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Comparison of adenosine, isoflurane, and desflurane on myocardial tissue oxygen pressure during coronary artery constriction in dogs.

OBJECTIVE: To compare adenosine-, isoflurane-, or desflurane-induced hypotension with and without left anterior descending (LAD) coronary artery constriction for the effects on myocardial tissue oxygen pressure (PmO(2)) in dogs. DESIGN: Prospective, randomized, nonblinded. SETTING: University teaching hospital. PARTICIPANTS: Male nonpurpose-bred dogs (n = 18). INTERVENTIONS: Dogs were anesthetized with 1.5% isoflurane (n = 12) or 8% desflurane (n = 6). A flow probe and balloon occluder were placed on the LAD artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial minus coronary sinus oxygen content. MEASURES AND MAIN RESULTS: Measures were made during hypotension produced by adenosine infusion, 2.8% isoflurane, or 14% desflurane with and without LAD constriction to decrease blood flow 30%. Without LAD artery constriction, adenosine infusion increased LAD flow 90% and MVO(2) 70%, 2.8% isoflurane produced no change in MVO(2), and 14% desflurane decreased MVO(2) 25%, but no treatment changed PmO(2). LAD artery constriction decreased PmO(2) 50% by itself. Adenosine infusion during LAD constriction decreased tissue oxygen pressure an additional 60%, 2.8% isoflurane produced no change, and 14% desflurane increased PmO(2) 100%. CONCLUSION: There was an inverse relationship between the effect of adenosine, 2.8% isoflurane, and 14% desflurane on MVO(2) and PmO(2) during ischemia. This is consistent with reports that increasing oxygen demand worsens myocardial ischemia.

Adenosine↗

Early constriction or expansion of the external elastic membrane area determines the late remodeling response and cumulative lumen loss in transplant vasculopathy: an intravascular ultrasound study with 4-year follow-up.

BACKGROUND: Early constriction of the external elastic membrane (EEM) area has been observed after cardiac transplantation. The aim of this study was to compare the late disease process of transplant vasculopathy between coronary segments with early constrictive and expansive remodeling. METHODS: Serial intravascular ultrasound data obtained annually for 4 years after transplantation in 38 transplant recipients was available. In 135 matched segments from 59 coronary arteries ultrasound images were digitized at 1-mm intervals. Mean values of the external elastic membrane (EEM), lumen and intimal areas were calculated. On the basis of a decrease or increase in EEM area within the first year after transplantation, we defined segments with early constrictive remodeling (CR, n = 71) or early expansive remodeling (ER, n = 64). RESULTS: Annual changes in intimal area were similar between segments with early CR and ER throughout the follow-up period. However, during the second and third year, annual increases in EEM area were greater in segments with early CR than in segments with early ER (second year: 1.5 +/- 2.7 vs 0.6 +/- 2.8 mm(2), p = 0.052; third year: 1.3 +/- 2.5 vs -0.03 +/- 2.6 mm(2), p = 0.003). Despite this late expansion, segments with early CR showed a cumulative decrease in the EEM area and a greater lumen loss than segments with early ER (-2.5 +/- 3.4 vs -0.6 +/- 2.6 mm(2), p < 0.001). CONCLUSIONS: In transplant vasculopathy, the late remodeling response was different between segments with early constrictive and expansive remodeling, despite similar intimal thickening. Early constriction caused an overall decrease in EEM area and greater loss of lumen during follow-up.

Adolescent↗

The effect of cauda equina constriction on nitric oxide synthase activity.

Nitric oxide synthase (NOS) activity was studied in the gray and white matter regions of the spinal cord 2 and 5 days after multiple cauda equina constrictions of the central processes of L7-Co5 dorsal root ganglia neurons. The results show considerable differences in enzyme activity in the thoracic, upper lumbar, lower lumbar, and sacral segments. Increased NOS activity was observed at 2 days after multiple cauda equina constrictions in the dorsal, lateral, and ventral columns of the lower lumbar segments and in the ventral column of the upper lumbar segments. The values returned to control levels within 5 postconstriction days. In the lateral columns of thoracic segments taken 2 and 5 days after surgery, NOS activity was enhanced by 54% and 55% and in the upper lumbar segments by 130% and 163%, respectively. Multiple cauda equina constrictions performed surgically for 2 and 5 days caused a significant increase in NOS activity predominantly in the gray matter regions of thoracic segments. A quite different response was found 5 days postconstriction in the upper lumbar segments, where the enzyme activity was significantly decreased in the dorsal horn, intermediate zone, and ventral horn. No such extreme differences could be seen in the lower lumbar segments, where NOS activity was significantly enhanced only in the ventral horn. The data correspond with a higher number of NOS immunoreactive somata, quantitatively evaluated in the ventral horn of the lower lumbar segments at 5 days after multiple cauda equina constrictions. While the great region-dependent heterogeneity in NOS activity seen 2 and 5 days after multiple cauda equina constrictions is quite apparent and suggestive of an active role played by nitric oxide in neuroprotective or neurotoxic processes occurring in the gray and white matter of the spinal cord, the extent of damage or the degree of neuroprotection caused by nitric oxide in compartmentalized gray and white matter in this experimental paradigm would be possible only using longer postconstriction periods.

Animals↗

Effect of renal vein constriction on the localization of immune complexes in the kidney.

To determine the effect of renal venous constriction on the localization of immune complexes in the kidney, we performed unilateral renal venous constriction in 19 male albino rabbits 7 days after they were given an i.v. bolus (250 mg/kg) of bovine serum albumin (BSA) to induce the development of serum sickness nephritis. The rabbits were sacrificed on day 12 after BSA administration. Renal histology was evaluated by (1) light microscopy, with semiquantitative grading and enumeration of glomerular nuclei and (2) fluorescent microscopy. Six rabbits were nonresponders and did not exhibit nephritis. The remaining 13 rabbits had differential degrees of severity of nephritis between the control and experimental kidneys as assessed by light microscopy (in 7 rabbits) and by fluorescent microscopy (in 12 and 9 rabbits when examined for deposits of IgG and C3, respectively). In all instances, the experimental kidney (with the constricted vein) showed less severe alterations. The degree of protection appeared to correlate with the degree of renal venous constriction, as manifested by tubulointerstitial changes [rs = 0.77, P less than 0.01). We concluded that renal venous constriction exercises a protective effect on the impaction of immune complexes in the glomeruli and development of acute serum sickness nephritis.

Animals↗

Indomethacin and corticosteroids: an additive constrictive effect on the fetal ductus arteriosus.

The objective of this paper is to study the possible additive effect of corticosteroids to the known effect of indomethacin on potency of the human ductus arteriosus. Systolic and diastolic blood flow of the fetal ductus arteriosus was measured by echo Doppler at 26-32 weeks of gestation. Four groups of patients were studied according to the treatment they have received: group A (exposure to indomethacin and betamethasone); group B (indomethacin alone); group C (betamethasone); and group D (controls). Children in whom ductal constriction was noted in utero were followed by repeat cardiac echo Doppler examinations at the age of 1 to 2 years. In group A (indomethacin and betamethasone) fetal ductal constriction was significantly higher (p = 0.02) and occurred in 11 out of 15 fetuses (73.3%), compared with 5 out of 14 (37.2%) of the fetuses in group B (indomethacin alone). In group C (betamethasone) and D fetuses (no treatment), no significant ductal constriction was observed. Pathological tricuspid regurgitation and right ventricular dilation were found more frequently in fetuses from group A. No long-term sequella was noted in the infants in whom ductal constriction had been noted in utero. Corticosteroids and indomethacin have a synergistic effect on the frequency and severity of fetal ductus arteriosus constriction. In short-term treatment this effect is transient, and has no deleterious effects on fetal and neonatal cardiac function.

Adrenal Cortex Hormones↗

Airway constriction by xanthine/xanthine oxidase in guinea pigs in vivo.

Reactive oxygens are considered to be one of the mediators involved in inflammation. We investigated the constrictive effects of reactive oxygens generated by aerosolized xanthine/xanthine oxidase (XOD) on the airways of anesthetized guinea pigs. Airway resistance was measured with a modified Konzett-Rössler method and expressed as a change in ventilation overflow (VO). Inhalation of xanthine (1.0 M)/XOD (10, 15 U/ml) caused a significant increase in VO. This airway constriction tended to be enhanced by pretreatment with inhaled superoxide dismutase, but was suppressed by inhaled catalase. Inhalation of hydrogen peroxide caused an airway constriction in a concentration-dependent manner (0.1-2.0 M). Xanthine/XOD significantly enhanced the maximal change in VO after inducing airway inflammation by SO2 exposure. The pretreatment with inhalation of xanthine/XOD did not affect the airway constriction induced by inhaled histamine. However, in SO2-exposed guinea pigs, the inhalation of xanthine/XOD significantly increased the sensitivity to histamine. These results indicate that hydrogen peroxide and other reactive oxygen intermediates produced by xanthine/XOD may cause an airway constriction and airway hyperresponsiveness.

Administration, Inhalation↗

Myocardial and peripheral catecholamine responses to acute coronary artery constriction before and after propranolol treatment in the anaesthetised dog.

The left anterior descending coronary artery was constricted for eight minutes on two occasions in 13 anaesthetised open-chest dogs. One group (n = 8) was studied before and afer 1 mg . kg-1 propranolol intravenously; a second group (n = 5) served as controls. Simultaneous blood samples were drawn from arterial and coronary sinus catheters for measurement of lactate and catecholamine concentrations. In controls, coronary artery constriction resulted in a reproducible fall in fractional myocardial lactate extraction and an increase in left atrial pressure, but caused no significant changes in blood pressure, heart rate or plasma concentrations of noradrenaline, adrenaline, or dopamine. In the treated group, heart rate was reduced but blood pressure was the same after propranolol; both remained unchanged during constriction and after release. The fall in fractional lactate extraction was abolished by propranolol. Arterial noradrenaline increased significantly after propranolol, fell during constriction and rose again after release. A similar trend was observed in coronary sinus noradrenaline. Reversible myocardial ischaemia is not associated with peripheral or myocardial release of catecholamines. Pre-treatment with propranolol appears to exert a protective effect on the myocardium even during reversible ischaemia. Although peripheral noradrenaline levels are increased after propranolol, this increase is not maintained during coronary artery constriction.

Acute Disease↗

Protein synthesis in pulmonary, cardiac, and skeletal muscle in acute hypertension induced by aortic constriction in the rat.

OBJECTIVE: The aim was to investigate nucleic acid composition and rates of protein synthesis in cardiopulmonary tissues and skeletal muscle in response to hypertension induced by aortic constriction. METHODS: After five days of abdominal aortic constriction, protein, RNA, and DNA contents were measured in the lung, the left and right atria, the left and right ventricles, and gastrocnemius muscle from young male Wistar rats weighing 120-140 g. Rates of protein synthesis were also measured in these tissues with L[4-3H]phenylalanine. RESULTS: Aortic constriction significantly increased the right atrial weight and in contrast reduced the lung weight, compared to pair fed and sham operated controls. The wet weights of all other tissues were unaffected. The concentrations of right atrial proteins, RNA, and DNA were also significantly reduced though total protein, RNA, and DNA contents were unaltered. The left ventricular RNA concentration increased and there were variable alterations in protein and DNA composition. The protein, RNA, and DNA compositions of the other tissues showed patterned responses, which included reductions in lung and skeletal muscle DNA concentrations, reductions in the skeletal muscle RNA/DNA ratio, and a decrease in the lung protein/DNA ratio. In response to aortic constriction there were increases in the left ventricular fractional rate of protein synthesis in mixed, high salt (myofibrillar), and low salt (sarcoplasmic) fractions. Rates of protein synthesis in all other regions of the heart, lung and skeletal muscle were not significantly changed. CONCLUSIONS: We conclude that in abdominal aortic constriction, the left ventricles display early adaptive responses without any concomitant change in mass. Those regions of the rat cardiopulmonary system which are not directly exposed to the acute pressure overloading, ie, right atrium, lungs, and skeletal muscle, also show disturbances.

Acute Disease↗

OP-1206, a prostaglandin E1 derivative, attenuates the thermal hyperesthesia induced by constriction injury to the sciatic nerve in the rat.

Nerve ischemia induces wallerian degeneration and peripheral neuropathy, the nerve constriction injury induces thermal hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal hyperesthesia in the nerve constriction injury model. Prostaglandin E1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal hyperesthesia induced by nerve constriction injury in the rat.

Alprostadil↗

Tracheal constriction by morphine and by fentanyl in man.

The effects of morphine and fentanyl on tracheal smooth muscle tone were studied in 38 patients during induction of anesthesia. Endotracheal tube cuff pressure was used to measure tracheal tone. Anesthesia was maintained with nitrous oxide, 70 per cent in oxygen, and pancuronium and ventilation was controlled with a respirator. Morphine, 0.5 mg/kg, produced a biphasic response, initially causing tracheal dilatation and then tracheal constriction. Ten minutes after morphine injection, cuff pressure increased to significantly (21 +/- 8 per cent) above control. Morphine-induced tracheal constriction could be completely blocked by the prior administration of atropine, 0.5 mg. Fentanyl, 0.006 mg/kg, also produced significant tracheal constriction, cuff pressures increasing to 44 +/- 11 per cent above control at 10 min. Fentanyl-induced tracheal constriction could be blocked by pretreatment with droperidol, 0.25 mg/kg. At equianalgesic doses, morphine and fentanyl produced similar tracheal constriction.

Adult↗

Mechanism of thiopental-induced constriction of guinea pig trachea.

The authors studied the effects of thiopental on baseline airway tone in intact guinea pig tracheas using a preparation where the epithelial (inside) and serosal (outside) surfaces were isolated. Whole tracheas were excised, cannulated, and mounted in 50-ml tissue baths. The serosal and epithelial surfaces were perfused via separate circuits with Krebs-Henseleit solution. All data were expressed as a percent of constriction produced by 2 X 10(-6) M carbachol (a concentration that elicited a 90 + % of maximal constriction). Thiopental elicited a dose-dependent constriction in all 25 tracheas. Increases in tone were first seen at 10(-5) M (14.3 +/- 1.84%; mean +/- SEM) and reached a peak at 10(-3) M (29 +/- 3.16%; P less than .0001). Responses to thiopental were similar when the epithelium was removed, when thiopental was added to the inner perfusate, and when tracheas were pretreated with 10(-5) M pyrilamine. Constriction was entirely inhibited by pretreatment with indomethacin 10(-5) M. The authors conclude that thiopental, at concentrations in the clinical range, causes a reproducible dose-dependent constriction of guinea pig trachea. This effect is mediated by constrictor prostaglandins.

Animals↗

Role of the injury discharge in the development of thermal hyperesthesia after sciatic nerve constriction injury in the rat.

BACKGROUND: Usually, a barrage of impulses ("injury discharge") is evoked following sensory nerve damage. It has been suggested that injury discharge may produce the hyperexcitatory state in the spinal cord, and this hyperexcitability may cause neurogenic pain. In the present study, the authors examined the role of injury discharge in developing the hyperesthetic state following nerve constriction injury. METHODS: A model of thermal hyperesthesia caused by a constriction injury created by making four loose ligations around the rat sciatic nerve was examined. To block the injury discharge, 0.5% bupivacaine was applied to the sciatic nerve before constriction injury. To block the hyperexcitatory state, (+)-MK-801, an N-methyl-D-aspartate antagonist, was administered intrathecally 15 min before the nerve lesion. RESULTS: Blocking injury discharge significantly delayed the development of hyperesthesia. Bupivacaine had no effect on the development of hyperesthesia when bupivacaine was applied to the sciatic nerve 15 min after the nerve constriction injury. Systemic bupivacaine had no effect on the development of thermal hyperesthesia. Intrathecal (+)-MK-801 also delayed the development of hyperesthesia when (+)-MK-801 was administered intrathecally 15 min before the nerve injury. When (+)-MK-801 was administered 15 min after the nerve injury, (+)-MK-801 had no effect on the development of hyperesthesia. CONCLUSION: These results suggest that injury discharge may induce facilitation of spinal dorsal horn neurons, and this spinal facilitation may play an important role in developing thermal hyperesthesia following sciatic nerve constriction injury.

Animals↗

Compliance and formation of distal anastomotic intimal hyperplasia in Dacron mesh tube constricted veins used as arterial bypass grafts.

Dilated and varicose veins constricted with a Dacron mesh tube were successfully used as arterial bypass grafts to avoid nonautogenous vascular prostheses. Mesh constriction has also been used to adapt the venous graft lumen to the diameters of grafted arteries. The influence of the external mesh on the wall elasticity of such venous grafts and the reactions of the host artery were not investigated. Elastic properties of mesh constricted autologous veins used as arterial grafts in femoropopliteal reconstructions, as well as consecutive formation of distal anastomotic intimal hyperplasia (DAIH), were investigated in this experiment. Twenty-four autologous venous grafts were implanted in 12 sheep. Grafts were left natural (Groups 1 and 3) or were constricted with an external Dacron mesh (Groups 2 and 4); their diameters were left unchanged (Groups 1 and 2) or were matched to the diameter of the host artery (Groups 3 and 4). Wall elasticity of the graft, distal anastomosis, and distal artery were measured by locally applied crystal transducers during surgery and follow-up. Formation and localization of DAIH was evaluated histomorphologically after a median of 8.3 months. Graft wall elasticity was found to be lower (54.6 vs. 147.9, P = 0.006) and overall DAIH was found to be higher in mesh tube grafts (49.42 vs. 20.8 microns, P = 0.001, Mann-Whitney U-test). No differences in elasticity and DAIH formation were observed between grafts with adapted and large diameters. Constriction of venous grafts by a Dacron mesh tube reduces graft wall elasticity and promotes formation of DAIH. To avoid such an increased mismatch in compliance while making use of the advantages of this method, the external mesh tube must not be brought close to the distal anastomotic area itself.

Anastomosis, Surgical↗

Constrictive pericarditis in chronic ulcerative colitis.

Acute pericarditis has been described as an extraintestinal manifestation of inflammatory bowel disease (IBD), as well as a consequence of IBD treatment, specifically sulfasalazine and mesalamine. Until now, there have been no reported cases of constrictive pericarditis associated with IBD or its treatment. A 37-year-old woman with a 24-year history of chronic ulcerative colitis (CUC) presented with a 3-month history of fevers, palpitations, dyspnea, syncope, and retrosternal chest pain. Two weeks before symptoms, she had initiated oral mesalamine for an ongoing CUC flare. Physical examination suggested constrictive pericarditis. An echocardiogram revealed a thickened pericardium with a nearly circumferential fibrinous effusion, with Doppler confirming diastolic compromise. The patient proceeded to radical pericardectomy. Pathological examination showed grossly hemorrhagic acute and chronic pericarditis, with cultures and cytology negative. To date, only 104 cases of IBD with acute pericarditis have been reported, with fewer than 10 cases of mesalamine-induced acute pericarditis reported. This is the first reported case of constrictive pericarditis related to IBD or its treatment. Although our patient may have had IBD-associated constrictive pericarditis, her mesalamine use raises the possibility of a drug-induced constrictive pericarditis.

Adult↗

Late diagnosis of pericardial constriction associated with defibrillator patches and deformation of the left ventricle.

We report a case of pericardial constriction associated with defibrillator patches developing 4.5 years after implantation. This constriction was related to the presence of a large pericardial mass that had developed above the defibrillator patch. This mass, which had a calcified superior border, suggested former hematoma associated with pericardial fibrosis. It induced significant compression of the right ventricle and a dumb-bell deformity of the left ventricle. The hemodynamic picture was of elastic-form constrictive pericarditis. Because of previous cerebral stroke during cardiac surgery, the patient was discharged on pharmacologic treatment after improvement of his functional status. Since removal of epicardial patches is an effective treatment of constriction, constrictive pericarditis should be systematically considered in patients with epicardial patch electrodes and impairment of functional status.

Cardiac Catheterization↗

Usefulness of systolic time intervals in differential diagnosis of constrictive pericarditis and restrictive cardiomyopathy.

Systolic time intervals in 15 patients with constrictive pericarditis and seven patients with restrictive cardiomyopathy were compared in order to assess their value in the differential diagnosis of the two disorders. Clinical examination had failed to make the distinction. Right heart catheterization was helpful in diagnosing restriction but failed to differentiate patients with constrictive pericarditis from those with restrictive cardiomyopathy. The systolic time intervals clearly separated the two groups. The PEP/LVET was normal in all patients with constrictive pericarditis (0.34 +/- 0.01) and abnormal in all patients with restrictive cardiomyopathy (0.70 +/- 0.09, P less than 0.001). In 13 patients (five with restrictive cardiomyopathy and eight with constrictive pericarditis) the results of quantitative left ventricular angiocardiography were available. A high correlation (r=-0.90, P less than 0.01) between the PEP/LVET and the ejection fraction confirmed the validity of the PEP/LVET as a measure of left ventricular performance in these patients. Thus the systolic time intervals clearly distinguished between constrictive pericarditis and restrictive cardiomyopathy and are a reliable non-invasive technique for making the difficult differential diagnosis.

Adult↗

Constrictive pericarditis as a complication of coronary artery bypass surgery.

Although it is now recognised as a rare complication of cardiac surgery, constrictive pericarditis was diagnosed in three patients after coronary artery bypass surgery. The time interval between cardiac surgery and the development of constrictive features varied from two to six weeks. All three patients presented with severe congestive heart failure. Haemodynamic findings were characteristic of constrictive pericarditis. Pericardial thickening detected by computed tomography in one patient was useful in establishing a definite diagnosis. One of the patients had a serous constrictive effusive pericarditis, and surgical pericardial drainage was needed. The other patient underwent pericardiectomy with preservation of the grafts. The diagnosis of constrictive pericarditis should be considered in patients presenting with unexplained right sided heart failure after cardiac surgery.

Aged↗

Restrictive cardiomyopathy and constrictive pericarditis: non-invasive distinction by digitised M mode echocardiography.

It is difficult to distinguish between restrictive cardiomyopathy and constrictive pericarditis on the basis of clinical findings and simple investigation. Cardiac catheterisation has been the reference standard for diagnosis but even this does not always permit an accurate distinction. A Summagraphics digitiser and Prime 750 computer system were used to digitise the echocardiograms of 15 patients with restrictive cardiomyopathy, 10 with constrictive pericarditis and a group of 20 age and sex matched normal subjects of similar age and sex distribution. Compared with controls, patients with restrictive cardiomyopathy showed a significant reduction in the following variables (a) decreased fractional shortening, (b) decreased peak left ventricular filling and emptying rates, (c) decreased percentage posterior wall thickening, and (d) decreased peak left ventricular posterior wall thickening and thinning rates. Whereas patients with constrictive pericarditis only had significantly reduced peak left ventricular filling and posterior wall thinning rates and significantly increased posterior wall thinning rate. When patients with restrictive cardiomyopathy were compared with those with constrictive pericarditis the significant differences were: (a) decreased peak left ventricular emptying rate, (b) decreased percentage posterior wall thickening, and (c) decreased peak left ventricular posterior wall thickening and thinning rates. Digitisation of M mode echocardiograms, with particular attention to posterior wall function, may be a useful adjunct to cardiac catheterisation in distinguishing restrictive cardiomyopathy from constrictive pericarditis.

Adult↗