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PubMed1977

Spastic constriction of cerebral vessels after electric convulsive treatment.

The brains of nine cats were subjected to bitemporal electric convulsive treatment. The current (AC, 220 V, 50 Hz, ca. 500 mA, 500 ms) was applied two to five times. Pial vessels were observed through a skull window. Immediately after current application, some pial arteries exhibited segmental spastic constriction which usually did not disappear until the animals were killed. Before sacrificing the animals, 20 min after convulsive treatment they were perfused with a carbon suspension. In some cortical areas blackening was impaired indicating that perfusion was not complete. Electron-microscopic investigation revealed that spasm also occurred in arterioles of the brain parenchyma. Many arterial vessels, some of them possessing only one muscular cell sheat, had collapsed so that the lumen was merely a small cleft. The spasms were irregularly distributed and confined to small segments of the vessel. Small arteriolar vessels were more affected than large pial arteries. Arterial spasms continued for 20 min. In a total of 39 control animals spastic constriction was observed only once; this animal had been subjected to prolonged hypocapnia.

Animals↗
PubMed1976

The interaction between prostaglandin E1 and delta 9-tetrahydrocannabinol on intestinal motility and on the abdominal constriction response in the mouse.

The interaction between delta9-tetrahydrocannabinol (THC) and PGE1 was studied using two pharmacological parameters-the rate of passage of a charcoal meal through mouse small intestine and the abdominal constriction response in the mouse. PGE1 administered intraperitoneally produced a dose-dependent decrease in intestinal motility, and this effect was antagonized by low (0.25 mg/kg) doses of THC and potentiated by higher doses of THC (1 mg/kg). Kinetic analysis suggested that the interaction was of a mixed but predominantly competitive type. PGF2alpha produced an increase in intestinal motility but this was not dose-dependent. THC antagonized the effect of PGF2alpha in a dose-dependent manner suggestive of a physiological antagonism. THC (0.25-2 mg/kg) antagonized the dose-dependent PGE1 abdominal constriction response in a fashion which suggested a mixed (though mainly competitive) antagonism. It would ssem, therefore, that on the two pharmacological parameters studied THC appears to be interacting with PGE1 at the same receptor site. Although the doses of THC used are within the range of those used in man, it is not implied that these results are necessarily implicated in the psychoactivity of the drug.

Analgesia↗
PubMed1995

Local cerebral hyperthermia induces spontaneous thrombosis and arteriolar constriction in the pia mater of the mouse.

The effect of local cerebral hyperthermia on responses of pial microvessels of the mouse was investigated. A set protocol was followed, involving the performance of a craniotomy on anaesthetized animals and using intravital microscope-television closed circuitry. Controlled hyperthermic exposure was applied regionally by heating the brain surface with irrigating artificial cerebrospinal fluid. Microvascular responses such as changes in diameter, thrombosis and embolism were monitored and video-taped observations were further viewed and analysed. When both brain surface and core body temperatures were kept at 37 degrees C, no changes in pial microvessels were noted. With core body temperature kept at 37 degrees C and at a brain surface temperature of 43.1 degrees C, passing emboli and arteriolar constriction were observed. A few minutes later, visible thrombosis was prevalent. Further spontaneous thrombo-embolic activity continued and at the end of a 50-min hyperthermic exposure, arterioles attained a constriction of 37%. Thrombus formation was sometimes massive enough to occlude fully the microvessel. The protocol followed in this study can be adopted to other small animal species and for a variety of experimental procedures involving hyperthermia and the pial microcirculation.

Animals↗
PubMed1996

Effect of ketanserin on 5-hydroxytryptamine-induced constriction in isolated, perfused canine basilar arteries exposed to blood.

The blocking effect of ketanserin, a 5-hydroxytryptamine (5-HT)2 receptor antagonist, was examined on responses to intra-luminal 5-HT or potassium chloride (KCl) in isolated and perfused canine basilar arteries before and after extraluminal whole blood by means of the stainless-steel cannula inserting method. Four hours after the application of blood, the constriction to 5-HT was significantly enhanced, while that to KCl was significantly attenuated. The absolute value in the decrease of perfusion pressure for the 5-HT-induced constriction sensitive to ketanserin was much greater after the blood application than that before the application. It is suggested that the augmentation of cerebrovascular responses to 5-HT in the early stage immediately after subarachnoid haemorrhage (SAH) might be mediated by 5-HT2 receptors at least in part. This early constrictor mechanism may be implicated in the aetiology of the following late stage of cerebral vasospasm after SAH.

Animals↗
PubMed1990

Adenosine constricts the isolated and perfused monkey coronary artery.

Adenosine constricted 37 of 58 isolated and perfused monkey coronary arteries, whereas it dilated dog coronary arteries in all cases. The vasoconstriction induced by 0.1-10 micrograms (0.37-37.4 nmol) of adenosine was examined, since adenosine in large doses produced tachyphylaxis. The adenosine-induced vasoconstriction was significantly attenuated by diltiazem (100 micrograms [0.24 mumol]), although it was not affected by aminophylline (100 micrograms [0.23 mumol]), phentolamine (100 micrograms [0.36 mumol]), or methysergide (10 micrograms [28 nmol]. Forty-minute treatment with indomethacin (5 x 10(-6) mol/l) completely prevented the adenosine-induced vasoconstriction, but it did not significantly inhibit vasoconstriction induced by KCl (3 mg [40 mumol])- or norepinephrine (NE, 0.1 micrograms [0.59 nmol]). These results suggest that: (1) adenosine constricts monkey coronary arteries by increasing Ca2+ influx across the smooth muscle cell membrane; (2) cyclooxygenase products may be involved in the adenosine-induced vasoconstriction; (3) adenosine receptors may not be involved in the vasoconstriction.

Adenosine↗
PubMed1999

Acidosis-induced coronary constriction in the rat heart: evidence for the activation of L-type calcium channels.

Perfused rat hearts were used to study the effects of acidosis on coronary tone. When pH was decreased, over the range pH 7.4 to pH 6.2, by reducing perfusate bicarbonate levels, under constant flow conditions, there was a transient decrease in coronary perfusion pressure (CPP), followed by a sustained acidosis-dependent increase in CPP, which reversed when pH was returned to pH 7.4. This increase in CPP was seen at perfusion rates of 5, 10, and 20 ml/min(-1). When using constant pressure perfusion acidosis reduced coronary flow. In a HEPES-buffered bicarbonate-free solution, acidosis did not cause a transient fall in CPP but it did produce a sustained increase in CPP. Addition of ammonium chloride (10 mM) reduced CPP, while washout of ammonium chloride increased CPP. The acidosis-induced increase in CPP was not affected by indomethacin, nitro-L-arginine, the nonselective adenosine receptor antagonist, 8-phenyl theophylline, or the thromboxane receptor antagonist, ZD 1542. The acidosis-induced increase in CPP was independent of the myocardial depressant effects of acidosis, but was attenuated by three different L-type calcium channel blockers. These results demonstrate that the coronary circulation of the rat constricts in response to acidosis. Experiments performed with L-type calcium channel blockers, and the calcium channel activator BAY K8644, suggest that constriction occurs via activation of L-type calcium channels. This would not be expected on the basis of electrophysiological studies, which have shown an inhibition of L-type calcium channels by acidosis.

Acidosis↗
PubMed2002

Site-directed mutagenesis within the central constriction site of ScrY (sucroseporin): effect on ion transport and comparison of maltooligosaccharide binding to LamB of Escherichia coli.

The 3-D structures of the maltooligosaccharide-specific LamB-channel of Escherichia coli (also called maltoporin) and sucrose-specific ScrY (sucroseporin) are known from X-ray crystallography. The central constriction of the channels formed by the external loop 3 is controlled by a number of different amino acids. The most prominent one of these, N192, D201 and F204, were replaced by site-directed mutagenesis into those of LamB, which, according to the 3-D model of both channels are localized at similar places. The ScrY single mutants ScrYN192R, ScrYD201Y and ScrYF204D and the ScrY triple mutant ScrY3113 (N192R + D201Y + F204D) were created together with the triple mutant ScrY3213, which lacks also amino acids 1 to 61 from the N-terminal end. The mutant proteins were purified to homogeneity and were reconstituted into lipid bilayer membranes. In these experiments, the single-channel conductance of the mutants in different salt solutions and the stability constants for binding of different maltooligosaccharides to the mutant channels was measured using titration experiments with carbohydrates. The carbohydrate-induced block of the channel function could also be used for the study of current noise through the different mutant ScrY-channels. The analysis of the power density spectra allowed the evaluation of the on- and off-rate constants (k1 and k-1) of carbohydrate-binding to the binding site inside the channels. The results suggest that both on- and off-rate constants were affected by the mutations. Most of them showed a substantial effect on carbohydrate binding kinetics. Nevertheless, single-channel conductance and carbohydrate binding of ScrY3113 mutant were still different from that of LamB, suggesting that not only the amino acids of the central constriction but also the general architecture of both channels have a substantial influence on channel properties.

Bacterial Outer Membrane Proteins↗
PubMed2005

Primary synovial osteochondromatosis presenting as constrictive capsulitis.

Primary synovial chondromatosis of the joints can present as capsular constriction with peri-articular osteopenia. This rare presentation is highlighted in three cases (two hips and one shoulder). The diagnosis in all the patients was made on arthrography and/or MRI/CT and was confirmed histologically. Synovial chondromatosis should be considered in patients with this presentation. Arthrography is the best imaging modality to confirm the cause (synovial chondromatosis) and effect (constrictive capsulitis).

Adult↗
PubMed2003

[Vigabatrin-associated bilateral simple optic nerve atrophy with visual field constriction. A case report and a survey of the literature].

CASE REPORT: A 70-year-old male with optic disc pallor and visual field constriction up to 35 degrees bilaterally was previously treated with vigabatrin. The cumulative dosage was 3.7 kg. The b-wave was reduced in photopic and scotopic electroretinography and the patient had delayed visual evoked potentials. The retinal nerve fiber thickness was pathologically reduced in the Heidelberg retinal tomography (HRT) and the retinal nerve fiber layer analyzer (GDx). CONCLUSION: Vigabatrin is an antiepileptic drug and may increase the intraretinal GABA level due to an inhibition of the enzyme GABA-transaminase and may induce an ascending simple optic nerve atrophy. Vigabatrin-associated visual field defects may be irreversible. A visual field control is recommended before starting the treatment with vigabatrin and at regular 6-month intervals thereafter. In cases of visual field constriction, the therapy should be stopped. If the cumulative dosage is more than 3 kg of vigabatrin, the visual field controls should be performed more frequently because of the dosage-toxicity relationship.

Aged↗
PubMed2002

Is visual field constriction in epilepsy patients treated with vigabatrin reversible?

OBJECTIVE: To evaluate the reversibility of vigabatrin associated visual field constriction. BACKGROUND: Visual field constriction (VFC) occurs in approximately 40 % of epilepsy patients under treatment with vigabatrin (VGB). There is still controversy about whether VGB-associated VFC is reversible. From a cross-sectional study there is evidence that VFC does not reverse three to six months after stopping VGB treatment. So far, there are no long term studies on this subject. METHODS: We performed a follow-up study on 15 epilepsy patients (eight women, seven men, median age 45 (21-58) years) with VGB-associated VFC but otherwise normal ophthalmological examination. Kinetic and static perimetry was performed one and two years after VFC was diagnosed (baseline examination). Visual field size at first and at second year-follow-up was compared with the baseline examination. Because discontinuation of VGB-treatment was dependant on clinical needs, patients either stopped VGB treatment before or after VFC was diagnosed. In a small group of patients VGB treatment was continued despite of VFC. RESULTS: There was no statistically significant difference in visual field size comparing baseline values with first year and second year follow-up examinations either in patients who stopped VGB treatment (n = 11) or in patients who continued VGB treatment on a reduced dosage (n = 4). CONCLUSION: Although our data are based on a relatively small group of patients there is evidence that VFC resulting from VGB treatment is not reversible in epilepsy patients after stopping the drug.

Adult↗
PubMed2006

Evaluation of residual retinal function by pupillary constrictions and phosphenes using transcorneal electrical stimulation in patients with retinal degeneration.

BACKGROUND: To evaluate inner-retinal function by pupillary constrictions and phosphenes evoked by transcorneal electrical stimulation (TES) in patients with hereditary retinal degeneration. METHODS: Consecutive 20 eyes of 20 patients (16 with retinitis pigmentosa (RP); and four with cone-rod dystrophy (CRD)) whose visual acuity was equal to or worse than 20/2000 at Osaka University Hospital and eight eyes of eight healthy subjects were enrolled. TES was performed on with a contact lens stimulating electrode. The electrically evoked pupillary response (EEPR) was recorded by a pupillometer, and the phosphenes by the subjective responses. Three electrical current thresholds were determined: T1, threshold current for initial phosphene; T2, threshold for eliciting a phosphene extending into the central field; and P, threshold for a relative pupillary constriction > or = 3%. The EEPR and phosphene thresholds were compared with the visual acuity or the visual field. RESULTS: All T1, T2 and P were significantly higher in patients than in normals (Mann-Whitney, P<0.001). Both T1 and T2 were not correlated with visual acuity but depended on the area and location of the residual visual field. T1 and T2 in RP eyes with a EEPR was significantly lower than that in RP eyes without an EEPR. During TES, all subjects and patients had no pain, and no complications except for a slight corneal superficial punctuate keratopathy. CONCLUSIONS: The safety and the efficacy of TES to estimate the residual inner-retinal function in patients with retinal degeneration indicate that TES can be used as one of the most important test to select candidates for retinal prostheses.

Adult↗
PubMed2006

Renal microvascular constriction to membrane depolarization and other stimuli: pivotal role for rho-kinase.

Contraction of vascular smooth muscle is determined not only by levels of intracellular free calcium but also by the sensitivity of its contractile apparatus. A potential modulator of the latter is rho-kinase. We addressed the question of a possible central role for rho-kinase in the regulation of periglomerular microvascular tone. In the rat hydronephrotic kidney model, diameter changes of distal interlobular arteries, afferent and efferent arterioles were measured using three distinctly different stimuli: intravascular pressure changes, angiotensin II (AngII) and membrane depolarization, which is a physiological component of many signaling pathways, as evoked in two ways. Two selective, structurally different rho-kinase inhibitors, Y-27632 and HA-1077, were employed, as well as a selective protein kinase C alpha inhibitor. Preglomerular vasoconstriction induced by direct membrane depolarization, increases in pressure or AngII all depended for their effect on rho-kinase. A differing role for rho-kinase in efferent arteriolar constriction to AngII as compared to preglomerular microvessels was not found. In conclusion, our data indicate that in the kidney, rho-kinase is involved in a variety of signaling pathways leading to microvascular constriction. It plays a pivotal role not only in preglomerular but also in postglomerular tone.

Animals↗
PubMed2005

Volatile anesthetics constrict pulmonary artery in rabbit lung perfusion model.

Volatile anesthetics are generally considered to possess a vasodilator action. Some of their actions on pulmonary vessels, however, are not clearly understood. We examined the effects of various volatile anesthetics on pulmonary vessels using an in situ rabbit isolated-lung perfusion model. We prepared a rabbit constant-flow lung-perfusion model by sending blood to the pulmonary artery and removing blood from the left atrium, and observed the changes in pulmonary arterial perfusion pressure caused by inhalation of 0.5, 1, 2, and 3 minimum alveolar concentration (MAC) volatile anesthetics: halothane, enflurane, isoflurane, and sevoflurane, in random order. These volatile anesthetics increased pulmonary arterial perfusion pressure in a dose-dependent manner and caused the pulmonary arteries to constrict. In particular, halothane at all concentrations induced significantly greater pulmonary vasoconstriction than the other volatile anesthetics. Therefore, it is suggested that volatile inhalation anesthetics induce the pulmonary arteries to constrict, and halothane exhibits the most potent pulmonary vasoconstrictor effect among the volatile anesthetics tested.

Anesthetics, Inhalation↗
PubMed2006

Acidosis augments myogenic constriction in rat coronary arteries.

The myogenic response is a process by which blood vessels autoregulate vascular smooth muscle tone in response to changes in transmural pressure. It is characterized by vessel contraction or dilation with increased or decreased pressure, respectively. We sought to identify whether acidosis impacts the myogenic response in rat coronary resistance arteries. Ventricular septal arteries were isolated from male Sprague-Dawley rats and mounted on a pressure myograph. The myogenic response was assessed by measuring the arterial diameter at pressures of 10-120 mm Hg. The fluorescence indicators 2',7'-bis-(carboxyethyl)-5(and-6)-carboxyfluorescein and Fura-2 were utilized to measure intracellular pH (pH(i)) and intracellular free calcium concentration ([Ca(2+)](i)), respectively. A decrease in the extracellular pH (pH(o)) from 7.4 to 6.9 produced a fall in pH(i) and an increase in the myogenic response. Under nominally HCO (3) (-) /CO(2)-free conditions at a constant pH(o), blockade of the sodium-hydrogen exchanger with HOE694 also resulted in a fall in pH(i) and a similar enhancement of myogenic activity. Concentration response curves were constructed to measure the potencies of the HOE694 effects: the EC(50) was 34 microM for the pH(i) change and 19 microM for vessel constriction. Apparent [Ca(2+)](i) remained unchanged during HOE694-induced intracellular acidification. Furthermore, in the presence of HCO (3) (-) , HOE694 did not markedly affect pH(i) and vascular tone remained unaltered. Our data demonstrate that acidosis augments myogenic constriction of rat coronary arteries. These effects are due to a fall in pH(i) consequent upon the reduction in pH(o) and may reflect an increased myofilament [Ca(2+)](i) sensitivity within vascular smooth muscle cells.

Acidosis↗
PubMedDate not supplied

Effects of topically instilled bunazosin hydrochloride and other ocular hypotensive drugs on endothelin-1-induced constriction in rabbit retinal arteries.

PURPOSE: To compare the inhibitory effect of topically instilled bunazosin hydrochloride (bunazosin), a selective alpha(1)-adrenoceptor antagonist, on the endothelin (ET)-1-induced vasoconstriction in rabbit retinal arteries with the effects of other ocular hypotensive drugs. METHODS: ET-1 was injected into the central part of the vitreous of both eyes of pigmented rabbits. Color fundus photographs were taken 5 min before and 60 min after the injection. The average diameters of the two major retinal arteries at the rim of the optic nerve head (ONH) were normalized with respect to ONH diameter. Fifty microliters of 0.01% bunazosin, or 0.12% isopropyl unoprostone (unoprostone), 1% dorzolamide hydrochloride (dorzolamide), 0.25% nipradilol, 0.5% betaxolol hydrochloride (betaxolol), or 0.5% timolol maleate (timolol) was instilled into one eye of each rabbit 60 min before the ET-1 injection. The series of experiments was performed as masked tests. RESULTS: Bunazosin and unoprostone inhibited the ET-1-induced constriction of retinal arteries by 103% (P = 0.012 versus contralateral eyes) and 50% (P = 0.037), respectively. Dorzolamide, nipradilol, betaxolol, and timolol had no significant effects in this experiment. CONCLUSIONS: Under our experimental conditions, bunazosin and unoprostone inhibited the ET-1-induced constriction. Hence, bunazosin and unoprostone may be clinically more effective against ET-1-related retinal diseases.

Administration, Topical↗
PubMed1999

Constrictive Pericarditis.

Constrictive pericarditis is an uncommon but treatable cause of heart failure that results from a variety of acute inflammatory processes. Corticosteroids appear to prevent the development of constriction in selected patients with active pericardial inflammation. Symptoms of right-sided heart failure usually predominate and can be adequately managed with diuretics. Complete surgical pericardiectomy remains the only definitive treatment. The mortality risk is markedly increased in patients with advanced symptoms, and surgery should be performed in earlier stages. The majority of patients (95% on average) will survive the surgery; complete relief of symptoms occurs in about 50% of survivors. Ten percent of patients will have persistent symptomatic heart failure (New York Heart Association functional class III or IV) and experience poor late outcomes, however, particularly when residual myocardial dysfunction coexists.

Journal Article↗
PubMed1983

Coronary constriction by leukotriene C4, D4, and E4 in the intact pig heart.

Leukotrienes are naturally occurring vasoactive metabolites of arachidonic acid that increase during inflammatory reactions and anaphylaxis. Coronary constriction and reduced myocardial contractility after leukotriene C4 and D4 administration were demonstrated in the isolated guinea pig heart. To explore the effects of leukotrienes in the in situ, blood-perfused heart, we administered leukotrienes C4, D4, and E4 into the coronary artery of the domestic pig. Increasing doses (0.1, 0.3, 1.0, and 3.0 micrograms) of leukotrienes C4, D4, and E4 were injected into the left anterior descending coronary artery of 8 open-chest domestic pigs. Significant dose-related reduction in coronary blood flow was observed after each leukotriene administration. Three micrograms of each leukotriene produced the following maximal decreases (mean +/- standard error); C4 = 80 +/- 9%, p less than 0.001; D4 = 81 +/- 3%, p less than 0.001; E4 = 64 +/- 12%, p less than 0.005. In several instances, surface electrograms recorded from the myocardial region exposed to leukotrienes showed signs of focal myocardial ischemia, sometimes accompanied by ventricular arrhythmia. Significant elevation of left ventricular end-diastolic pressure was observed after large doses (1 or 3 micrograms) of leukotrienes C4 and D4. Minimal (5 to 10%) decreases in mean arterial pressure and no change in heart rate were observed after leukotriene injection. We conclude that leukotrienes C4, D4, and E4 are extremely potent coronary constrictors in the in situ heart. The intensity of response and associated electrocardiographic signs of ischemia suggest that constriction is mainly due to a primary effect on vascular smooth muscle. However, coronary flow reduction may also reflect consequences of a primary negative inotropic action. Leukotrienes may play a significant role in the pathogenesis of a variety of cardiac disorders, particularly those associated with extensive inflammatory changes.

Animals↗
PubMed1987

Relative roles of preload increase and coronary constriction in ergonovine-induced myocardial ischemia in stable angina pectoris.

To assess the relative role of increased ventricular preload and critical coronary lesions in ergonovine-induced myocardial ischemia, 9 normal subjects (group A), 7 patients with stable angina (group B) and 5 with variant angina (group C) were studied. In all patients, the 12-lead electrocardiogram, blood pressure and left ventricular (LV) volume (technetium-99m blood pool) were continuously recorded before and during administration of incremental doses of ergonovine given at 5-minute intervals. In all subjects, an initial LV dilatation developed; in group B and C patients, this was followed by a decrease in stroke volume and ejection fraction with subsequent onset of electrocardiographic changes and angina. The interval between these events was significantly shorter in group C and in 3 group B patients; in these patients, signs of ischemia appeared with smaller ergonovine doses and at minimal preload increase, coronary constriction being the likely mechanism of ischemia. In the remaining 4 group B patients, the onset of stroke volume, ejection fraction, electrocardiographic changes and angina was significantly delayed, occurring after administration of larger ergonovine doses when LV volume was already considerably increased. This finding suggests that the loading effect of ergonovine on LV volume, rather than on coronary constriction, could be the prevailing mechanism of ergonovine-induced ischemia in these patients.

Angina Pectoris↗