the HPA axis plays an important role in the regulation of wakefulness, central oxytocin may modulate sleep-wake behaviour. In the present vehicle-controlled study, we assessed the influence of a selective oxytocin receptor antagonist (des-Gly-NH2d(CH2)5 [Tyr(Me)2,Thr4] OVT; 0.75 microg/5 microl) or of synthetic oxytocin (0.1 microg and 1 microg/5 microl), infused into the lateral ventricle (i.c.v.), on the sleep pattern in male Wistar rats (n=7). Compared to vehicle, the oxytocin antagonist slightly but persistently increased wakefulness at the expense of all sleep states. This finding indicates that endogenous brain oxytocin promotes sleep. However, acute icv infusion of oxytocin delayed sleep onset latency, which resulted in a transient reduction of non-REMS and REMS, and augmented high-frequency activity in the electroencephalogram (EEG) within non-REMS. These observations agree with previous reports that icv oxytocin induces a state of arousal. Based on these findings, we postulate that oxytocin has a dual mechanism of action in dependence of the physiological state. Under basal, stress-free conditions, endogenous oxytocin may promote sleep. Conversely, the high brain levels of oxytocin after central oxytocin infusion may reflect a condition of stress accompanied by behavioural arousal and, possibly via an excitatory action on the CRH system, increase vigilance.

Animals↗
PubMed2005

Aluminum chloride does not facilitate deposition of human synthetic amyloid beta1-42 peptide in the rat ventricular system of a short-term infusion model.

Recent data have demonstrated that a 39-43 amino acid peptide called beta-amyloid peptide (Abeta), which predominantly contains 42 residues (Abeta1-42), has a strong tendency to form insoluble aggregates and that the toxic effects of Abeta are based on its aggregation. In a previous study, we reported that infusion of 100 microg of human synthetic Abeta1-42 (sAbeta1-42), which is a main component of diffuse plaques, into the lateral ventricle of the rat brain of a short-term infusion model resulted in almost complete disappearance of sAbeta1-42 aggregates from the ventricles by 28 days. In addition, aluminum is considered a potential etiological factor in Alzheimer's disease (AD). Neurotoxicity from excess brain exposure to aluminum has been documented from both clinical observations and animal experiments, although a direct relationship between aluminum and AD has yet to be clearly established. We therefore investigated the effects of sAbeta1-42 aggregates with aluminum chloride (AlCl3) in the ventricular system of the rat brain of a short-term infusion model. At either 2 or 7 days following infusion, sAbeta1-42 formed aggregates with AlCl3 that spread throughout the entire ventricular system. However, sAbeta1-42 aggregates with AlCl3 had almost disappeared from the ventricles by 28 days, resulting in similarities with respect to the time-course and the neuropathological changes observed in sAbeta1-42 aggregation without AlCl3. We herein report for the first time that considerable amounts of sAbeta1-42 aggregates with AlCl3 almost disappear from the rat ventricular system by 28 days post-infusion.

Aluminum Chloride↗
PubMed1991

Impairment of active avoidance response in rats with continuous infusion of quinolinic acid into the lateral ventricle.

Continuous infusion of quinolinic acid (QA) at low doses into the lateral ventricle has been previously shown to cause a reduction of the hippocampal and cortical ChAT activities in rats although GAD activities were unchanged. In the present study, we have studied behavioral changes in rats with continuous infusion of QA in an active avoidance task. Acquisition of active avoidance was significantly impaired in rats with QA infusion compared to control. These results suggest that continuous infusion of QA is a useful technique for the study of chronic neurodegenerative diseases associated with memory impairment.

Animals↗
PubMedDate not supplied

[Effect of the novel III class anti-arrhythmia preparation (AL-275) in experimental myocardium and sympathetic stimulation].

AL-275, a new antiarrhythmic agent, exhibits the properties typical of the class III antiarrhythmogen: (i) prolongs the ventricular repolarization; (ii) inhibits the sinus node automatism; (iii) increases the effective refractory periods in atrium and ventricles; and (iv) does not modify AV and intraventricular conduction. AL-275 produces a pronounced antiarrhythmic and antifibrillatory action. The effect of AL-275 is independent of the heart rate, which is an advantage over the other class III agents. Both character and intensity of the electrophysiological and antiarrhythmic activity of AL-275 were fully retained upon the preliminary infusion of isoproterenol. Independence of the drug action of both the heart rate and the isoproterenol-induced changes in refractoriness are related to the ability of AL-275 to block a slow component (IKs) of the potassium current.

Adrenergic Agonists↗
PubMed2005

A noninvasive method for assessing impaired diastolic suction in patients with dilated cardiomyopathy.

BACKGROUND: Diastolic suction is a major determinant of early left ventricular filling in animal experiments. However, suction remains incompletely characterized in the clinical setting. METHODS AND RESULTS: First, we validated a method for measuring the spatio-temporal distributions of diastolic intraventricular pressure gradients and differences (DIVPDs) by digital processing color Doppler M-mode recordings. In 4 pigs, the error of peak DIVPD was 0.0+/-0.2 mm Hg (intraclass correlation coefficient, 0.95) compared with micromanometry. Forty patients with dilated cardiomyopathy (DCM) and 20 healthy volunteers were studied at baseline and during dobutamine infusion. A positive DIVPD (toward the apex) originated during isovolumic relaxation, reaching its peak shortly after mitral valve opening. Peak DIVPD was less than half in patients with DCM than in control subjects (1.2+/-0.6 versus 2.5+/-0.8 mm Hg, P<0.001). Dobutamine increased DIVPD in control subjects by 44% (P<0.001) but only by 23% in patients with DCM (P=NS). DIVPDs were the consequence of 2 opposite forces: a driving force caused by local acceleration, and a reversed (opposed to filling) convective force that lowered the total DIVPD by more than one third. In turn, local acceleration correlated with E-wave velocity and ejection fraction, whereas convective deceleration correlated with E-wave velocity and ventriculo:annular disproportion. Convective deceleration was highest among patients showing a restrictive filling pattern. CONCLUSIONS: Patients with DCM show an abnormally low diastolic suction and a blunted capacity to recruit suction with stress. By raising the ventriculo:annular disproportion, chamber remodeling proportionally increases convective deceleration and adversely affects left ventricular filling. These previously unreported mechanisms of diastolic dysfunction can be studied by using Doppler echocardiography.

Adult↗
PubMed1986

Echovirus polymyositis in patients with hypogammaglobulinemia. Failure of high-dose intravenous gammaglobulin therapy and review of the literature.

A 29-year-old man with X-linked hypogammaglobulinemia was treated with prednisone and methotrexate for polymyositis. Subsequently, it was established that disseminated echovirus 11 infection was causing the polymyositis. Treatment with large doses of intravenous gammaglobulin did not result in improvement. Viral cultures of blood, urine, and cerebrospinal fluid gave positive results throughout treatment and at postmortem examination. Multiple cultures of other tissues, including muscle, also gave positive results at postmortem examination. Severity of infection and treatment with prednisone and methotrexate prior to referral, diagnosis, and gammaglobulin treatment may explain the lack of response. A review of 23 cases of echovirus infection in patients with hypogammaglobulinemia revealed that the infection in these patients may cause meningoencephalitis or a polymyositis-like syndrome or both. Treatment with immunosuppressive agents, the standard therapy for polymyositis, is contraindicated, and intravenous or intraventricular gammaglobulin or both may be helpful.

Adolescent↗