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At least 991 records · Page 55Linked to original sources
PubMed2001

Adenovirus-mediated gene transfer of a secreted transforming growth factor-beta type II receptor inhibits luminal loss and constrictive remodeling after coronary angioplasty and enhances adventitial collagen deposition.

BACKGROUND: Extracellular matrix (ECM) remodeling is central to the development of restenosis after coronary angioplasty (PTCA). As a regulator of ECM deposition by vascular cells, substantial evidence implicates transforming growth factor-beta1 (TGF-beta1) in the pathogenesis of restenosis. We investigated the effects of intracoronary expression of a transgenic antagonist of TGF-beta1 on luminal loss after PTCA. METHODS AND RESULTS: Porcine coronary arteries were randomized to receive a recombinant adenovirus expressing a secreted form of TGF-beta type II receptor (Ad5-RIIs), an adenovirus expressing beta-galactosidase (Ad5-lacZ), or vehicle only by intramural injection at the site of PTCA. Computerized morphometry 28 days after angioplasty revealed a greater minimum luminal area in Ad5-RIIs-injected arteries (1.71+/-0.12 mm(2)) than in the Ad5-lacZ (1.33+/-0.13 mm(2)) or vehicle-only (1.08+/-0.17 mm(2); P=0.010 by ANOVA) groups. This was accompanied by greater areas within the internal (P=0.013) and external (P=0.031) elastic laminae in Ad5-RIIs-treated vessels. Adventitial collagen content at the site of injury was increased in the Ad5-RIIs group, in contrast to decreases in the Ad5-lacZ and vehicle-only groups (P=0.004). CONCLUSIONS: Adenovirus-mediated antagonism of TGF-beta1 at the site of PTCA reduces luminal loss after PTCA by inhibiting constrictive remodeling. Antagonism of TGF-beta1 stimulates the formation of a dense collagenous adventitia, which prevents constrictive remodeling by acting as an external scaffold. These findings demonstrate the potential of gene therapy-mediated antagonism of TGF-beta1 as prophylactic therapy for restenosis.

Adenoviridae↗
PubMed1974

Normal contractile state of hypertrophied myocardium after pulmonary artery constriction in the cat.

The contractile function of right ventricular papillary muscles from normal cats and cats in which the pulmonary artery had been constricted for 6 or 24 wk was examined. Acute pulmonary artery constriction reduced cross-sectional area by an average of 70%, resulting in a 30% mortality from congestive heart failure, all such deaths occurring within the first 3 wk after banding. The increase in right ventricular mass in animals surviving for 6 or 24 wk was similar, averaging 70%. No banded animals had evidence of congestive heart failure at the time of sacrifice, and cardiac output and right atrial pressures were similar to those in control animals.6 wk after banding, the active length-tension curve, maximal rate of rise of isometric force, force-velocity relations, and isometric force with paired stimulation and norepinephrine were all significantly depressed when compared to their respective values in control animals. In contrast, none of these variables was significantly different from control values in animals banded for 24 wk. These observations indicate that depressed contractile state is not a fundamental characteristic of pressure-induced hypertrophied myocardium and reemphasize the important temporal relationship between contractile state and the imposition of sudden sustained loads.

Animals↗
PubMedDate not supplied

Effusive constrictive pericarditis due to rheumatoid arthritis revealed by pericardiocentesis with simultaneous pressure recording--a case report.

A 59-year-old man had a history of rheumatoid arthritis. He presented with incurable pericardial effusion. He was repeatedly treated with pericardiocentesis with only transient attenuation of his symptoms because the underlying pericardial constriction had been overlooked. This time the authors diagnosed effusive constrictive pericarditis due to rheumatoid arthritis using the hemodynamic findings observed before and after pericardiocentesis.

Arthritis, Rheumatoid↗
PubMed1991

An immunofluorescence test to determine the occurrence of type II collagen in muscle biopsies from cattle with rectovaginal constriction.

Type II collagen occurs in the muscles of rectovaginal constriction (RVC) affected and carrier cattle but not in normal cattle. Muscle biopsies from known RVC affected and carrier cattle and normal cattle were examined for the presence of Type II collagen using affinity purified goat anti-collagen II serum in a fluorescent antibody test. Type II collagen was consistently found in RVC affected animals (22 of 23 samples score positive). Rectovaginal constriction carrier animals had variable staining for the Type II collagen (25 of 47 samples scored positive). Some positive staining was also observed in the control animals (8 of 34 samples scored positive). Because of the variable occurrence of Type II collagen, the value of fluorescent antibody staining to identify RVC carrier animals is uncertain.

Animals↗
PubMed1981

Constriction of the fetal ductus arteriosus by glucocorticoid hormones.

Hydrocortisone, prednisolone, and betamethasone were injected into a rat that was 21 days pregnant, and the fetal ductus arteriosus was studied using the rapid whole-body freezing technique. All these glucocorticoids constricted the fetal ductus arteriosus in a dose-dependent relationship. Fetal ductal constriction was maximum 1 to 4 hr after injection and was significantly more prominent in premature fetuses than in mature ones.

Animals↗
PubMed2005

A behavioral and pharmacological validation of the acetone spray test in gerbils with a chronic constriction injury.

UNLABELLED: Cold and mechanical allodynia are important symptoms in patients with neuropathic pain. The study of cold allodynia in animals can help us to understand the underlying pathophysiological mechanisms of neuropathic pain and to validate drugs. The evaluation of cold allodynia in gerbils with a chronic constriction injury of the sciatic nerve on the cold plate is not always stable. We developed a new application method of acetone using a specific spray technique with an Eppendorf multistepper pipette. The chronic constriction injury of the sciatic nerve in gerbils resulted in a long-lasting mechanical and acetone spray-induced hyperreactivity throughout the testing period, which is clearly different from what was seen in sham-operated animals. The acetone spray test incorporates a multimodal stimulus different from direct cold stimulation. The reactivity to the acetone spray coincides in time and strength with the reactivity observed in mechanical allodynia in gerbils and with mechanical and thermal allodynia in other species. Furthermore, a pharmacological validation of the acetone spray test by different reference compounds was performed. Different compounds effective in neuropathic pain models in rodents influence the hyperreactivity to the acetone spray after acute and chronic administration. This study indicates that the multimodal acetone spray test is a valuable tool in the study of neuropathic pain in rodents. IMPLICATIONS: The acetone spray test is a multimodal and valuable tool in the evaluation of neuropathic pain behavior in gerbils.

Acetone↗
PubMed2005

Both milrinone and colforsin daropate attenuate the sustained pial arteriolar constriction seen after unclamping of an abdominal aortic cross-clamp in rabbits.

We previously reported that unclamping of an abdominal aortic cross-clamp causes initial dilation of pial arteries followed by sustained constriction. Both milrinone and colforsin daropate have a vasodilator action, and both have been used in such critical conditions as abdominal aortic aneurysmectomy. We measured cerebral pial arteriolar diameters using a rabbit closed cranial window preparation before (baseline) and 15 min after the start of an IV infusion of 0.9% saline (control group), milrinone, or colforsin daropate (0.05 and 0.5 microg . /kg(-1) . min(-1)) (pre-clamp), just after aortic clamping, 20 min after clamping, and at 0 to 60 min after unclamping. In the control group, a significant decrease in diameter persisted for at least 60 min after unclamping (maximum, -15% for large and -26% for small arterioles versus baseline). These values were significantly smaller after both doses of milrinone and the larger dose of colforsin daropate (-5% and -8%, 10% and 12%, and -2% and -5%, respectively vs baseline, at 60 min). In a second experiment, changes in regional cerebral blood flow and tissue oxygen tension reflected changes in vascular variables. Thus, sustained cerebral pial arteriolar constriction induced by aortic unclamping can be attenuated by IV milrinone or colforsin daropate.

Animals↗
PubMed2005

A role for endothelin in neuropathic pain after chronic constriction injury of the sciatic nerve.

The purpose of this study was to explore the role of endothelin in neuropathic pain. Endothelins (ET) are a family (ET-1, ET-2, ET-3) of ubiquitously expressed peptides involved in control of vascular tone. Injected ET-1 causes intense pain via activation of ETA receptors, modulated by analgesic signals initiated by ETB receptor activation. Using a rat model of chronic constriction injury of the sciatic nerve, we found that pharmacologic ETA receptor antagonism acutely and significantly reduced thermal and mechanical hyperalgesic responses 5 days after injury. Furthermore, ET-1 and the ETA receptor are locally upregulated at the site of chronic constriction injury at both the message and the protein levels, suggesting that ET-1 may be involved in establishing pain after the injury. These data point to ET-1 as an important mediator of pain in general and suggest that ETA antagonism deserves study as a potential novel therapy for neuropathic pain.

Animals↗
PubMed2000

Degos' disease with constrictive pericarditis: a case report.

A 47-year-old man with Degos' disease was examined by echocardiography, which showed hypokinesis of the apical left ventricular wall with pericardial effusion. To evaluate the myocardial perfusion and coronary flow reserve, 201Tl scintigraphy and intracoronary Doppler flowmetry were performed. The coronary flow reserve was not decreased nor was there angiographical coronary stenosis, although a pressure study revealed constrictive dysfunction of both ventricles. The constrictive pericarditis might have been induced by pericardial vasculitis, thereby causing the left ventricular wall motion abnormality.

Humans↗
PubMed1992

Implantable cardioverter defibrillator infection causing constrictive pericarditis.

A case of severe constrictive pericarditis resulting from an indolent Pseudomonas aeruginosa infection of the automatic internal cardiac defibrillator is described. Total explanation of the device was attempted after nine months but was unsuccessful because of dense adhesions under the patch electrodes. The patient subsequently developed clinical and hemodynamic findings of constrictive pericarditis and a second desperate attempt to remove the patches resulted in operative death. Diagnostic modalities for detecting infection of the AICD are reviewed. As soon as there is infection involving any component, the entire lead system and pulse generator should be removed.

Aged↗
PubMed1994

Platypnea related to constrictive pericarditis.

Platypnea is the rare symptom of dyspnea in the upright position, which is relieved by assumption of the recumbent position. This symptom has been previously described in association with several conditions, but never with constrictive pericarditis. The authors report the case of a patient with constrictive pericarditis and severe platypnea, which resolved after pericardiectomy.

Dyspnea↗
PubMed1996

Tracheobronchial constriction in asthmatics induced by isocapnic hyperventilation with dry cold air.

Although it is well known that isocapnic hyperventilation (IHV) with dry cold air produces airway constriction in asthmatic subjects, the site of airway narrowing is nuclear. To address this issue, we have quantified the tracheal and bronchial response to IHV with dry cold air in 15 patients with mild asthma and 7 healthy control subjects. We employed the acoustic reflection technique to evaluate changes in airway cross-sectional areas caused by IHV with dry cold air. Airway areas were measured during tidal breathing before and 5 to 10, 30, 60, and 90 min following cold air challenge. For analysis purposes, airway areas were divided into three anatomic segments: extrathoracic tracheal segment, intrathoracic tracheal segment, and main bronchial segment. These segments were assessed at a fixed volume below total lung capacity. Maximal and partial expiratory flow-volume curves were also obtained before each set of area measurements. In normal subjects, IHV with dry cold air caused no significant changes in FEV1, flow at 30% of the vital capacity in the partial curve (V30p), or airway areas. In asthmatics, at 5 to 10 min after challenge, we found that FEV1 decreased by 22 +/- 5% (mean +/- SEM) (p < 0.0001), V30p by 33 +/- 8% (p < 0.003), intrathoracic tracheal area by 10.7% +/- 2% (p < 0.03), and main bronchial area by 14 +/- 3% (p < 0.003). At 30 min, tracheal and main bronchial areas were returned to baseline levels; however, FEV1 and V30p were still significantly decreased, by 13 +/- 3% and 16 +/- 4%, respectively. We conclude that in asthmatics, IHV with dry cold air causes both tracheal and bronchial constriction, and that recovery seems to occur first in the central airways.

Acoustics↗
PubMed2002

Cardiac decortication (epicardiectomy) for occult constrictive cardiac physiology after left extrapleural pneumonectomy.

Constrictive cardiac physiology typically does not occur in the absence of parietal pericardium. However, we report eight patients who, after left extrapleural pneumonectomy and removal of the parietal pericardium for malignancy, presented with dyspnea, jugular venous distension, and peripheral or generalized edema unresponsive to diuretics. Cardiac decortication (epicardiectomy) was performed whereby a thickened peel encasing the heart was surgically excised, resulting in vigorous contraction and expansion of the heart. In one patient, decortication occurred early after pneumonectomy and was incomplete. Acute signs of inflammation were present, and recurrence necessitated repeat decortication. When patients present with dyspnea, hepatojugular reflux, and peripheral edema refractory to diuretics, constrictive cardiac physiology should be considered in the differential diagnosis, even in the absence of parietal pericardium.

Constriction, Pathologic↗
PubMed1979

Epicardial pacemaker complicated by cardiac tamponade and constrictive pericarditis.

Following insertion of an epicardial pacemaker, our patient developed cardiac tamponade complicated by subacute constrictive pericarditis. Echocardiographic findings and intracardiac pressures were typical of constrictive pericarditis, which was confirmed at surgery. Although rare, these unusual complications should be considered in patients who develop evidence of reduced cardiac output following either transvenous or epicardial electrode placement.

Aged↗
PubMed1981

Motion of pulmonic valve and constrictive pericarditis.

Extreme respiratory variation in the depth of the "a" wave of the pulmonic valve echo was demonstrated in a patient with constrictive pericarditis; a mechanism for this finding is offered. Disparity in systolic and diastolic ventricular function in constriction is also useful in ruling out restrictive cardiomyopathy.

Aged↗
PubMed1975

Rheumatic valvulitis and constrictive pericarditis. Report of case.

A 13-year-old girl was admitted with congestive heart failure, edema, ascites, and jaundice. There was an apical pansystolic murmur of mitral insufficiency and marked cardiomegaly. Her venous pressure was elevated. Despite medical treatment her condition deteriorated, hepatic and renal failure as well as disseminated intravascular coagulation ensued, leading to her death. At post mortem she was found to have rheumatic mitral valvulitis and constrictive pericarditis. The pathologic picture of pericarditis was nonspecific, but in presence of a positive skin test for tuberculosis the latter is considered to be the most likely cause of the pericarditis, nevertheless, rheumatic etiology of pericarditis in this case cannot be excluded. The presence of rheumatic heart disease and cardiomegaly may have led to the exacerbation of symptoms and signs of constrictive pericarditis and severe right heart failure.

Adolescent↗
PubMed1979

Presystolic pulmonary valve opening in constrictive pericarditis.

Right heart pressure tracings were studied in 5 cases with constrictive pericarditis. The pressure of the A-wave in the right atrium of these cases was higher than the pulmonary arterial diastolic pressure. In addition, a presystolic wave appeared in the pulmonary arterial and the right ventricular pressure tracings, in coincidence with atrial systole. The pressure of this presystolic wave was similar to that of the right atrial A-wave. This suggests that the pulmonary valve opens following atrial systole, and then the blood flows into the pulmonary artery in the presystolic phase in patients with constrictive pericarditis. In 2 cases, pulmonary valve echograms were recorded. The a-dip in these 2 cases was as deep as 8.4 mm and 9.6 mm (1.8-4.1 mm with a mean of 2.80 mm for normal men), and its duration was prolonged to 0.17 sec and 0.18 sec (0.10-0.13 sec with a mean of 0.115 sec for normal men). In conclusion, such a deep and prolonged a-dip on pulmonary valve echogram is presumably a sign of presystolic pulmonary valve opening.

Adult↗
PubMed1987

Effects of the rise in aortic pressure on coronary flow reserve in dogs. Comparison between constriction of the descending thoracic aorta and injection of methoxamine.

In order to investigate the effect of a rise in aortic pressure on coronary flow reserve and also on the difference of its effect according to the methods used to raise aortic pressure, this experiment was performed. Using 7 anesthetized dogs with heart rate held constant by a pacemaker, both the resting and the peak reactive hyperemic left circumflex coronary flow were measured following raising of the aortic pressure by either descending thoracic aorta constriction or methoxamine injection. The resting and peak reactive hyperemic coronary flows both increased linearly following the rise in aortic pressure. The magnitude of the resting flow increment and the resting coronary vascular resistance following raising aortic pressure did not differ significantly between the two different methods. However, the magnitude of the peak hyperemic flow increment and the peak hyperemic coronary vascular resistance following raising aortic pressure were significantly smaller with methoxamine injection than with aortic constriction. These data indicate that coronary flow reserve increases proportionally with a rise in aortic pressure. However, the magnitude of the increment of coronary flow reserve is smaller following an alpha-adrenoceptor-mediated rise in aortic pressure, because the maximal coronary vasodilation was reduced by alpha-stimulated coronary vasoconstriction.

Animals↗