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PubMed1994

Coronary flow dynamics and reserve assessed by transesophageal echocardiography in obstructive hypertrophic cardiomyopathy.

Myocardial ischemia is frequently associated with left ventricular outflow obstruction. To assess coronary flow impairment in obstructive hypertrophic cardiomyopathy (HC), 10 patients with echo-Doppler-detected obstructive HC and normal coronary arteries underwent transesophageal echo-Doppler examination of both coronary flow velocity (CFV) at rest, recorded in the proximal left anterior descending coronary artery, and coronary flow reserve (CFR) evaluated by means of dipyridamole infusion response. Ten normal patients were similarly studied and served as a control group. Two relevant alterations in coronary flow dynamics were detected in patients with HC: (1) a significantly increased diastolic/systolic CFV ratio, and (2) a significantly reduced dipyridamole/baseline CFV ratio. Compared with normal subjects, the CFV pattern showed a significantly greater diastolic and a significantly lower systolic component at rest (in some patients it was reversed). Diastolic/systolic CFV ratio was significantly higher in patients with HC at baseline (3.1 +/- 1 vs 1.6 +/- 0.5; p < 0.01) and increased further after dipyridamole infusion (4.9 +/- 2 vs 2.2 +/- 0.7; p < 0.01). In addition, CFR was impaired in patients with HC (1.8 +/- 0.3 vs 3.1 +/- 0.5; p < 0.01). Furthermore, a significant correlation between CFR and intraventricular pressure gradient was found. Thus, transesophageal echo-Doppler examination is a useful tool for evaluating CFV dynamics and CFR as demonstrated in patients with obstructive HC.

Aged↗
PubMed1998

Modification of phosphorothioate oligonucleotides yields potent analogs with minimal toxicity for antisense experiments in the CNS.

There is increasing evidence that phosphorothioate oligonucleotides infused into the brain can cause a host of undesired side effects which compromise the antisense experiment. In studies on the corticotropin releasing factor type-2 receptor, several phosphorothioate oligonucleotides administered intraventricularly produced significant weight loss in rats. Four different phosphodiester and phosphorothioate oligonucleotide analogs were examined to identify molecules which could eliminate these side effects while maintaining good potency for antisense inhibition. Of these, chimeric oligonucleotides consisting of a mixed phosphodiester-phosphorothioate backbone, and having 2'-methoxyribonucleotide modifications in 60% of the oligonucleotide were the most optimal. Rats treated with these chimeric oligonucleotides gained weight at rates identical to that of saline-treated controls. In addition, the antisense oligonucleotide but not the mismatch control sequence reduced corticotropin releasing factor type-2 receptor binding of 125iodo-sauvagine in the lateral septum by 40-60% after 5 daily injections. Increasing the dosing period to 9 days reduced receptor binding by 78%. Reductions in protein binding were accompanied by comparable reductions in the in situ hybridization signal of the corticotropin releasing factor type-2 receptor mRNA. However, when an oligonucleotide analog incapable of supporting ribonuclease H activity was used, neither protein nor RNA binding levels were changed compared to saline-treated controls. These results suggest that ribonuclease H or enzymes with similar activity are critical to the antisense inhibition observed in the lateral septum.

Amphibian Proteins↗
PubMed2001

Selective blockade of neurokinin-2 receptors produces antidepressant-like effects associated with reduced corticotropin-releasing factor function.

The present study investigated the effects of the selective neurokinin-2 (NK2) receptor antagonist SR48968 in behavioral, electrophysiological, and biochemical tests sensitive to the action of prototypical antidepressants (fluoxetine, imipramine) or to corticotropin-releasing factor (CRF) receptor antagonists, which have been proposed recently as potential antidepressants. Results showed that SR48968 (0.3-10 mg/kg i.p.) produced antidepressant-like activity because it reduced immobility in the forced swimming test in both mice and rats, and decreased the amount of maternal separation-induced vocalizations in guinea pig pups. This latter effect appears to involve a reduction of stress-induced substance P release because SR48968 reduced the separation-induced increase in the number of neurons displaying neurokinin-1 receptor internalization in the amygdala. Furthermore, SR48968 increased the expression of the cAMP response-element binding protein mRNA in the rat hippocampus after repeated (1 mg/kg i.p., 21 days), but not acute administration. Finally, neuronal firing of the locus coeruleus (LC) and noradrenergic (NE) release in the prefrontal cortex both elicited by an uncontrollable stressor or an intraventricular administration of CRF were reduced by SR48968 (0.3-1 mg/kg i.p.). The finding that SR48968 (1 mg/kg i.p.) blocked the cortical release of NE induced by an intra-LC infusion of the preferential NK2 receptor agonist neurokinin A suggested the presence of NK2 receptors in this latter region. Importantly, SR48965 (1-10 mg/kg i.p.), the optical antipode of SR48968, which is devoid of affinity for the NK2 receptor, was inactive in all the models used. These data suggest that NK2 receptor blockade may constitute a novel mechanism in the treatment of depression and CRF-related disorders.

Animals↗
PubMed1980

Reversal of ischemic damage with amino acid substrate enhancement during reperfusion.

Twenty dogs underwent 15 minutes of normothermic ischemic arrest and 30 minutes of reperfusion while on cardiopulmonary bypass. In 10 control dogs, the reperfusate blood was not modified. In 10 other dogs, the aorta was reclamped and the heart reperfused for 5 minutes with blood containing L-glutamate (0.026M). We measured coronary blood flow (microspheres), left ventricular (LV) metabolism [O2 content, adenosine triphosphate (ATP)], LV compliance (intraventricular balloon), and LV performance (balloon and Starling curves) before and 30 minutes after ischemia. Fifteen minutes of ischemic arrest produced significant depression in contractility and oxidative metabolism. L-Glutamate infusion resulted in higher oxygen uptakes (9.7 versus 6.9 cc/100 gm/min) and allowed more complete recovery of ATP content (80% versus 67%). Glutamate-treated hearts had more complete recovery in the rate of contraction, +dP/dt, (96% versus 68%), and relaxation, --dP/dt (99% versus 72%), the best recovery of compliance (74% versus 88%), and complete (100%) recovery of stroke work index (1.55% versus 0.87% gm - m/kg). We conclude that the addition of L-glutamate to reperfusate blood reverses ischemic damage. We suspect that l-glutamate acts by replenishing Krebs' cycle intermediates lost during ischemia, thereby stimulating oxidative metabolism and enhancing ATP production.

Adenosine Triphosphate↗
PubMed2004

Intraventricular transplantation of embryonic stem cell-derived neural stem cells in intracerebral hemorrhage rats.

In the present study, we attempted to explore cell transplantation therapy for intracerebral hemorrhage (ICH) using embryonic stem (ES) cells. Collagenase-induced ICH rats were used as model animals. Mouse ES cells were differentiated into nestin-positive neural stem cells in vitro by alltrans retinoic acid (ATRA). ATRA-treated ES cells (10(5)) were transplanted into the lateral ventricle in the hemisphere contralateral to the hemorrhage 7 days after collagenase infusion. Twenty-eight days after transplantation, ES-derived neurons and astrocytes were observed around the hematoma cavities of the brain in all of the ten rats receiving grafts. Graft-derived neurons were found in the subependymal area of the lateral ventricle as cellular nodules. Although one of the ten rats receiving grafts showed uncontrolled growth of astroglia derived from the ES cells, intraventricular transplantation of ATRA-treated ES cells is an effective delivery system of neuronal lineage-committed progenitor cells toward the site of ICH.

Animals↗
PubMed1985

Treatment of haemodynamic and electrocardiographic side-effects resulting from imipramine toxicity in rats and dogs.

This study was designed to analyze the effects of carbocromene and dipyridamole on the haemodynamic and electrocardiographic side-effects resulting from imipramine infusion in anaesthetised rats and dogs. Imipramine was infused at 1 mg/kg/min until cardiac failure and vascular collapse terminated the experiment at 21 +/- 2.3 min in rats and at 29.5 +/- 2.1 min in dogs. This was characterized by hypotension, bradycardia, intraventricular conduction delay, cardiac tachyarrhythmia and A-V block. Carbocromene (4 mg/kg i.v., followed by 80 micrograms/kg/min) protected the animals against heart failure. This was associated with delayed hypotension and negative inotropy, and lower incidence of heart block. Survival time increased to 37 +/- 1.5 min (P less than 0.05), and 54.2 +/- 2.6 min (P less than 0.02) in rats and dogs, respectively. Dipyridamole (0.5 mg/kg i.v., followed by 80 micrograms/kg/min) failed to decrease imipramine toxicity as judged by the haemodynamic and electrocardiographic parameters and did not alter survival time of imipramine controls. These results suggest that carbocromene is an effective treatment for imipramine-induced cardiovascular collapse and cardiac arrhythmias, the beneficial effects being largely due to metabolic and membrane stabilizing effects. Carbocromene has both therapeutic and prophylactic value and appears to be superior to dipyridamole therapy.

Animals↗
PubMed1979

The effect of selective lesions of brain noradrenergic systems on the development of barbiturate tolerance in rats.

A method for chronic infusion of barbiturates into the central nervous system of rats was developed and used to study the importance of noradrenergic systems in the development of barbiturate tolerance. Destruction of noradrenergic neurons by intraventricular administration of 6-hydroxydopamine or by specific lesions of the dorsal or ventral noradrenergic bundles prevented the development of barbiturate tolerance without altering the animal's response to the acute administration of barbiturate.

Animals↗
PubMed2003

A case of hypereosinophilic cardiomyopathy: additional value of the myocardial contrast agent SonoVue for the differential diagnosis of a cardiac mass.

We describe the case of a 37-year-old male referred because of hypereosinophilia associated with dyspnea. Transthoracic harmonic echocardiography showed an extensive myocardial infiltration and highlighted an intraventricular "in plus" image, whose characteristics were compatible with a diagnosis of intracardiac thrombus. The use of the myocardial contrast agent SonoVue (1 ml in bolus i.v. and 4 ml at an infusion velocity of 2 ml/min) allowed us to immediately identify, during left ventricular chamber opacification, the exact endocardial border of the left ventricular cavity and, later (when the residual SonoVue was evident only at the level of the myocardial walls), the true characteristics of the "in plus" image. This approach revealed the infiltration of the myocardial tissue and of both papillary muscles and chordae tendinae. The use of the myocardial contrast agent SonoVue may be, therefore, useful to distinguish the origin of "in plus" images often evident at echocardiography in the hypereosinophilic syndrome.

Adult↗
PubMedDate not supplied

Inability of metoprolol to achieve a sustained limitation of infarct size 24 h after coronary artery embolization in the closed chest dog.

Studies were undertaken to ascertain whether metoprolol, a beta 1-selective adrenergic blocking agent, could offer a limitation of myocardial injury throughout a 24-h period of coronary embolization in the dog. Regional myocardial ischaemia was induced through the use of a bead embolization technique which did not require thoracotomy. In order to delineate the zone at risk of infarction (hypoperfused area), radioactive microspheres (141Ce) were administered intraventricularly immediately after embolization. In the drug-treated group (n = 8) metoprolol administration was initiated by an intravenous bolus injection (0.3 mg X kg-1). This was followed by a continuous infusion (0.003 mg X kg-1 X min-1) during the 24-h experimental period. In the control group (n = 8) saline was administered throughout the 24-h period. Electrocardiographic activity was monitored throughout the experiment and this confirmed the negative chronotropic and antiarrhythmic properties of metoprolol. After 24 h, the hearts were excised and transverse myocardial sections (3 mm) prepared. Areas of necrosis were visualized by tetrazolium staining and risk zones were defined by microsphere autoradiography. In the control and metoprolol-treated groups, 73.3 +/- 7.7% and 68.2 +/- 6.1% of the risk zone became necrotic, respectively. There was no significant difference between these groups.

Animals↗
PubMed1976

Accidental quinidine poisoning in two children.

Two cases of acute accidental quinidine poisioning in two children are presented. Both cases are characterized by the same ECG abnormalities consisting of rhythm disorders and AV and intraventricular conduction defects. It is suggested that there is a causal relationship between the electrophysiologic cardiac effects of quinidine and the ECG abnormalities observed. Both patients were successfully treated by continuous intravenous infusion of a hypertonic sodium chloride solution and lidocaine.

Accidents, Home↗
PubMed1983

Safety and efficacy of intravenous quinidine.

The safety and efficacy of intravenous quinidine were evaluated in a patient population with a high prevalence of left ventricular dysfunction and intraventricular conduction delays. Quinidine gluconate (mean dose 9.1 +/- 1.6 mg/kg) was administered during electrophysiologic study to 100 patients with ventricular or supraventricular tachyarrhythmias. Clinical heart failure was present in 68 percent of the patients. Left ventricular end-diastolic pressure, cardiac index, and left ventricular ejection fraction were abnormal in 62, 48, and 70 percent, respectively. Major intraventricular conduction delays (QRS of 120 msec or more) were present in 27 percent, and the H-V interval was prolonged (over 55 msec) in 28 percent. Despite the prevalence of these abnormalities, quinidine was discontinued because of hypotension in only 10 patients. Saline solution was infused to maintain preload in 37 percent, and hypotension responded promptly to saline solution infusion or discontinuation of quinidine infusion in all subjects. Hypotension was not more common in patients with more severe left ventricular dysfunction. QRS duration, H-V interval, QTc, and right ventricular effective refractory period increased significantly (p less than 0.001) after quinidine administration. Heart block or QRS widening of 50 percent or more did not occur. Quinidine prevented arrhythmia induction in 26 percent of patients who received full doses. Ventricular tachycardia cycle length increased in all 41 patients in whom identical forms were induced before and after quinidine (287 +/- 71 msec versus 361 +/- 93 msec, p less than 0.001). Intravenous quinidine may be administered safely to patients with intraventricular conduction delays and moderate heart failure. When antiarrhythmic efficacy is assessed by electrophysiologic study, quinidine compares favorably with other antiarrhythmic agents.

Arrhythmias, Cardiac↗
PubMed1989

Intraventricular self-administration of heroin in the rat: reward seems dissociated from analgesia and physical dependence.

Experimentally naive rats were implanted with a cannula in the lateral ventricle of the brain and were allowed to self-administer heroin in doses of 0.125, 0.25, 0.5, 1 or 2 micrograms/infusion or placebo for five daily sessions of 3 h. The number of self-injections was related to the unit dose in an inverted U-shaped manner: the 0.5 microgram/infusion dose induced the highest infusion rate. The total heroin intake was proportionally related to the unit dose. A hot-plate test performed immediately after the fourth session revealed no analgesic effects in any of the groups that self-administered heroin. A naloxone (10 mg/kg) challenge given immediately after the fifth session induced very mild withdrawal signs only in the group that administered the highest dose of heroin. The results indicate that rats readily acquire intraventricular heroin self-administration behaviour and suggest that the rewarding effects of heroin can be dissociated from its analgesic and physical dependence-inducing effects.

Analgesics↗
PubMed1986

Effect of adenosine-induced controlled hypotension on canine myocardial performance, blood flow and metabolism.

The effect of adenosine-induced controlled hypotension (CH) on myocardial performance, blood flow, and metabolism was studied in nine pentobarbital-anaesthetized, open-chest dogs. Adenosine was continuously infused i.v. (0.69 +/- 0.06 and 1.36 +/- 0.11 mg/kg/min) at two stepwise increased rates (12-14 min-periods) in order to induce approximately 20 and 40% reduction of the mean arterial pressure (MAP 62 +/- 4 and 43 +/- 1 mmHg, respectively). The reduction of MAP was associated with decreases in heart rate (6 +/- 2%, P less than 0.05 and 21 +/- 4%, P less than 0.01), left intraventricular systolic pressure (14 +/- 3%, P less than 0.01 and 32 +/- 3%, P less than 0.01), left ventricular end-diastolic pressure (23 +/- 9%, P less than 0.05 and 42 +/- 9%, P less than 0.01) and ventricular intramyocardial systolic pressure (15 +/- 6% n.s. and 27 +/- 6%, P less than 0.01). The rate pressure product was markedly reduced by 49 +/- 3% (P less than 0.01) at the highest infusion rate. The mean coronary vein pressure (20.3 +/- 2.8 mmHg) was unaffected by the adenosine infusion. The systolic pressure time index (SPTI) was decreased by 33 +/- 3% (P less than 0.01) during the highest infusion rate of adenosine, while the diastolic perfusion time index (DPTI) was 15.4 +/- 2.2 mmHg X s and remained unchanged. The DPTI:SPTI ratio increased by 40 +/- 13% (P less than 0.05), suggesting a sufficient endocardial oxygen supply.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1997

Prognostic significance of coexistent bulky metastatic central nervous system disease in patients with leptomeningeal metastases.

OBJECTIVE: To assess the clinical significance of bulky metastatic central nervous system disease in patients with leptomeningeal metastases. PATIENTS AND METHODS: Forty patients (24 women and 16 men) ranging in age from 32 to 74 years (median, 56.5 years) with cytologically documented leptomeningeal metastases were demonstrated by cranial or spinal magnetic resonance imaging to have either no bulky central nervous system metastatic disease (group A; 20 patients) or bulky central nervous system metastatic disease (group B; 20 patients). Twenty-nine patients were treated with involved-field radiotherapy, and all patients were treated with sequential intraventricular chemotherapy. RESULTS: Median survival was 7 months in group A (range, 5-12 months) as compared with 4 months in group B (range, 2-12 months) (P < .01; Mantel-Cox log rank analysis). Cause of death was similar in both patient groups. CONCLUSIONS: In patients with leptomeningeal metastases, neuroradiographic demonstration of bulky metastatic central nervous system disease independently predicts survival and is useful in determining which patients are candidates for intraventricular chemotherapy.

Adult↗
PubMed1994

Ischemic preconditioning, cardioplegia or both?

UNLABELLED: With the continuing search for superior methods of myocardial protection, we compared the protective efficacy of ischemic preconditioning with that of St Thomas' cardioplegia, alone and in combination, against vascular and myocyte injury during ischemia and reperfusion. Rat hearts were perfused with blood for 20 min, subjected to zero flow global ischemia for 35 min (37 degrees C) and reperfused for 40 min. Left ventricular developed pressure (LVDP) was assessed with an intraventricular balloon. Coronary flow was measured at a constant perfusion pressure. Study groups (n = 8 hearts/group) were: (i) controls (unprotected ischemia), (ii) preconditioning (PC, 3 min ischemia + 3 min reperfusion), (iii) cardioplegia (CP, infused for 1 min before ischemia) and (iv) PC + CP. The post-ischemic recoveries of LVDP were 26 +/- 6, 44 +/- 2, 53 +/- 3 and 54 +/- 4% respectively (P < 0.05 all others v control). Post-ischemic coronary vascular resistance increased in controls by 167 +/- 60% from its pre-ischemic baseline value but was well protected with PC, CP and PC + CP (changing by only + 11 +/- 7, + 27 +/- 10 and -2 +/- 6% respectively). CONCLUSIONS: Preconditioning and cardioplegia alone afford similar and substantial protection of post-ischemic contractile and vascular function. The combination of the two affords no significant additional protection.

Animals↗