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PubMedDate not supplied

Uterine venous permeability in the rat is altered in response to pregnancy, vascular endothelial growth factor, and venous constriction.

Venoarterial communication is a potential short-loop signaling pathway for the local control of uteroplacental perfusion. As this pathway is permeability-dependent, this study investigated the effects of molecular weight, gestation, vascular endothelial growth factor (VEGF), wall tension, and constriction on solute flux across the venous wall. Experiments utilized fluorimetry to quantitate solute flux (3- and 70-kDa dextran) in isolated segments of uterine vein from virgin (NP) and late-pregnant (LP; day 20) rats as a function of endothelial surface area and time. Uterine veins were > 10-fold more permeable to the 3- versus 70-kDa dextran in both NP and LP groups. Flux was increased during gestation ( 2.5-fold), and by VEGF (NP, 3 kDa: 3.3-fold, 70 kDa: 4.8-fold; LP, 3-kDa: 3.3-fold, 70 kDa: 7.4-fold). Permeability to the 3 kDa dextran correlated directly with wall tension (r2 = .74 in both groups), whereas permeability to both dextrans correlated inversely with constriction (NP: r2 = .85 and .76; LP: r2 = .89 and .79, respectively). Uterine veins demonstrate permeability to 3- and 70-kDa tracers resulting from molecular weight dependence and an apparent difference in transport mechanisms. Permeability is enhanced by gestational remodeling and subject to modulation by placental factors, indicating the presence of a regulated pathway for the transfer of molecules across the venous wall.

Animals↗
PubMed2003

Effects of three different L-type Ca2+ entry blockers on airway constriction induced by muscarinic receptor stimulation.

BACKGROUND: The crucial role of L-type Ca(2+) channels in airway smooth muscle contraction suggests that these channels could be an important therapeutic target. There are three separate drug binding sites on this channel: those for dihydropyridines, benzothiazepines and phenyl alkylamines. In this study, we examined the effects of the dihydropyridines nifedipine and nicardipine, the benzothiazepine diltiazem, and the phenylalkylamine verapamil on airway constriction. METHODS: Tension of guinea-pig tracheal strips was measured isometrically in vitro with a force displacement transducer. Strips were precontracted with carbachol 10(-7) M with or without 4-aminopyridine 10(-3) M, a voltage-sensitive K(+ )channel blocker. Then, nifedipine 10(-8)-10(-4) M, diltiazem 10(-8)-3 x 10(-4) M or verapamil 10(-8)-3 x 10(-4) M was added cumulatively to the organ bath (n=6 each). The bronchial cross-sectional area of pentobarbital-anaesthetized dogs was assessed using a bronchoscopy method. Bronchoconstriction was elicited with methacholine 0.5 micro g kg(-1) plus 5 micro g kg(-1) min(-1), and then nicardipine 0-1000 micro g kg(-1), diltiazem 0-3000 micro g kg(-1) or verapamil 0-3000 micro g kg(-1) were given i.v. (n=7 each). RESULTS: In the in vitro experiments, nifedipine and diltiazem fully reversed carbachol-mediated tracheal contraction with logIC(50) values of 4.76 (SEM 0.22) (mean 17.5 micro M) and 4.60 (0.33) (mean 24.8 micro M), respectively. Although verapamil 10(-6)-10(-4) M reversed the contraction by 87.2%, strip tension re-increased by 18.1% following maximal relaxation with verapamil 3 x 10(-4 )M. This re-increase was almost fully abolished by pretreatment with 4-aminopyridine. In the in vivo experiments, nicardipine and diltiazem dose-dependently reversed methacholine-induced bronchoconstriction, with logID(50) values of 3.22 (0.05) (mean 0.60 mg kg(-1)) and 1.85 (0.32) (mean 14.0 mg kg(-1)), respectively. Verapamil worsened methacholine-induced bronchoconstriction. CONCLUSIONS: Although supraclinical doses of dihydropyridines and benzothiazepines can produce airway relaxant effects, these agents are unlikely to be used in the treatment of bronchoconstriction. In addition, verapamil may aggravate airway constriction.

Animals↗
PubMed1999

Differential pupillary constriction and awareness in the absence of striate cortex.

The fact that the pupil constricts differentially to visual stimuli in the absence of changes in light energy makes it a valuable tool for studying normal function as well as residual capacity in hemianopic subjects. When pupillometrically effective stimuli such as equiluminant gratings or coloured patches with an abrupt onset and offset are presented to the 'blind' hemifield, a hemianopic subject with damage largely restricted to striate cortex (V1) sometimes reports being 'aware' of the transient onset/offset, although without 'seeing' as such. The question addressed here is whether the pupil still responds in the condition of blindsight in its strict sense--i.e. discriminative capacity in the absence of acknowledged awareness--when stimuli are deliberately designed to eliminate awareness. This was accomplished by making stimulus onset and offset slow and gradual. The results with a well-studied hemianope, G.Y., demonstrate that there is still a pupillary constriction to isoluminant achromatic gratings and red-coloured stimuli, although reduced in size, in the absence of acknowledged awareness.

Accidents, Traffic↗
PubMed2005

Ion changes in spreading ischaemia induce rat middle cerebral artery constriction in the absence of NO.

In rats, cortical spreading hyperaemia is coupled to a spreading neuroglial depolarization wave (spreading depression) under physiological conditions, whereas cortical spreading ischaemia is coupled to it if red blood cell products are present in the subarachnoid space. Spreading ischaemia has been proposed as the pathophysiological correlate of the widespread cortical infarcts abundantly found in autopsy studies of patients with subarachnoid haemorrhage. The purpose of the present study was to investigate whether the extracellular ion changes associated with the depolarization wave may cause the vasoconstriction underlying spreading ischaemia. We induced spreading ischaemia in vivo with the nitric oxide (NO) scavenger oxyhaemoglobin and an elevated K+ concentration in the subarachnoid space while slow potential, pH, extracellular volume and concentrations of K+, Na+, Ca2+ and Cl- were measured in the cortex with microelectrodes. We then extraluminally applied an ionic cocktail (cocktail(SI)) to the isolated middle cerebral artery in vitro, matching the ionic composition of the extracellular space as measured during spreading ischaemia in vivo. Extraluminal application of cocktail(SI) caused middle cerebral artery dilatation in the absence and constriction in the presence of NO synthase inhibition in vitro, corresponding with the occurrence of spreading hyperaemia in the presence and spreading ischaemia in the absence of NO in vivo. The L-type Ca2+ inhibitor nimodipine caused the cocktail(SI)-induced vasoconstriction to revert to vasodilatation in the absence of NO in vitro similar to the reversal of spreading ischaemia to spreading hyperaemia in response to nimodipine in vivo. We found that K+ was the predominant vasoconstrictor contained in cocktail(SI). Its vasoconstrictor action was augmented by NO synthase inhibition. Our results suggest that, under elevated baseline K+ as a hallmark of any condition of energy deficiency, the extracellular ion changes represent the essential mediator of the vascular response to spreading neuroglial depolarization. In the presence of NO they mediate vasodilatation and in its absence they mediate constriction.

Animals↗
PubMed2003

Preliminary investigation of a modified Huddart/Bodenham scoring system for assessment of maxillary arch constriction in unilateral cleft lip and palate subjects.

The objective of this study was to describe a numerical scoring system for the measurement of maxillary arch constriction in patients born with unilateral cleft lip and palate (UCLP). A modification of the Huddart/Bodenham scoring system was compared and contrasted with the current methods of measuring treatment outcome, the GOSLON and 5-year indices. The GOSLON and 5-year indices are represented by 10 sets of study models grouped into five categories representing the range of possible outcomes in terms of dental arch relationship, with two sets of models in each of the five categories, whilst the modified Huddart/Bodenham method uses the frequency and severity of crossbite of the dental occlusion to evaluate maxillary arch constriction. The latter system was found to be more objective and reliable, and to correlate well with current recommended standards. It was also more versatile and more sensitive to interarch discrepancies. However, further work is required to refine it to reflect the potential for orthodontic treatment to mask interarch discrepancy following surgery.

Child↗
PubMed2004

Direct pericardial involvement of non-small cell lung cancer rapidly developing pericardial constriction.

A 71-year-old male, who had been followed up after being treated with chemo-radiotherapy for non-small cell lung cancer (adenocarcinoma), rapidly developed dyspnea and mild fever. Radiographs showed left pleural effusion and cardiomegaly, and echocardiographic examination revealed echo-free space, suggesting a pericardial effusion. The patient was treated conservatively without any surgical procedures such as pericardiocentesis. Disappearance of the echo-free space was followed by development of pericardial constriction within two months. At post-mortem examination, a direct extension to the pericardium from the primary lesion of the right upper lobe through the mediastinum was observed. The rapid development of pericardial constriction is extremely rare in patients with malignant pericarditis.

Adenocarcinoma↗
PubMed2004

In vitro hypoxia differentially affects constriction and relaxation responses of isolated pulmonary arteries from broiler and leghorn chickens.

Under normoxic conditions in vitro, isolated pulmonary arteries from broilers exhibit reduced endothelium-dependent relaxation responses when compared with Leghorns. In vivo, hypoxia increases the susceptibility of broiler chickens to pulmonary hypertension syndrome (PHS), whereas Leghorns are considered resistant to PHS. Because L-arginine supplementation decreases the incidence of PHS in vivo and improves the relaxation responses of broiler isolated pulmonary arteries in vitro, we hypothesized that in vitro hypoxia would further reduce the relaxation responses of broilers to endothelium-derived nitric oxide (EDNO)-dependent vasodilators and that L-arginine supplementation would alleviate this impairment. As a test of this hypothesis, pulmonary arteries from broiler and Leghorn chickens were isolated and exposed to normoxia or hypoxia in the presence or absence of L-arginine while their constriction and relaxation responses to vasoactive compounds were recorded. In broilers, hypoxia did not affect the constriction responses of isolated pulmonary arteries but decreased EDNO-dependent acetylcholine-induced relaxation responses. In contrast, in Leghorns hypoxia increased endothelin-1-induced vasoconstriction responses and reduced the EDNO-dependent relaxation responses only to the lowest concentration of acetylcholine used. L-Arginine supplementation augmented the relaxation responses to acetylcholine in broilers and Leghorns under normoxia but failed to augment them under hypoxia. Relaxation responses to the NO donor, sodium nitroprusside, were not affected by hypoxia in Leghorns but were increased by hypoxia in broilers. These results suggest that the increased incidence of PHS in broiler chickens reared under hypoxia may be associated with a hypoxia-induced reduction in the synthesis or activity of EDNO in the pulmonary circulation.

Acetylcholine↗
PubMed2001

A prostaglandin E2 receptor subtype EP1 receptor antagonist (ONO-8711) reduces hyperalgesia, allodynia, and c-fos gene expression in rats with chronic nerve constriction.

UNLABELLED: Chronic constriction injury (CCI) of the sciatic nerve in rats induces persistent mechanical hyperalgesia and allodynia. CCI is widely known as a model of neuropathic pain, and many studies using this model have been reported. Recently, c-fos has been used as a neural marker of pain, and various studies have assessed the relationship between hyperalgesia and c-fos expression in the lumbar spinal cord. In this study, we examined the role of a prostaglandin E2 receptor subtype EP1 receptor antagonist (ONO-8711) in a rat CCI model. EP1 receptor antagonist (EP1-ra) oral administration from day 8 to day 14 significantly reduced hyperalgesia and allodynia in the three pain tests on day 15. EP1-ra treatment from day 8 to 14 also reduced c-fos-positive cells in laminae I-II, III-IV, and V-X compared with saline treatment. A single dose of EP1-ra treatment on day 8 significantly reduced hyperalgesia and allodynia at 1 h and 2 h after administration, but the efficacy was not observed at 24 h. We conclude that EP1-ra treatment may be useful for hyperalgesia and allodynia and that EP1 receptor mechanisms are involved in the maintenance of c-fos gene expression induced by nerve injury. IMPLICATIONS: We examined whether a prostaglandin E2 receptor subtype EP1 receptor antagonist abrogates neuropathic pain induced by chronic constriction injury model in rats. The EP1 receptor antagonist significantly reduced hyperalgesia, allodynia, and c-fos positive cells. These findings suggested that EP1 receptor antagonists may have a role in treatment of neuropathic pain.

Animals↗
PubMed1987

C5a and thromboxane generation associated with pulmonary vaso- and broncho-constriction during protamine reversal of heparin.

The authors conducted a study in humans to determine the mediators associated with acute pulmonary vaso- and broncho-constriction occurring episodically with protamine reversal of heparin anticoagulation. Of 48 adult patients investigated prospectively after termination of cardiopulmonary bypass, two presented a sudden increase of airway pressure, acute pulmonary hypertension, and systemic hypotension 1-3 min after right atrial protamine injection. In these two subjects, plasma levels of C5a increased from 0.7 and 2.2 to 9.8 and 9.9 ng/ml, respectively, and thromboxane B2 increased from 0.26 and 0.34 to 7.5 and 16.2 ng/ml 1 minute after drug injection. A third subject not identified prospectively had an identical reaction and mediator profile (C5a, 10.2 ng/ml; TxB2, 18.6 ng/ml at 1 min). The plasma levels of these mediators were unchanged in the remaining patients (C5a, 0.7 +/- 1.1 [x +/- S.D.] to 0.6 +/- 0.9 ng/ml; TxB2, 0.16 +/- 0.12 to 0.15 +/- 0.07 ng/ml). Plasma histamine was not involved in this type of reaction, but increased from 0.7-10.4 ng/ml in a fourth patient who became hypotensive without acute pulmonary hypertension, bronchoconstriction, or elevation of C5a or TxB2. The authors' data indicate that the generation of high plasma levels of C5a anaphylatoxins and thromboxane is associated with pulmonary vaso- and broncho-constriction induced by protamine reversal of heparin in humans.

Adult↗
PubMed1987

Nitrous oxide constricts epicardial coronary arteries without effect on coronary arterioles.

The authors sought to determine the effects of nitrous oxide on both epicardial coronary artery dimensions and intramyocardial coronary arteriolar tone. Nine dogs were anesthetized with fentanyl-pentobarbital-oxygen. High resolution angiograms of the left coronary system were obtained, and cross-sectional areas of the proximal, mid, and distal left anterior descending and proximal circumflex coronary arteries were quantitated using a computerized analysis system. Measurements were made at three coronary perfusion pressures before nitrous oxide administration, and then repeated following the addition of both 30% and 60% nitrous oxide. At the same time, coronary arteriolar tone was assessed by measuring coronary blood flow using 133Xenon washout. Sixty percent nitrous oxide was accompanied by constriction of the epicardial coronary arteries. Thirty percent nitrous oxide had a less marked effect. At 70 mmHg coronary perfusion pressure, following 60% nitrous oxide, mid left anterior descending cross-sectional area decreased from 4.6 +/- 0.3 mm2 (mean +/- SD) to 3.5 +/- 0.3 mm2. At 90 mmHg, area decreased from 4.57 +/- 0.3 mm2 to 3.69 +/- 0.4 mm2, and, at 110 mmHg, from 4.7 +/- 0.4 mm2 to 3.9 +/- 0.4 mm2 (P less than 0.01). Nitrous oxide had no effect on the relationship between coronary blood flow and myocardial oxygen consumption, indicating an absence of effect on coronary arteriolar tone. It is concluded that intramyocardial coronary arterioles and epicardial coronary arteries are dissimilar in their response to nitrous oxide. In the intact, anesthetized, normal dog, nitrous oxide does not affect coronary arteriolar tone. Sixty percent nitrous oxide produces constriction of epicardial coronary arteries.

Animals↗
PubMed1994

Halothane and enflurane constrict canine mesenteric arteries by releasing Ca2+ from intracellular Ca2+ stores.

BACKGROUND: Recent studies suggest that volatile anesthetics cause not only vasodilation but also vasoconstriction, depending on the experimental conditions. However, the mechanism of the constrictive effect of volatile anesthetics has not been clarified. The aim of this study was to evaluate the vasoconstrictor effects of halothane, enflurane, and isoflurane and to elucidate the underlying mechanism. METHODS: Vascular rings of canine mesenteric arteries were mounted in organ baths, and isometric tension changes were recorded. Changes in intracellular free Ca2+ concentration of vascular smooth muscle were examined by using the fluorescent Ca2+ indicator fura 2 and a dual-wavelength fluorometer. RESULTS: Halothane (0.75-2.3%) and enflurane (1.7-3.4%), but not isoflurane (1.2-3.5%), induced a concentration-dependent transient contraction, followed by a slight, sustained contraction. Halothane (1.5%)- and enflurane (3.4%)-induced contractions were reduced by endothelial denudation and enhanced by indomethacin (10(-5) M) treatment but were not affected by L-NG-nitroarginine (10(-5) M) or nifedipine (2 x 10(-7) M) treatment. Ryanodine (2 x 10(-5) M) treatment completely abolished the transient increases in tension and Ca2+ concentration. Even in ryanodine-treated arteries, however, both anesthetics induced a slowly developing sustained contraction, and the sustained contraction induced by enflurane (3.4%) was not accompanied by a significant increase in Ca2+ concentration. CONCLUSIONS: Halothane and enflurane, but not isoflurane, induce vasoconstriction by releasing Ca2+ from intracellular stores. Release of a vasodilating prostanoid and endothelium-derived constricting factor may also be involved in the vasoconstrictor effect. Furthermore, increased Ca2+ sensitivity of contractile machinery may be involved in the effect of enflurane.

Animals↗
PubMed1987

Single-stage correction of constriction ring syndrome.

The accepted method of treatment for the constricting ring syndrome of the extremities is serial excision and repair with Z-plasties. A series of 4 patients operated upon in different centers by single-stage excision of the ring and multiple Z-plasty repair is presented. In 1 patient there was absence of a major nerve trunk underneath and distal to a constriction ring. None of the patients suffered any significant circulatory embarrassment. This surgical approach is anatomically sound and clinically safe. It should be considered as an alternative method of treatment to the currently accepted procedure.

Amniotic Band Syndrome↗
PubMed1993

The influence of nodal constriction on conduction velocity in myelinated nerve fibers.

Myelinated nerve fibers exhibit a complex anatomy in the nodal region which includes a marked nodal-paranodal constriction and an intricate paranodal structure where the myelin sheath is separated from the axon by a narrow periaxonal space. In this study, a recently developed computational model of the mammalian myelinated nerve fiber based on electron microscopic data was employed to examine the effect of the nodal-paranodal axonal radius and periaxonal space width on the conduction of action potentials. These findings indicate that the nodal-paranodal constriction promotes higher conduction velocities by minimizing the component of the nodal capacity contributed by the paranodal axolemma. Model prediction of optimal nodal-paranodal radii is correlated with radii determined in experimental anatomical studies.

Action Potentials↗
PubMed1994

A study of early ongoing activity in dorsal horn units following sciatic nerve constriction.

An analysis was made of the background activity of spinal neurones involved in nociceptive processes during, and in the first hour after, sciatic nerve constriction in normal rats and in rats in which sciatic nerve conduction had been previously blocked with local anaesthetic. In both pure noxious and WDR neurones the results showed high frequency discharges at the time of ligation, followed by a slight but persistent increase in activity that reached, after 1 h, values 6-8 times those preligature. The increased post-injury discharge could be reduced by secondarily applying lidocaine on the peripheral site of constriction. There were no neuronal activity changes after the ligatures in rats with sciatic nerve pretreated with local anaesthetic. The likelihood that the early persistent increase in activity may have a role in the excitability change of spinal neurones observed in neuropathic pain is discussed.

Animals↗
PubMed1996

Clubfeet in congenital annular constricting bands.

Thirty-five children who had congenital annular constricting bands (Streeter's dysplasia) with associated clubfeet seen by the author from September 1989 to March 1992 were reviewed with respect to quality of the clubfeet,the relationship of the bands with the clubfeet, possible prenatal factors, and treatment results. It was noted that all the clubfeet were rigid even if there were no constricting bands in the leg with the clubfoot. The clubfeet responded poorly to casting (6% success) and 77% required surgical correction. Z-plasties of deep bands were done before clubfoot correction. There was a high incidence of abnormal pregnancies with attempts at abortion in 66% of the cases, suggesting intrauterine insult early in the pregnancy as a factor causing both the clubfeet and the Streeter's dysplasia.

Adult↗
PubMed1997

Arteriolar constriction in mild-to-moderate essential hypertension: an old concept requiring reconsideration?

OBJECTIVE: To investigate differences between in-vivo properties of a vascular bed in hypertensive patients and normotensive controls. DESIGN: Despite the controversy about the origin of essential hypertension and its accompanying vascular changes, it is generally assumed that the characteristic increase in peripheral resistance when hypertension progresses is caused by arteriolar constriction. Yet, there is little experimental evidence that this assumption generally holds in vivo. METHODS: A non-invasive technique was used for studying properties of the complete vascular bed of an upper arm segment under an occluding cuff in 23 previously untreated hypertensive patients and their matched normotensive controls. The method used the segment's electrical impedance to assess the volumes of extravascular fluid and of arterial and venous blood under varying arterial transmural pressures. RESULTS: Compared with that of matched normotensive controls, the compliance of the large arteries of the vascular bed was on average 50.9% lower (P < 0.001) in the hypertensive patients. The compliance of the complete arterial bed at the operating blood pressure level was also lower (40.0%, P < 0.01), but appeared to be significantly higher (45.9%, P < 0.05) at the normotensive blood pressure level. On the venous side, the patients had a higher blood volume (60.0%, P < 0.01) and an increased myogenic response (68.5%, P < 0.05). CONCLUSIONS: The increase in vascular resistance in the hypertensive patients is due primarily to changes in the large and small vessels of the arterial bed. We found no evidence for a generally increased arteriolar constriction.

Adult↗
PubMed1991

An alpha-adrenergic coronary constriction during esophageal distention in the dog.

Previous work has shown an increase in sympathetic stimulation of the heart during chemical or mechanical irritation of visceral organs, but the involvement of the coronary circulation in such reflexes is not clear. In five preliminary experiments in anesthetized dogs, esophageal distention produced a sympathetic stimulation of the heart, as evidenced by an increase in heart rate, which was abolished by non-selective beta-adrenergic and muscarinic blockades. On the basis of these preliminary data, we further examined a sympathetic coronary constriction during acute esophageal distension in which any direct adrenergic coronary constriction was unmasked by muscarinic blockade with atropine (100 micrograms/kg, i.v.), and non-selective beta-adrenergic blockade with propranolol (1 mg/kg, i.v.). In seven dogs anesthetized with alpha-chloralose in an open-chest procedure, the esophagus was rapidly distended to a pressure of 36 +/- 2 mm Hg, which was not significantly different from the distending pressure used in the preliminary experiments. During esophageal distention, the mean circumflex blood flow decreased to 77 +/- 10% (SEM) of the predistention value. This decrease was statistically significant (p less than 0.05). There was no change in left ventricular pressure, mean arterial pressure dP/dtmax, or heart rate. Intracoronary administration of the nonselective alpha-adrenergic antagonist phentolamine completely abolished the reduction in mean circumflex coronary blood flow caused by esophageal distention in the presence of beta-adrenergic and muscarinic blockades. These results demonstrate a direct sympathetic coronary vasoconstriction elicited by esophageal distention. This vasoconstriction was due to activation of coronary alpha-adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed2000

Deletion of the endothelin-A-receptor suppresses oxygen-induced constriction but not postnatal closure of the ductus arteriosus.

Experiments were carried out in mutant 129/SvEv mice lacking the endothelin-A (ET(A))-receptor to determine whether endothelin-1 (ET-1), acting as a messenger for oxygen constriction, is responsible for closure of the ductus arteriosus at birth. The isolated ductus from ET(A) -/- fetuses, unlike that from ET(A) +/+ littermates, contracted marginally to oxygen and ET-1 but responded to a thromboxane analog. In vivo, reduction in ductus lumen was equally pronounced in tracheotomized ET(A) -/- and ET(A) +/+ newborns. Conversely, no such vessel narrowing was seen in hyperoxic ET(A), -/- fetuses, although it occurred in ET(A) +/+ littermates. Notwithstanding the uneven behaviour of the ductus in vitro and in vivo, no ET(A) genotype-related difference was noted in the morphology of the vessel on both light and electron microscopy. We conclude that ET-1 mediates the ductus constriction to oxygen. Without ET-1, however, the vessel still closes postnatally probably as a result of the withdrawal of the relaxing influence of prostaglandin E2 (PGE2).

Animals↗