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PubMed2000

Endothelin and prostaglandin H(2)/thromboxane A(2) enhance myogenic constriction in hypertension by increasing Ca(2+) sensitivity of arteriolar smooth muscle.

The myogenic response of skeletal muscle arterioles is enhanced in hypertension because of the release of endothelin (ET) and prostaglandin H(2) (PGH(2))/thromboxane A(2) (TxA(2)) from the endothelium. We hypothesized that ET and PGH(2)/TxA(2) modulate Ca(2+) signaling in arteriolar smooth muscle and thereby enhance myogenic constriction. Thus, simultaneous changes in intracellular Ca(2+) concentration in smooth muscle ([Ca(2+)](i)), measured by fura 2 microfluorometry (expressed as Ca(2+) fluorescence ratio [R(Ca)]), and diameter were obtained as a function of intraluminal pressure (P(i)) in isolated cannulated gracilis muscle arterioles (diameter approximately 120 micrometer) of normotensive Wistar rats (WR) and spontaneously hypertensive rats (SHR). In the absence of extracellular Ca(2+), increases in P(i) from 20 to 160 mm Hg increased the passive diameter of arterioles without changes in R(Ca). In the presence of extracellular Ca(2+) and endothelium, increases in P(i) elicited similar increases in R(Ca) (30+/-7% for control and 33+/-8% for SHR at 160 mm Hg) but a significantly (P<0.05) greater constriction of SHR arterioles compared with WR arterioles (at 160 mm Hg, 55+/-4% versus 38+/-2%, respectively, of passive diameter). In the absence of the endothelium, P(i)-induced changes in the R(Ca) and diameter of SHR and WR arterioles did not differ significantly. Also, a step increase in P(i) (from 80 to 140 mm Hg) elicited a similar increase in R(Ca) but greater constrictions in SHR versus WR arterioles. In the presence of the TxA(2) receptor inhibitor SQ29,548 and the ET(A) receptor inhibitor BQ123, there was no difference between responses of SHR and WR arterioles. In WR arterioles, increasing concentrations of KCl elicited a significant increase in R(Ca) (38+/-7% at 80 mmol/L) and completely constricted the arterioles. In contrast, constrictions to ET (52+/-7% at 3x10(-12) mol/L) and the TxA(2) agonist U46619 (40+/-8% at 3x10(-9) mol/L) were not accompanied by increases in R(Ca) at submaximal concentrations. Collectively, these findings suggest that in hypertension, endothelium-derived ET and PGH(2)/TxA(2) increase the Ca(2+) sensitivity of the contractile apparatus of arteriolar smooth muscle; thus, the similar increases in [Ca(2+)](i) in response to the elevation of intraluminal pressure elicit greater myogenic constriction.

Animals↗
PubMed1981

Effects of indomethacin, renal denervation, and propranolol on plasma renin activity in conscious dogs with chronic thoracic caval constriction.

The role of renal prostaglandins and the adrenergic nervous system in the control of renin release was studied in conscious dogs with thoracic caval constriction. Indomethacin reduced plasma renin activity (PRA) in intact animals with thoracic caval constriction by 43% but failed to change PRA after surgical renal denervation and during chronic propranolol administration; adrenergic blockade reduced the initial control level of PRA before indomethacin from 15 to 4 ng angiotensin I/ml per hr. Renal hemodynamic function was markedly reduced by indomethacin both before and after adrenergic blockade. These observations indicate that prostaglandins are involved in the control of renin release, but they appear to have a more important role in the control of renal arterial resistance. The adrenergic nervous system also plays a role in the hyperreninemia of caval constriction and, possibly, a greater role than the renal prostaglandins. In the first experimental design, surgical renal denervation and daily oral propranolol administration in dogs with caval constriction reduced PRA to normal in two of seven dogs and a natriuresis occurred. In four of the five remaining animals, PRA fell, but not to normal, and renal sodium excretion failed to increase. In a second experimental design, the kidneys were denervated and propranolol was given before the dogs were subjected to caval constriction and propranolol was continued for 5 days; PRA increased markedly, sodium retention occurred, and ascites formed. Under these circumstances, compensatory mechanisms secondary to caval constriction led to increased PRA in spite of adrenergic blockade.

Animals↗
PubMed1985

Pulmonary artery constriction produces a greater right ventricular dynamic afterload than lung microvascular injury in the open chest dog.

Investigators model noncardiogenic pulmonary hypertension by constricting the pulmonary artery to increase right ventricular afterload. To investigate this model's validity, we compared the right ventricular afterload, quantified as pulmonary input impedance, created by constricting the pulmonary artery and by inducing a pulmonary microvascular injury (with glass beads infused into the pulmonary circulation). The pulmonary injury constriction produced a different right ventricular afterload than the microvascular injury. The constriction increased both the input resistance and the characteristic impedance. Microvascular injury increased only input resistance. Physiological levels of lung inflation did not influence pulmonary impedance, but lung hyperinflation increased input resistance both before and while constricting the pulmonary artery or after producing microvascular injury. Total right ventricular power output and stroke work were unchanged during each vascular intervention. Pulmonary artery constriction did not affect power output distribution, whereas microvascular injury decreased oscillatory power and its relative contribution to total power. Lung hyperinflation dramatically reduced right ventricular power and left ventricular stroke work. These effects appeared mediated by right ventricular afterload increase uncompensated for by right ventricular preload increase. These observations help explain the hemodynamic consequences of acute pulmonary hypertension and the effects of lung hyperinflation with positive end-expiratory pressure respiration in such patients.

Animals↗
PubMed1974

Mechanism of effect of thoracic inferior vena cava constriction on renal water excretion.

Persistent secretion of vasopressin and/ or diminished distal fluid delivery have been proposed to explain the impaired water excretion associated with low-output cardiac failure. In the present investigation cardiac output (CO) was diminished in anesthetized dogs undergoing a water diuresis by constriction of the thoracic inferior vena cava (TIVC). In intact animals (group I) acute TIVC constriction decreased CO from 3.5 to 2.2 liters/min (P < 0.005) as urinary osmolality (U(osm)) increased from 103 to 543 mosmols/ kg (P < 0.001) and free water clearance (C(H2o)) decreased from 2.1 to -0.6 ml/min (P < 0.001). This antidiuretic effect was disassociated from changes in renal arterial and venous pressures, glomerular filtration rate, solute excretion, and renal innervation. To examine the role of vasopressin in this antidiuresis, studies (group II) were performed in acutely hypophysectomized, steroid-replaced animals. In these animals TIVC constriction decreased CO to a similar degree from 3.4 to 2.1 liters/min (P < 0.001). However, the effects on U(osm) (87-104 mosmols/kg) and C(H2o) (2.1-1.6 ml/min) were significantly less than in intact dogs. In another group of hypophysectomized animals, (group III) renal arterial and venous pressures were not controlled, and the effect of TIVC constriction on U(osm) was not significant (65-79 mosmols/kg) although C(H2o) decreased from 3.3 to 1.9 ml/min (P < 0.001). In both the group II and III studies, there were linear correlations between the changes in C(H2o) and the urine flow. Studies were also performed in baroreceptor-denervated animals with intact hypothalamo-neurohypophyseal tracts, and acute TIVC constriction altered neither U(osm) nor C(H2o) when renal arterial pressure was controlled. These results therefore indicate that the effect of TIVC constriction on U(osm) is primarily vasopressin mediated while the effect on C(H2o) is mediated both by vasopressin release and diminished distal fluid delivery. A decrease in renal arterial pressure, or some consequence thereof, seems to be an important determinant of the latter effect.

Animals↗
PubMed2000

Calcific constrictive pericarditis: is it still with us?

BACKGROUND: The presence of pericardial calcification on a plain radiograph strongly suggests constrictive pericarditis in patients with heart failure. However, calcific constrictive pericarditis is considered rare in the United States since tuberculosis incidence has decreased, and doubt has therefore been raised about the importance of this radiologic finding in modern cardiovascular practice. OBJECTIVE: To determine the clinical and prognostic significance of pericardial calcification on radiography in patients with constrictive pericarditis. DESIGN: Retrospective cohort study. SETTING: Tertiary referral center. PATIENTS: A consecutive series of 135 patients (mean age +/- SD, 56 +/- 16 years) who from 1985 through 1995 had constrictive pericarditis confirmed surgically (n = 133) or by autopsy (n = 2). Patients were divided into two groups: those with pericardial calcification on chest radiography (group I) and those without (group II). MEASUREMENTS: Clinical and diagnostic findings were compared in both groups, and outcome was compared in 132 patients who had pericardiectomy. RESULTS: Pericardial calcification was seen in 36 patients (27%). The cause of constrictive pericardial disease was indeterminate in 67% of patients in group I and in 21% of patients in group II (P < 0.001). Patients in group I had had symptoms for a longer period and were more likely to have pericardial knock, larger atrial size, and atrial arrhythmia. Significantly more perioperative deaths were seen in group I, but incidence of late survival and incidence of noncalcific disease were similar in both groups. CONCLUSIONS: Pericardial calcification is a common finding in patients with constrictive pericarditis. It is often associated with idiopathic disease and other markers of disease chronicity and is an independent predictor of increased perioperative mortality rates.

Adolescent↗
PubMed1999

Hemodynamic and neurohumoral changes after abdominal aortic constriction in rats.

Cardiac after-load, neurohumoral reaction and the secondary cardiac hypertrophy were studied in six groups of Sprague-Dawley (SD) rats with abdominal aortic constriction. We found that abdominal aortic constriction above the renal arteries decreased the heart rate and cardiac output, and increased the pulse pressure. These abnormalities would return to normal after constriction ended. Captopril, propranolol and prazosin could reduce the increase of pulse pressure but still had decreased in cardiac output of rats with abdominal constriction. Aortic constriction also increased the aortic impedance and cardiac load but decreased aortic compliance. These changes could also be lessened by captopril, propranolol and prazosin. We have confirmed that aortic constriction can induce secondary cardiac hypertrophy, but the pathogenesis might be due to multiple factors.

Animals↗
PubMed2000

[Annular constriction of popliteal vein for treating severe venous insufficiency].

OBJECTIVE: To study the mechanism and therapeutic effects of annular constriction for severe venous insufficiency of legs. METHODS: Annular constriction of popliteal vein was performed by Gore-Tex vascular graft in 82 patients. Among them, 78 patients had deep venous valve insufficiency of legs (III, IV degree), 2 postphlebitic syndrome, and 2 valve absence of deep vein. Under normal respiration and breath holding, venous pressure was measured at the proximal and distal part from the constricting site. RESULTS: Great difference was noted in the venous pressure between the proximal and distal part from the constricting site. The pressure was (9.4 +/- 4.5) mm Hg, (41.2 +/- 28.1) mm Hg at calm and (32.4 +/- 16.2) mm Hg, (41.2 +/- 28.1)mm Hg at breath holding (P < 0.01). Symptoms disappeared or released after operation. Ulcer healed in all patients. Venous pressure decreased by over 60%. Pressure recovery time was over 22 seconds. There was no reflux distal to the constricting site. Deep venous angiography and color Doppler showed an effect similar to venous valve. CONCLUSION: Annular constriction is effective in treating severe venous insufficiency of legs.

Constriction↗
PubMed1991

[Chronic constrictive pericarditis. 27 cases].

Twenty-seven cases of chronic constrictive pericarditis seen between 1975 and 1990 in an internal medicine department were analyzed retrospectively. The chronic pericarditis was consecutive to one (n = 5) or several (n = 7) episodes of acute pericarditis. Echography demonstrated the presence of pericardial effusion in 74 percent of the cases, pericardial thickening in 41 percent and/or compression of right heart cavities in 55 percent. Computerized tomography of the chest, performed in 16 cases, showed pericardial effusion in 63 percent of the cases, pericardial thickening in 37 percent and lymph node enlargement in 19 percent. Magnetic resonance imaging of the chest was carried out in 2 patients but showed no abnormality. All 11 patients who underwent cardiac catheterization were found to be adiastolic. The cause of constrictive pericarditis, elicited in 13 patients was neoplasia in 4, sequelae of radiotherapy in 2, injuries in 2, mediastinal and retroperitoneal fibrosis in 2, myocardial infarction in 1, purulent pericarditis in 1 and bacteriologically proven tuberculosis in 1. Medical treatment with corticosteroids (n = 16) and/or antituberculous therapy (n = 15) was successful in 2 patients; 25 patients had to undergo surgery 7 +/- 11 months after constriction was diagnosed. Pericardial drainage (through a pericardiopleural window in 4 cases) proved to be sufficient in 10/15 patients but failed in 5. Pericardectomy was performed initially in 3 cases and after failure of medical treatment and/or drainage in 11 cases. The 4 patients with neoplastic constrictive pericarditis died 10 months on average after the diagnosis, but the remaining 23 patients were alive after à 9 to 48 months (mean: 19 +/- 15) follow-up. These results suggest that the data provided by echocardiography and computerized tomography of the chest usually point to the relevant therapeutic measures without a need for invasive haemodynamic exploration. Idiopathic constrictive pericarditis now accounts for 50 percent of the cases; tuberculosis has become exceptional, but the other, previously exceptional causes (neoplasia, heart surgery, radiotherapy, connective tissue diseases) are more frequent. Corticosteroids should be used in chronic constrictive pericarditis occurring after cardiac surgery or in the course of a connective tissue disease, but they are effective only in highly inflammatory forms of the disease. Modern treatment relies on early surgery, since functional results and patient's survival are closely related to the date of pericardectomy which must be carried out before very important myocardial repercussions develop.

Adrenal Cortex Hormones↗
PubMed1994

Constriction of the umbilical cord leading to fetal death. A report of three cases.

Constriction of the umbilical cord is characterized by localized absence of Wharton's jelly, leading to narrowing of the cord, thickening of the vascular walls and narrowing of the vascular lumens. This may result in a compromised fetal blood supply, leading to fetal anoxia and eventual fetal death. Approximately 50 cases have been reported in the world literature over the last three centuries. Three cases of umbilical cord constriction leading to intrauterine fetal demise are reported. Two of the patients presented during the late second trimester with loss of sensation of fetal movements. Intrauterine fetal demise was diagnosed, and autopsy revealed constricted umbilical cords associated with torsion. The third patient is unique in that fetal death was precipitated by a routine, technically uncomplicated, transplacental amniocentesis procedure performed in the early second trimester. At the time of termination of the pregnancy we found marked stenosis with torsion over a 1-cm segment of the umbilical cord juxtaposed against the fetal insertion site. Umbilical cord constriction is a rare, almost invariably fatal condition, usually undiagnosed antenatally. In case 3, disruption of the placenta by amniocentesis may have initiated a terminal event in a fetus already compromised by a cord constriction. Three possible mechanisms could have contributed to the fetal death after amniocentesis in the presence of cord constriction: acute vasospasm, acute oligohydramnios and uterine contraction, or an obliterating thrombus.

Adult↗
PubMed1995

Vacuum constriction device and topical minoxidil for management of impotence.

OBJECTIVE: We report our preliminary experience with a vacuum constriction device and topical minoxidil for the management of impotence. METHODS: We evaluated 18 patients, 8 with neurogenic and 10 with psychogenic impotence with a vacuum constriction device and topical minoxidil (1 ml 2% solution). RESULTS AND CONCLUSIONS: All patients responded to treatment but 100 cases refused home use because of psychological impact. Twelve patients did not need the application of the constrictive ring because of the erection facilitation effect of minoxidil. No side effects were observed. In our opinion the association of the vacuum constriction device with topical minoxidil might be useful in the treatment of impotence; however, several factors must be evaluated in selecting patients. Application of minoxidil before vacuum constriction device might be useful to reduce the time of device application, to increase the efficacy of the device and in some cases to avoid the use of the constrictive ring.

Administration, Topical↗
PubMed1992

Constrictive amniotic bands, amniotic adhesions, and limb-body wall complex: discrete disruption sequences with pathogenetic overlap.

In a fetopathologic evaluation of 18 cases with amniotic bands, we discerned 3 types of lesions: (1) constrictive tissue bands, (2) amniotic adhesions, and (3) more complex anomaly patterns, designated as limb-body wall complex (LBWC). Constrictive bands are caused by primary amnion rupture with subsequent entanglement of fetal parts (mostly limbs) by shriveled amniotic strands. Adhesive bands are the result of a broad fusion between disrupted fetal parts (mostly cephalic) and an intact amniotic membrane. Most of the craniofacial defects (encephaloceles and/or facial clefts) occurring in these fetuses are not caused by constrictive amniotic bands, but are the result of a vascular disruption sequence with or without cephalo-amniotic adhesion. Our observations confirm the fact that amnion rupture is not a conditio sine qua non for the development of LBWC. However, LBWC is often complicated by rupture of the unsupported amnion with ensuing formation of constrictive bands. We think that the concept that considers the 3 lesions in question as a single pathogenetic entity is erroneous and will inevitably lead to a never-ending debate between followers of the 2 prevailing theories. In our view, the theories of Streeter and Torpin are not mutually exclusive but rather apply to different types of lesions. The recognition of constrictive amniotic bands, amniotic adhesions, and LBWC as discrete but often combined disruption sequences with important pathogenetic overlap may resolve many dilemmas in interpretation when a fetus exhibits classical constrictive bands beside more severe defects.

Amnion↗
PubMed2005

GABA receptors and nitric oxide ameliorate constrictive collagen remodeling in hyperhomocysteinemia.

Elevated plasma levels of homocysteine (Hcy) are associated with vascular dementias and Alzheimer's disease. The role of Hcy in brain microvascular endothelial cell (MVEC) remodeling is unclear. Hcy competes with muscimol, an gamma-amino butyric acid (GABA)-A receptor agonist. GABA is the primary inhibitory neurotransmitter in the brain. Our hypothesis is that Hcy induces constrictive microvascular remodeling by altering GABA-A/B receptors. MVEC from wild type, matrix metalloproteinase-9 (MMP-9) knockout (-/-), heterozygote cystathionine beta synthase (CBS-/+), and endothelial nitric oxide synthase knockout (eNOS-/-) mouse brains were isolated. The MVEC were incorporated into collagen (3.2 mg/ml) gels and the decrease in collagen gel diameter at 24 h was used as an index of constrictive MVEC remodeling. Gels in the absence or presence of Hcy were incubated with muscimol or baclofen, a GABA-B receptor agonist. The results suggested that Hcy-mediated MVEC collagen gel constriction was ameliorated by muscimol, baclofen, MMP-9, and eNOS gene ablations. There was no effect of anti-alpha 3 integrin. However, Hcy-mediated brain MVEC collagen constriction was abrogated with anti-beta-1 integrin. The co-incubation of Hcy with L-arginine ameliorated the Hcy-mediated collagen gel constriction. The results of this study indicated amelioration of Hcy-induced MVEC collagen gel constriction by induction of nitric oxide through GABA-A and -B receptors.

Animals↗
PubMed1984

Division of constricted and urethane-treated sand dollar eggs: a test of the polar stimulation hypothesis.

In spherical cells with a central mitotic apparatus, the centers of the asters are closer to the poles than to the equator. This circumstance is basic to several hypothetical explanations of the way in which the mitotic apparatus establishes the division mechanism. This investigation was designed to determine whether that geometrical relationship is necessary for division. Fertilized, mechanically denuded sand dollar eggs were inserted into glass loops, which reduced the diameter in the constriction plane from the normal 142 to 78-80 microns and partly constricted the cell into equal parts. The mitotic apparatus straddled the constriction, and its length was not significantly changed. The manipulation increased the distance from the astral centers to the poles and decreased the distance from the astral centers to the equator to a degree that reversed the normal distance relations. These cells divided normally. Ethyl urethane (0.06 M) reduces the size of the mitotic apparatus and blocks cleavage in spherical cells. When treated cells are confined in 80-microns i.d. capillaries, they divide. Treated cells also divide when they are constricted by an 80-microns i.d. glass loop if the mitotic apparatus straddles the constriction. An equal degree of constriction in the subfurrow and subpolar areas did not reverse the effect of urethane. The results demonstrate that cleavage does not depend on the normal distance relation between the mitotic apparatus and the poles, and that the urethane effect can be remedied only by reducing the distance between the mitotic apparatus and the equatorial surface. Both findings are inconsistent with the polar stimulation hypothesis.

Animals↗
PubMed1996

Activated polymorphonuclear leukocytes induce constriction of canine coronary artery via Mac-1, but not LFA-1, and ICAM-1.

Polymorphonuclear leukocytes (PMNs) can induce endothelium-dependent constriction of the vascular ring. We evaluated the roles of adhesion molecules in PMNs-induced coronary vasoconstriction. We measured changes in the isometric tension of isolated rings of canine coronary arteries with and without endothelium suspended in an organ chamber after the addition of autologous PMNs. In concentration of 5 x 10(5) to 1 x 10(7) cells/ml, fMLP-stimulated PMNs increased the tension of coronary artery with endothelium in a dose-dependent manner (23 +/- 3 to 102 +/- 11% of KCl-induced constriction). PMNs did not damage the endothelial function of coronary arteries as determined by an acetylcholine exposure. Mechanical rubbing of the endothelial cells abolished the PMN-induced vasoconstriction. The PMN-induced vasoconstriction (5 x 10(6) cells/ml: 98 +/- 8% of KCl-induced constriction) was inhibited when PMNs were pretreated with the monoclonal antibody against Mac-1 (54 +/- 4% of KCl-induced constriction) but not against LFA-1 against ICAM-1 (31 +/- 2% of KCl-induced constriction). The PMN-induced vasoconstriction was inhibited when PMNs were pretreated with the monoclonal antibody against CD18, and the extent of inhibition was comparable with CD11b/CD18. The combination of pretreatments of PMNs with CD11b/CD18 and of endothelium with ICAM-1 did not inhibit the vasoconstriction more than ICAM-1 alone. These results suggest that activated PMNs may mediate adherent-dependent constriction of canine coronary artery via Mac-1 (CD11b/CD18), but not LFA-1 (CD11a/CD18), with ICAM-1.

Animals↗
PubMed2001

Role of prostanoids and 20-HETE in mediating oxygen-induced constriction of skeletal muscle resistance arteries.

This study determined the contribution of cytochrome P450 (CP450) 4A enzyme metabolites of arachidonic acid in mediating the constriction of isolated rat skeletal muscle resistance arteries in response to elevated PO2. Gracilis arteries (GA) were viewed via television microscopy and constrictor responses to elevated PO2 were measured with a video micrometer. Endothelium removal and treatment of GA with 17-octadecynoic acid (17-ODYA; suicide substrate inhibitor of CP450 4A enzymes) impaired oxygen-induced constriction of the vessels; treatment of endothelium-denuded GA with 17-ODYA eliminated responses to elevated PO2. NOS inhibition and inhibition of EET production had no effect on oxygen-induced constriction of the vessels, although cyclooxygenase inhibition with indomethacin impaired GA responses to elevated PO2. Treatment of GA with dibromododecenyl methylsulfimide (DDMS; inhibitor of 20-hydroxyeicosatetraenoic acid (20-HETE) production) or 6(Z),15(Z)-20-HEDE (antagonist for 20-HETE receptors) mimicked the effects of 17-ODYA on GA responses to elevated PO2. Treatment of vessels with iberiotoxin or glibenclamide reduced the constriction of the vessels in response to elevated PO2 while treatment with both K+ channel blockers eliminated oxygen-induced constriction of the vessels. Following treatment of GA with indomethacin and 20-HETE, the vessels failed to respond to elevated PO2. These results suggest that oxygen-induced constriction of skeletal muscle resistance arteries represents the combined effects of reduced prostanoid release from the vascular endothelium and enhanced 20-HETE production in vascular smooth muscle cells.

Animals↗
PubMed2002

Characterization of the constriction with neocentric activity of 5RL chromosome in wheat.

In wheat-5RL monotelosomic and ditelosomic addition lines, a proximal constriction located on the long arm of rye chromosome 5R shows neocentric activity at metaphase I of meiosis. In some pollen mother cells this region is unusually stretched, acquires kinetic activity and co-orients with the true centromeres. In the work described here we characterized the putative neocentric constriction of 5RL using various approaches. Fluorescence in situ hybridization (FISH) revealed that the rye subtelomeric repetitive DNA sequence pSc119.2 is a constituent of the 5RL constriction. This FISH site corresponds with a heterochromatic C-band in normal rye. Other subtelomeric (pSc34, pSc74, pSc200), centromeric (CCS1, Bilby) and Arabidopsis-type telomeric sequences produce no detectable hybridization signal on the constriction. Immunolocalization with anti-alpha-tubulin antibodies showed that microtubules are bound to the constriction in a similar way to their binding to true centromeres. Silver staining demonstrated that proteins are accumulated at the constriction, the signal being more prominent than that observed at the centromere and telomeres of 5RL. The frequency of neocentric activity in different plants varied dramatically in different generations and in siblings grown in different years, suggesting that activation of the neocentric site is dependent on internal features and environmental conditions.

Centromere↗
PubMed2001

Pharyngeal constriction in elderly dysphagic patients compared with young and elderly nondysphagic controls.

This article reports the results of our study to determine the incidence of abnormalities in timing and extent of pharyngeal constriction in an elderly population with complaints of dysphagia. We performed a retrospective analysis of videofluoroscopic studies, i.e.. dynamic swallow studies, that were performed between 1996 and 1999. Included in the study were patients over 65 years old without an obvious medical or surgical cause for their dysphagia complaints. The timing of maximum pharyngeal constriction was measured relative to the onset of bolus pharyngeal transit, relative to the arrival of the bolus at the upper esophageal sphincter, and relative to the exit of the tail of the bolus from the upper esophageal sphincter. The extent of maximum pharyngeal constriction was measured from a lateral view. Patient data were compared with data gathered from young (18-62 years old) nondysphagic controls and with data gathered from elderly (67-83 years old) nondysphagic controls. We found that 73% of the patient population demonstrated incomplete pharyngeal constriction relative to controls, although the timing of pharyngeal constriction remained coordinated relative to the position of the bolus in the pharynx. Poor pharyngeal constriction, suggestive of pharyngeal weakness, contributed to 75% of the cases of aspiration.

Adult↗
PubMed1993

Effects of an NK1 receptor antagonist, FK888, on constriction and plasma extravasation induced in guinea pig airway by neurokinins and capsaicin.

The effects of FK888, an NK1 receptor antagonist, on airway constriction and airway plasma extravasation induced by neurokinins and capsaicin were investigated in guinea pigs. FK888 inhibited substance P (10(-8) M)- and neurokinin A (10(-9) M)-induced contraction of isolated guinea pig trachea, with IC50 values of 3.2 x 10(-8) and 4.2 x 10(-6) M, respectively. FK888 given i.v. inhibited substance P (13.5 micrograms kg-1)-induced airway constriction with an ED50 value of 0.40 mg kg-1 but did not inhibit neurokinin A (1.1 micrograms kg-1)- and capsaicin (3.1 micrograms kg-1)-induced airway constriction at a dose of 1 mg kg-1. On the other hand, FK888 given i.v. inhibited airway plasma extravasation induced by substance P (1.3 micrograms kg-1), neurokinin A (11 micrograms kg-1) and capsaicin (100 micrograms kg-1) with equal potency and ED50 values of 0.011, 0.0063 and 0.019 mg kg-1, respectively. When FK888 was given locally (into the airway directly) inhibitory activities were more potent than following i.v. administration. In this case FK888 inhibited substance P-, neurokinin A- and capsaicin-induced airway constriction with ED50 values of 3.2, 190 and 550 micrograms kg-1, respectively, suggesting that an about 100 times higher dose is required to inhibit neurokinin A- and capsaicin-induced airway constriction than substance P-induced constriction. FK888 given orally was also effective in substance P-, neurokinin A- and capsaicin-induced airway plasma extravasation with ED50 values of 4.2, 5.9 and 9.5 mg kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗