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PubMedDate not supplied

Constricting effect of leukotrienes on cerebral arterioles of mice.

Three leukotrienes (LTB4, C4, D4) were locally applied to cerebral arterioles in doses varying from 3 X 10(-8) to 4 X 10(-7) M and each produced a dose related constriction. LTC was tested in the presence and absence of FPL-55712, a relatively specific inhibitor of leukotriene receptors. A low dose (10(-8) M) of FPL-55712 did markedly reduce the response to the LTC and did not significantly alter an equally pronounced constriction produced by norepinephrine. The constricting properties of the leukotrienes shown by our data support the suggestion that these products of lipoxygenase's action on arachidonic acid have the potential to modify cerebrovascular tone. This potential may be important in view of recent evidence showing that the brain can make significant amounts of leukotrienes from arachidonic acid.

Animals↗
PubMedDate not supplied

Evidence that in vivo constriction of cerebral arterioles by local application of tert-butyl hydroperoxide is mediated by release of endogenous thromboxane.

Pial arterioles of mice were suffused in situ with tert-butyl hydroperoxide (TBHP). This agent has been reported to stimulate synthesis or release of the constrictor, thromboxane. In the present study we observed pial arterioles by in vivo microscopy. Locally applied TBHP produced dose-dependent constriction, significantly inhibited by each of three drugs: acetylsalicylic acid, OKY-046, and SQ-29548. These drugs are respectively a cyclooxygenase inhibitor, a thromboxane synthetase inhibitor, and a thromboxane receptor blocker. Since each acts by a different mechanism to interfere with thromboxane-mediated responses and each inhibited the contractile response to TBHP, thromboxane appears to be a mediator of this response. Platelet aggregation was not seen after local application of TBHP, and the dwell time of platelets at the site of TBHP application is less than 1 second. Thus, platelets are an unlikely source of the thromboxane mediating the local constriction. It is much more likely that the source of thromboxane is either the wall of the pial vessels or the underlying brain and/or its vessels. These data do not distinguish between the latter two possibilities, but if this suggestion is correct, then the data show for the first time that thromboxane can be released from normal brain and/or brain vessels in amounts sufficient to cause arteriolar constriction.

Animals↗
PubMed1990

Leukotriene constriction of mouse pial arterioles in vivo is endothelium-dependent and receptor-mediated.

The diameters of pial arterioles of mice were monitored in vivo with an image-splitting technique and television microscopy. Concentrations of leukotriene C4 as low as 10(-7) M constricted the arterioles. The leukotriene C4-D4 receptor blocker ICI 198615 (10(-8) M) inhibited the response. Endothelial injury by helium-neon laser/Evans blue technique eliminated the constriction and unmasked a slight but consistent relaxation that was not inhibited by 10(-8) M ICI 198615. Since leukotrienes are produced by the brain and enter the cerebrospinal fluid in ischemia, head trauma, and subarachnoid hemorrhage, the possibility that leukotrienes C4 and D4 contribute to decreases in cerebral blood flow during these conditions should be considered. However, the present data makes such a possibility far less likely because the endothelium is frequently injured in these conditions, and therefore the ability of leukotrienes to constrict vessels would be severely curtailed.

Animals↗
PubMedDate not supplied

Constriction of pial arterioles produced by prostaglandin F2alpha.

Prostaglandin F2alpha constricted pial arterioles when locally applied to the cerebral surface. Norepinephrine and serotonin each elicted similar contractile effects. The constriction produced by F2alpha in combination with either biogenic amine was greater than the constriction elicited by F2alpha or amine acting alone. The effect of one agent on the other was additive rather than potentiating. Since F2alpha norepinephrine and serotonin are all naturally occurring agents, it is possible that their combined effect is important under pathological circumstances and this combined effect should not be overlooked in the search for single spasmogens of great potency. Before ascribing a pathologically important effect of F2alpha, either alone or in combination, evidence is required showing that doses effective in experiments are similar to the concentrations occurring during disease states and/or that vessels may become hypersensitive to F2alpha during such states.

Animals↗
PubMed1990

C3a57-77, a C-terminal peptide, causes thromboxane-dependent pulmonary vascular constriction in isolated perfused rat lungs.

Pulmonary hypertension occurs after the intravascular activation of complement. However, it is unclear which activated complement fragments are responsible for the pulmonary vascular constriction. We investigated the 21-carboxy-terminal peptide of C3a (C3a57-77) to see if it would cause pulmonary vascular constriction when infused into isolated buffer-perfused rat lungs. Injection of C3a57-77 (225 to 450 micrograms) caused mean pulmonary arterial pressure (Ppa) to rapidly increase. However, the response was transient, with Ppa returning to baseline within 10 min of its administration. C3a57-77 also resulted in an increase in lung effluent thromboxane B2 (TXB2), concomitant with the peak increase in Ppa. C3a57-77 did not affect the amount of 6-keto-PGF1 alpha in the same effluent samples. Indomethacin inhibited the C3a57-77-induced pulmonary artery pressor response and the associated TXB2 production. Indomethacin also decreased lung effluent 6-keto-PGF1 alpha. The thromboxane synthetase inhibitors CGS 13080 and U63,357 inhibited the C3a57-77-induced pulmonary artery pressor response and TXB2 production without affecting 6-keto-PGF1 alpha. These inhibitors did not inhibit pulmonary artery pressor responses to angiotensin II. Tachyphylaxis to C3a57-77 occurred because a second dose of C3a57-77 administered to the same lung failed to cause a pulmonary artery pressor response or TXB2 production. The loss of the pressor response was not due to a C3a57-77-induced decrease in pulmonary vascular responsiveness because pressor responses elicited by angiotensin II were not altered by lung contact with C3a57-77. Thus, C3a57-77 caused thromboxane-dependent pulmonary vascular constriction in isolated buffer perfused rat lungs.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

Absence of stellate ganglion influence on alveolar-duct constriction.

Previous work has shown decreased lung compliance with high wash fluid surface tensions, but normal ratios of lung weight to body weight during stellate ganglion stimulation (SGS) in cats and monkeys. In the present study, effects of SGS on diameters of alveolar ducts were determined in spontaneously breathing cats under ketamine anesthesia. Compliance and pulmonary resistance were also measured. A fluorocarbon cooled to - 100 degrees C was poured onto an exposed lung lobe after rapidly opening the chest after sham operation and during SGS. Examination of the outer 2 mm of the lungs by light microscopy revealed no alveolar-duct constriction by SGS, although compliance decreased by 15%. Pulmonary resistance was unchanged. Alveolar-duct diameters were 157 +/- 4.3 micron (mean +/- SEM) in control animals and 163 +/- 4.6 micron in SGS cats. Absence of alveolar-duct constriction suggests that peripheral airway constriction did not contribute to the decrease in compliance during SGS.

Airway Resistance↗
PubMed1985

Effective sites by sympathetic beta-adrenergic and vagal nonadrenergic inhibitory stimulation in constricted airways.

In an attempt to identify the site and nature of nonadrenergic inhibitory nervous regulation in airways, we studied the relative effectiveness of the nervous system in reversing bronchoconstriction along various generations of airways by comparing it with that seen during sympathetic (beta-adrenergic) stimulation in 9 cats. After giving atropine (3 mg/kg), airway dimensions were obtained from roentgenograms after insufflation of powdered tantalum. Baseline bronchoconstriction was then induced by an intravenous infusion of serotonin (50 to 250 micrograms/kg/min). Electrical stimulation of the sympathetic nerves inhibited constriction throughout the airways from trachea down to bronchioli less than 0.5 mm in diameter, with the maximal effect in airways 1 to 4 mm in diameter. The vagi were then stimulated after blocking the adrenergic inhibitory nervous system with propranolol (2 mg/kg). The distribution and potency of the remaining nonadrenergic inhibitory nerve's effect on airway constriction induced by serotonin was comparable to that obtained with sympathetic stimulation. We conclude that the nonadrenergic inhibitory nerves preferentially dilate the midsized airways, which essentially correspond to the sites maximally constricted by vagal stimulation without atropine. The largest (tracheal) and the peripheral airways (less than 1 mm in diameter) are only slightly affected by either inhibitory system.

Animals↗
PubMed1971

The relative contributions of reabsorptive rate and redistributed nephron filtration rate to changes in proximal tubular fractional reabsorption during acute saline infusion and aortic constriction in the rat.

The absolute rate of reabsorption by superficial rat proximal tubules was measured by the in situ microperfusion technique under conditions of hydropenia, infusion of saline, and infusion of saline plus aortic constriction sufficient to decrease whole kidney filtration rate below hydropenic levels. Fractional reabsorption was measured in adjacent filtering nephrons by collecting and recollecting tubular fluid from late proximal convolutions during each experimental condition. During hydropenia, the absolute rate of proximal tubular reabsorption averaged 3.56 +/-0.60 nl/min per mm and late proximal tubular fractional reabsorption averaged 0.56 +/-0.10. From these two measurements and measurements of tubule length to the site of micropuncture, a value for filtration rate was calculated for filtering nephrons. During hydropenia this value averaged 32.9 +/-7.1 nl/min. Saline infusion increased sodium excretion to 5.5% of the filtered load as the absolute rate of proximal tubular reabsorption decreased 38% and fractional reabsorption decreased 45%. Calculated superficial nephron filtration rate increased 21% which on the average was identical with the simultaneously measured increase in whole kidney filtration rate. Similar results were obtained in a separate group of animals by the technique of total collection of late proximal tubular fluid. Aortic constriction during saline infusion decreased whole kidney and calculated nephron filtration rate to the same degree and to values lower than those during hydropenia. Fractional reabsorption increased but not to hydropenic values. The persistent natriuresis during aortic constriction was associated with a continued depression of the absolute rate of proximal tubular reabsorption which was sufficient to maintain an increased delivery of filtrate out of the proximal tubule despite the fall in nephron filtration rate. These results indicate that depressed fractional reabsorption in the proximal tubule during acute saline infusion is due predominantly to a decrease in absolute reabsorptive rate and to a lesser extent to an increase in superficial nephron filtration rate which is proportional to the increase in whole kidney filtration. Continued natriuresis when filtration rate is decreased during saline infusion can be accounted for entirely by the persistent large reduction in the absolute rate of proximal tubular reabsorption.

Aminohippuric Acids↗
PubMed2005

Pharmacological reversal of endothelin-1 mediated constriction of the spiral modiolar artery: a potential new treatment for sudden sensorineural hearing loss.

BACKGROUND: Vasospasm of the spiral modiolar artery (SMA) may cause ischemic stroke of the inner ear. Endothelin-1 (ET-1) induces a strong, long-lasting constriction of the SMA by increasing contractile apparatus Ca2+ sensitivity via Rho-kinase. We therefore tested several Rho-kinase inhibitors and a cell-permeable analogue of cAMP (dbcAMP) for their ability to reverse ET-1-induced constriction and Ca2+-sensitization. METHODS: The present study employed SMA isolated from gerbil temporal bones. Ca2+sensitivity was evaluated by correlating vascular diameter and smooth muscle cell [Ca2+]i, measured by fluo-4-microfluorometry and videomicroscopy. RESULTS: The Rho-kinase inhibitors Y-27632, fasudil, and hydroxy-fasudil reversed ET-1-induced vasoconstriction with an IC50 of 3, 15, and 111 micromol/L, respectively. DbcAMP stimulated a dose-dependent vasodilation (Ec50 = 1 mmol/L) and a reduction of [Ca2+]i (EC50 = 0.3 micromol/L) of ET-1-preconstricted vessels (1 nmol/L). Fasudil and dbcAMP both reversed the ET-1-induced increase in Ca2+ sensitivity. CONCLUSION: Rho-kinase inhibition and dbcAMP reversed ET-1-induced vasoconstriction and Ca2+-sensitization. Therefore, Rho-kinase inhibitors or cAMP modulators could possess promise as pharmacological tools for the treatment of ET-1-induced constriction, ischemic stroke and sudden hearing loss.

Journal Article↗
PubMed2006

Lack of flow-mediated dilation and enhanced angiotensin II-induced constriction in skeletal muscle arterioles of lupus-prone autoimmune mice.

Systemic lupus erythematosus (SLE) is associated with disturbances in the microcirculation of various tissues, yet the nature of arteriolar dysfunction has not been characterized. Thus, changes in diameter of isolated, pressurized skeletal muscle arterioles of mice with systemic autoimmune disease (lupus prone, MRL/lpr four-month old female) and control (MRL) mice were investigated by video-microscopy. Arteriolar responses to changes in intraluminal pressure, flow, and to vasoactive agents with known mechanisms of action were compared. The active and passive (in Ca2+ free solution) diameter of MRL/lpr arterioles were not significantly different compared to MRL and morphometric changes were not apparent. Compared to MRL mice the endothelium-dependent dilations to increase in flow, acetylcholine and bradykinin were markedly reduced in arterioles of MRL/lpr mice. Endothelium-independent dilations to sodium-nitroprusside and adenosine were similar in MRL and MRL/lpr arterioles. Furthermore, angiotensin II elicited greater constrictions in MRL/lpr arterioles, whereas serotonin-induced constrictions were similar in both groups. Thus, in arterioles of MRL/lpr mice endothelium-dependent dilator mechanisms are impaired and constriction to angiotensin II is enhanced, suggesting specific alterations in the vasomotor function of microvessels that are likely contribute to the disturbance of skeletal muscle blood flow observed in systemic lupus erythematosus.

Acetylcholine↗
PubMed1993

Nitrous oxide constricts epicardial coronary arteries in pigs: evidence suggesting inhibitory effects on the endothelium.

Nitrous oxide increases peripheral vascular tone in animals and humans and constricts epicardial coronary arteries in dogs. Current studies sought both to determine whether nitrous oxide caused epicardial coronary artery constriction in a second animal species, pigs, and to investigate mechanisms. Left anterior descending coronary artery diameters were measured by using computer-assisted angiography in intact pigs anesthetized with ketamine and fentanyl. In separate experiments, isolated porcine coronary arteries were used to assess nitrous oxide effects on both vascular tone and norepinephrine overflow. Agonist-induced increases in [Ca2+]i were estimated in cultured porcine coronary endothelial cells. Nitrous oxide caused epicardial coronary artery vasoconstriction in vivo by about 20%. Nitrous oxide did not affect endothelium-dependent relaxations and contractions in isolated vessels. Norepinephrine overflow was increased but only in vessels with endothelium. The anesthetic attenuated Ca2+ mobilization in endothelial cells. We conclude that nitrous oxide induces epicardial coronary artery constriction in pigs and suggest that the mechanism may involve the inhibition of endothelium-dependent norepinephrine turnover.

Animals↗
PubMed2007

Abelson kinase (Abl) and RhoGEF2 regulate actin organization during cell constriction in Drosophila.

Morphogenesis involves the interplay of different cytoskeletal regulators. Investigating how they interact during a given morphogenetic event will help us understand animal development. Studies of ventral furrow formation, a morphogenetic event during Drosophila gastrulation, have identified a signaling pathway involving the G-protein Concertina (Cta) and the Rho activator RhoGEF2. Although these regulators act to promote stable myosin accumulation and apical cell constriction, loss-of-function phenotypes for each of these pathway members is not equivalent, suggesting the existence of additional ventral furrow regulators. Here, we report the identification of Abelson kinase (Abl) as a novel ventral furrow regulator. We find that Abl acts apically to suppress the accumulation of both Enabled (Ena) and actin in mesodermal cells during ventral furrow formation. Further, RhoGEF2 also regulates ordered actin localization during ventral furrow formation, whereas its activator, Cta, does not. Taken together, our data suggest that there are two crucial preconditions for apical constriction in the ventral furrow: myosin stabilization/activation, regulated by Cta and RhoGEF2; and the organization of apical actin, regulated by Abl and RhoGEF2. These observations identify an important morphogenetic role for Abl and suggest a conserved mechanism for this kinase during apical cell constriction.

Actins↗
PubMed1990

Inhibitory modulation of the reflex tracheal constriction induced by afferent vagal stimulation.

Afferent cervical vagal electrical stimulation caused a reflex tracheal constriction. Atropine changed the tracheal constriction into a tracheal dilatation that was almost inhibited by propranolol. In the hypertonic trachea with 5-hydroxytryptamine, a reflex dilatation following a constriction was observed by afferent vagal stimulation. The reflex dilatation was inhibited about 50% by propranolol and was abolished by hexamethonium. These results suggest that the adrenergic and nonadrenergic inhibitory innervations may mediate the reflex tracheal dilatation, especially in a hypertonic tracheal condition.

Animals↗
PubMed1994

Inhibitory effect of enalapril on the constriction of the ductus arteriosus in newborn rats.

Caesarean newborn rats were given subcutaneously enalapril maleate (EM), an angiotensin-converting enzyme inhibitor, (1) immediately or (2) 180 min after delivery. The ductus arteriosus (DA) in these newborn pups was calibrated 30, 60 and 90 min after the EM-treatment. The results were as follows: (1) DA calibers of the pups given 10 or 50 mg/kg EM just at caesarean delivery remained significantly larger than those of the controls thereafter until 90 min. (2) The DA was completely closed 180 min after caesarean delivery. However, with 50 mg/kg EM given at this time, the DA was temporarily re-opened and then constricted. It is concluded that, in newborn rats, EM has the direct inhibitory action on the constriction of the DA, and that it also has the re-opening action on the once-constricted DA.

Animals↗
PubMed2000

Visual field constriction in children with epilepsy on vigabatrin treatment.

Vigabatrin is considered the drug of choice for infantile spasms and simple and complex partial epilepsy in childhood. Its mechanism of action relies on the irreversible inhibition of gamma-aminobutyric acid (GABA) transaminase. Since June 1997 several articles have been published reporting visual field constriction in adult patients on vigabatrin therapy. Recently, 7 pediatric patients, 1 on vigabatrin monotherapy and 6 on add-on therapy with visual field constriction have been described. We have observed 30 pediatric patients with epilepsy (14 boys and 16 girls), ages ranging from 4 to 20 years (mean: 11 years and 2 months) treated with vigabatrin for infantile spasms, simple and complex partial epilepsy, who had never complained of ophthalmologic disturbances. Twenty-one patients underwent complete routine ophthalmologic examination (fundus oculi, visual acuity, intraocular pressure, and visual field tests); 9 children (<6 years old) underwent only fundus examination, because collaboration was lacking. We report on 4 children showing constriction of visual field, prevailing in nasal hemifield. In 1 child, visual abnormalities were stable even 10 months after vigabatrin discontinuation, while in another a greater improvement was observed 5 months after discontinuation. The possible mechanisms have been discussed and the cone dysfunction, connected with GABA augmentation in the outer retina, has been outlined. We suggest a possible protocol to control visual abnormalities in epileptic children.

Adolescent↗
PubMed2004

Mandibular widening by distraction osteogenesis in the treatment of a constricted mandible and telescopic bite.

OBJECTIVE: Documentation of the application of mandibular widening by distraction osteogenesis and orthodontics. PATIENTS: Three patients with telescopic bite resulting from an extremely constricted mandible related to hypoglossia-hypodactyly syndrome. INTERVENTION: Mandibular widening by distraction osteogenesis using an extraoral device and subsequent orthodontic treatment. RESULTS: The extremely constricted mandible and telescopic bite were dramatically improved by mandibular widening using distraction osteogenesis and subsequent orthodontics. Two of the three patients had transient complications; one reported temporomandibular joint pain and the other showed evidence of periodontal damage. CONCLUSION: Mandibular widening by distraction osteogenesis is an effective technique for the treatment of telescopic bite resulting from an extremely constricted mandible.

Child↗
PubMed1994

Proliferative and constrictive bronchiolitis: classification and radiologic features.

The small airways of the lung consist of the terminal bronchioles, respiratory bronchioles, and alveolar ducts. A recently introduced pathologic classification system divides bronchiolitis into proliferative and constrictive types. The histologic classification of small-airways disease into proliferative and constrictive bronchiolitis frequently correlates with the radiographic appearances. Proliferative bronchiolitis is characterized by air-space opacification, whereas constrictive bronchiolitis tends to be associated with lobular areas of decreased attenuation and airway dilatation. The purpose of this essay is to illustrate the radiographic and CT features of these two varieties of bronchiolitis.

Bronchiolitis↗
PubMed1999

Clinical analysis of breathing exercise during immersion in 38 degrees C water for obstructive and constrictive pulmonary diseases.

Breathing exercises during immersion in 38 degrees C water were performed in 22 patients with bronchial asthma, pulmonary emphysema and constrictive pulmonary diseases. The patients entered a pool filled with 38 degrees C water to shoulder level. While standing, they breathed in deeply and breathed out slowly through the mouth into water while sinking the nose below the water level. This breathing method was repeated for 20 min. with a 5-min. rest out of water and this cycle was performed twice a day for two months. Respiratory function test and arterial blood gas analysis were examined before and after the two-month exercise program. FEV1.0% was significantly increased in patients with asthma and emphysema (p = 0.042 and 0.032, respectively) but did not change in patients with constrictive pulmonary diseases. %FVC, PF and Vmf25 did not change in any of the diseases. PaO2 was significantly increased in emphysematous patients (p = 0.0002) and PaCO2 was significantly decreased in asthmatic and emphysematous patients (p = 0.034 and 0.046, respectively). These results suggest that our breathing exercise by immersion is useful in patients with asthma and emphysema but is less effective in patients with constrictive pulmonary diseases.

Aged↗