Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Constriction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,153 records · Page 64Linked to original sources
PubMed1993

Acute effect of cigarette smoking on the coronary circulation: constriction of epicardial and resistance vessels.

OBJECTIVES: This study was performed to determine the acute effect of cigarette smoking on proximal and distal epicardial conduit and coronary resistance vessels. BACKGROUND: Cigarette smoking causes constriction of epicardial arteries and a decrease in coronary blood flow in patients with coronary artery disease, despite an increase in myocardial oxygen demand. The role of changes in resistance vessel tone in the acute coronary hemodynamic effect of smoking has not been examined. METHODS: Twenty-four long-term smokers were studied during cardiac catheterization after vasoactive medications had been discontinued. The effect of smoking one cigarette 10 to 15 mm long on proximal and distal conduit vessel segments was assessed before and immediately after smoking and at 5, 15 and 30 min after smoking (n = 8). To determine the effect of smoking on resistance vessels, coronary flow velocity was measured in a nonobstructed artery with a 3F intracoronary Doppler catheter before and for 5 min after smoking (n = 8). Eight patients were studied without smoking to control for spontaneous changes in conduit arterial diameter (n = 5) and resistance vessel tone (n = 3). RESULTS: The average diameter of proximal coronary artery segments decreased from 2.56 +/- 0.12 mm (mean +/- SEM) before smoking to 2.41 +/- 0.09 mm 5 min after smoking (-5 +/- 2%, p < 0.05). Distal coronary diameter decreased from 1.51 +/- 0.07 to 1.39 +/- 0.06 mm (-8 +/- 2%, p < 0.01). Marked focal vasoconstriction after smoking was observed in two patients. Coronary diameter returned to baseline by 30 min after smoking. There was no change in vessel diameter in control patients. Despite a significant increase in the heart rate-mean arterial pressure product, coronary flow velocity decreased by 7 +/- 4% (p < 0.05) and coronary vascular resistance increased by 21 +/- 4% (p < 0.01) 5 min after smoking. There was no change in these variables in the control subjects. CONCLUSIONS: Smoking causes immediate constriction of proximal and distal epicardial coronary arteries and an increase in coronary resistance vessel tone, despite an increase in myocardial oxygen demand. These acute coronary hemodynamic effects may contribute to the adverse cardiovascular consequences of cigarette smoking.

Analysis of Variance↗
PubMed1993

Acetylcholine-induced constriction of angiographically normal coronary arteries is not time dependent in transplant recipients. Effects of stepwise infusion at 1, 6, 12 and more than 24 months after transplantation.

OBJECTIVES: The aim of this study was to evaluate whether acetylcholine may be a useful tool for detection of early angiographically undetectable coronary atherosclerosis in heart transplant recipients. BACKGROUND: Coronary artery disease is the main determinant of long-term prognosis in transplant recipients. Acetylcholine-induced constriction of angiographically normal coronary arteries in heart transplant recipients could be due to early atherosclerosis, and acetylcholine has been proposed for early detection of coronary artery disease. METHODS: The responses of large coronary arteries to stepwise intracoronary infusion of acetylcholine (10(-8) to 10(-5) mol/liter) were compared in five control subjects and in four groups of transplant recipients 1, 6, 12 and > 24 months postoperatively (group 1, n = 6; group 2, n = 7; group 3, n = 6; group 4, n = 6, respectively). All patients had normal coronary arteriographic findings. Vessel dimensions were measured in four segments in each patient. RESULTS: In control subjects, acetylcholine increased diameters significantly at 10(-8), 10(-7) and 10(-6) mol/liter (all p < 0.001 vs. basal value). No significant variation was observed at 10(-5) mol/liter. Intracoronary isosorbide dinitrate increased diameters of all segments (p < 0.001). In transplant recipients, vessel diameters did not vary significantly from baseline at 10(-8) and 10(-7) mol/liter concentrations in groups 1 and 3 and at 10(-8) mol/liter in group 4. Vessels constricted significantly in all the other cases. Comparisons of each group with control subjects showed that responses were significantly different for all concentrations but 10(-8) mol/liter in groups 3 and 4. Intracoronary isosorbide dinitrate elicited coronary vasodilation similar to that of control subjects in all groups of transplant recipients. CONCLUSIONS: This study indicates that the acetylcholine response is persistently abnormal in transplant recipients compared with that in normal control subjects and that this abnormality may not be related simply to the presence of atherosclerosis. Thus, acetylcholine may not be a useful tool for early detection of coronary atherosclerosis in heart transplant recipients.

Acetylcholine↗
PubMed2004

Epicardial coronary artery constriction to cold pressor test is predictive of cardiovascular events in hypertensive patients with angiographically normal coronary arteries and without other major coronary risk factor.

Epicardial coronary endothelial dysfunction independently predicts cardiovascular events in patients with coronary risk factors. This study was designed to evaluate outcome of hypertensive patients on the basis of their epicardial coronary function assessed by cold pressor test (CPT). Control subjects (n = 68, 48.8 +/- 7.6 years) and hypertensive patients (n = 83, 51.3 +/- 7.9 years) with angiographically normal coronary arteries and without other major coronary risk factor underwent epicardial coronary reactivity assessment to CPT using quantitative angiography. Cardiovascular events were recorded with a mean follow-up of 115 months (range 84-132). In control subjects, dilation occurred in 88.2%, no change in 11.8% (mean diameter change: +14.6 +/- 9.3%). In hypertensive patients, dilation occurred in 13.3%, no change in 25.3% (mean diameter change for both: +10.9 +/- 11.2%), and constriction in 61.4% (mean diameter change: -12.7 +/- 3.4%). Endothelium-independent dilation was normal in control subjects and hypertensive patients. In control subjects, there were three cardiovascular events in two subjects (2.9%). In hypertensive patients, there were 17 cardiovascular events in 12 patients (14.5%, P < 0.01 versus control subjects), with 15 cardiovascular events in the 10/51 patients (19.6%) with coronary artery constriction, and two cardiovascular events in the 2/32 patients (6.3%) with no change or dilation (P < 0.05). In conclusion, in hypertensive patients with angiographically normal coronary arteries and without other major coronary risk factors, epicardial coronary artery dysfunction assessed by the cold pressor test is predictive of long-term cardiovascular events.

Adult↗
PubMed2005

An alternative approach for correction of constricted ears of moderate severity.

Moderately severe constricted ears are characterised by lidding, moderate reduction of the vertical height of the upper ear (reduced scapha, absent superior crus) and prominence with absent antihelix. Techniques described for the correction of moderate constricted ear deformities included an attempt to expand the upper part of the ear by various cartilage transection and/or flap techniques. In the current paper, an alternative approach is presented and is based on the recreation of an antihelix (with Mustarde sutures) and excision of the lidding without performing cartilage expansion procedures. The technique was used in four patients with satisfactory results despite the persistence of the deficient scapha and triangular fossa. No recurrence of the cupping deformity was observed (follow up ranged from 6 months to 4 years with a mean of 2 years) and this was attributed to the use of a 'mastoid hitch' as an adjunctive technique to prevent recurrence.

Child↗
PubMed2004

Serotonin blockade protects against early microvascular constriction following atherosclerotic plaque rupture.

Early microvascular constriction following atherosclerotic plaque rupture may be mediated via serotonin and/or endothelin-1. Atherosclerotic lesions in the rabbit hindlimb underwent plaque rupture, resulting in a rapid reduction of distal flow (7.1+/-0.7 ml/min pre-rupture versus 3.6+/-0.6 ml/min post-rupture, P<0.001) and a rise in distal microvascular resistance (10.5+/-0.9 mm Hg min/ml pre-rupture versus 23.5+/-3.5 mm Hg min/ml post-rupture, P=0.01). Distal microvascular resistance remained elevated following endothelin-1 receptor antagonism and control vehicle, but normalised after serotonin receptor antagonism with ritanserin (10.5+/-0.9 mm Hg min/ml pre-rupture versus 22.2+/-6.0 mm Hg min/ml post-endothelin-1 receptor antagonism [P<0.05] versus 21.6+/-6.2 mm Hg min/ml post-control vehicle [P<0.05] versus 11.6+/-2.0 mm Hg min/ml post-ritanserin [P=NS]). Early antagonism of serotonin receptors protects against distal microvascular constriction following atherosclerotic plaque rupture.

Animals↗
PubMed2004

Ascorbate protects against impaired arteriolar constriction in sepsis by inhibiting inducible nitric oxide synthase expression.

Compromised microvascular responsiveness is one of the key factors associated with mortality of septic patients. The present study addresses the mechanism of protection by ascorbate against impaired vasoconstriction in septic mice. Sepsis (i.e., cecal ligation and puncture (CLP) model) elevated both plasma protein carbonyl (i.e., an index of oxidative stress) and plasma nitrite/nitrate (NOx) levels, reduced baseline mean arterial blood pressure (MABP), and inhibited the MABP pressor response to angiotensin II (Ang II) at 6 h post-CLP. At the microvascular level, sepsis increased the inducible nitric oxide synthase (iNOS) mRNA level in cremaster muscle arterioles (18-25 microm diameter) at 3 h post-CLP, and impaired vasoconstriction to Ang II in these arterioles at 6 h post-CLP. At 24 h post-CLP, sepsis resulted in 9% survival. An intravenous bolus of ascorbate (200 mg/kg body wt) given 30 min prior to CLP prevented the protein carbonyl and NOx increases, partially restored the baseline arterial pressure, and completely protected against all arteriolar iNOS mRNA increases, arteriolar constriction hyporesponsiveness, and pressor response impairment. Survival increased to 65%. In septic mice, iNOS gene knockout resulted in protection of arteriolar constriction and pressor responses identical to that provided by ascorbate. Ascorbate bolus given 3 h post-CLP protected against the increase in plasma NOx concentration and against the pressor response impairment. We conclude that ascorbate may protect arteriolar vasoconstrictor responsiveness in sepsis by inhibiting excessive NO production.

Angiotensin II↗
PubMed2006

The anatomical site of constriction of the median nerve in patients with severe idiopathic carpal tunnel syndrome.

During open carpal tunnel release in patients with severe idiopathic carpal tunnel syndrome, an area of constriction in the substance of the median nerve is frequently noted. In a prospective study of 30 patients, the central point of the constricted part of the nerve was determined intraoperatively and found to be, on average, 2.5 (range 2.2-2.8)cm from the distal wrist crease. This point always corresponded to the location of the hook of the hamate bone. These intraoperative findings were compared with the "narrowest" point of the carpal canal as determined by anatomical and radiological studies in the literature.

Adult↗
PubMed2006

Pharmacological correlation between the formalin test and the neuropathic pain behavior in different species with chronic constriction injury.

Research on mechanisms of drug action, and preclinical screening of molecules with a potential activity on neuropathic pain requires extensive animal work. The chronic constriction injury model is one of the best-characterized models of neuropathic pain behavior in rats, but requires extensive time consuming operations and animal handling. The formalin test is easier to perform, and a well validated model. The latter may serve as an effective prescreening test of molecules and may facilitate drug targeting. In the present study the activity of different pharmacological reference compounds was tested in rats and gerbils on the cold plate for animals that had undergone chronic constriction injury and in the second phase of the formalin test. In rats, a comparable outcome in both test conditions was observed for morphine, fentanyl, MK-801 and flunarizine. Clonidine had more activity in the second phase of the formalin test, whereas baclofen, tramadol, amitryptiline, ketamine and topiramate showed more activity in the cold plate. In gerbils, both test conditions yielded comparable results for fentanyl and ketoprofen. Tramadol and CP-96345 tended to have more activity in the second phase of the formalin test, whereas morphine, SR-48968, SR-142801 and R116301 demonstrated more activity in the cold plate test. This study demonstrates a good correlation between the second phase of the formalin test and the cold allodynia in the CCI model for, both for rats and gerbils. Drugs with a proven activity in humans, used as reference compounds, also showed good pharmacological activity in this animal study.

Animals↗
PubMed2003

Effect of the respiratory-related bronchial rhythmic constriction on alveolar ventilation in the dog.

The middle-sized bronchus constricts during mid-inspiration through early-expiration. The purpose of this study was to elucidate the physiological role of this respiratory-related bronchial rhythmic constriction (RRBRC). The following parameters were measured in 12 decerebrated and paralyzed dogs: pressure from a balloon-tipped catheter in the fifth-generation bronchus (to reveal RRBRC), efferent neurogram from C(5) phrenic, and ventilatory flow and volume. We found a small but significant reduction of peak expiratory flow of mechanical ventilation during RRBRC. During bilateral vagal cold block, RRBRC was simulated by intermittent electric stimulation of vagal fibers distal to the cold block. This stimulus evoked a decrease in peak expiratory flow and in Pa(CO2) (approximately 1.5 mmHg). After vagal warming, mechanical ventilation was terminated, and blood gases were maintained normal by extracorporeal oxygenation. During each RRBRC ventilatory volume decreased by approximately 3 ml. The changes in gas volume and RRBRC disappeared after bilateral vagotomy. These findings support the concept that the physiological role of RRBRC is to facilitate alveolar gas exchange by reducing expiratory flow, anatomical dead space, or both.

Action Potentials↗
PubMed2002

Site-directed mutagenesis of tyrosine 118 within the central constriction site of the LamB (Maltoporin) channel of Escherichia coli. I. Effect on ion transport.

The three-dimensional structure of the malto-oligosaccharide-specific LamB-channel of Escherichia coli (also called maltoporin) is known from x-ray crystallography. The central constriction of the channel formed by the external loop 3 is controlled by a tyrosine residue (Y118). Y118 was replaced by site-directed mutagenesis by ten other amino acids (alanine, isoleucine, asparagine, serine, cysteine, aspartic acid, arginine, histidine, phenylalanine, and tryptophane) including neutral ones, negatively and positively charged amino acids to study the effect of their size, hydrophobicity, and charge on ion transport through LamB. The mutant proteins were purified to homogeneity. They were reconstituted into lipid bilayer membranes and single-channel conductance and ion selectivity were measured to get insight into the mechanism of ion transport through LamB. The mutation of Y118 to any other nonaromatic amino acid led to a substantial increase of the single-channel conductance by more than a factor of six at maximum. The highest effect was observed for Y118D. Additionally, a nonlinear relationship between the salt concentration in the aqueous phase and the channel conductance was observed for this mutant, indicating strong discrete charge effects on ion conductance. For all other mutants, with the exception of Y118R, linear relationships were found between single-channel conductance and bulk aqueous concentration. The individual hydrophobicity indices of the amino acids introduced inside the central constriction of the LamB channel had a somewhat smaller effect on the single-channel conductance as compared with the effect of their size and charge.

Amino Acid Substitution↗
PubMed2003

Prefission constriction of Golgi tubular carriers driven by local lipid metabolism: a theoretical model.

Membrane transport within mammalian cells is mediated by small vesicular as well as large pleiomorphic transport carriers (TCs). A major step in the formation of TCs is the creation and subsequent narrowing of a membrane neck connecting the emerging carrier with the initial membrane. In the case of small vesicular TCs, neck formation may be directly induced by the coat proteins that cover the emerging vesicle. However, the mechanism underlying the creation and narrowing of a membrane neck in the generation of large TCs remains unknown. We present a theoretical model for neck formation based on the elastic model of membranes. Our calculations suggest a lipid-driven mechanism with a central role for diacylglycerol (DAG). The model is applied to a well-characterized in vitro system that reconstitutes TC formation from the Golgi complex, namely the pearling and fission of Golgi tubules induced by CtBP/BARS, a protein that catalyzes the conversion of lysophosphatidic acid into phosphatidic acid. In view of the importance of a PA-DAG cycle in the formation of Golgi TCs, we assume that the newly formed phosphatidic acid undergoes rapid dephosphorylation into DAG. DAG possesses a unique molecular shape characterized by an extremely large negative spontaneous curvature, and it redistributes rapidly between the membrane monolayers and along the membrane surface. Coupling between local membrane curvature and local lipid composition results, by mutual enhancement, in constrictions of the tubule into membrane necks, and a related inhomogeneous lateral partitioning of DAG. Our theoretical model predicts the exact dimensions of the constrictions observed in the pearling Golgi tubules. Moreover, the model is able to explain membrane neck formation by physiologically relevant mole fractions of DAG.

Biological Transport↗
PubMed2003

Attenuated arterial and venous constriction in conscious rats with streptozotocin-induced diabetes.

We examined if arterial or venous constriction is impaired in early diabetes. Dose-pressor and mean circulatory filling pressure (index of venous tone) response curves to noradrenaline and angiotensin II were constructed in four groups of conscious, instrumented, Wistar rats pretreated with streptozotocin (60 mg/kg i.v.) or vehicle at 2 weeks prior to the study. Rats with diabetes, relative to controls, had increased ED(50) (reduced potency) for the pressor (2.5-fold of control) and mean circulatory filling pressure (4.3-fold of control) response to noradrenaline, as well as reduced maximum pressor response (efficacy) to noradrenaline (diabetic, 74+/-8 mm Hg; control, 96+/-5 mm Hg). Diabetic rats also had reduced potency (ED(50), 5-fold of control) of the pressor response to angiotensin II; however, maximum pressor response and dose-mean circulatory filling pressure curve to angiotensin II were similar in both groups. Therefore, arterial and venous constrictions are impaired at an early phase of type I diabetes.

Angiotensin II↗
PubMed2003

S1P3 receptors mediate the potent constriction of cerebral arteries by sphingosine-1-phosphate.

We characterized the effect of Sphingosine-1-phosphate (S1P) on vascular tone. S1P selectively constricted isolated cerebral, but not peripheral arteries, despite ubiquitous expression of S1P(1), S1P(2), S1P(3) and S1P(5) receptor mRNA. Clostridium B and C3 toxins and the rho-kinase inhibitor Y27632 (trans-N-(4-pyridyl)-4-(l-aminoethyl)-cyclohexane carboxamide) reduced this vasoconstriction to S1P, indicating that the response was mediated through Rho. Pertussis toxin displayed only weak inhibition, suggesting minor involvement of G(i/o) protein. The S1P effect was specifically reduced by adenovirus bearing a s1p(3) but not s1p(2), antisense construct. Furthermore, suramin, which selectively blocks S1P(3) receptors, inhibited the vasoconstrictor effect of S1P, indicating that S1P(3) receptors account for at least part of S1P-mediated vasoconstriction in cerebral arteries. In vivo, intracarotid injection of S1P decreased cerebral blood flow, an effect prevented by suramin treatment. Because S1P constricts cerebral blood vessels and is released from platelets during clotting, the S1P/S1P(3) system constitutes a novel potential target for cerebrovascular disease therapy.

Animals↗
PubMed1998

The antimigraine agent alniditan selectively constricts porcine carotid arteriovenous anastomoses via 5-HT1B/1D receptors.

In previous studies, we have shown that several 5-HT1B/1D receptor agonists, including sumatriptan, potently constrict porcine carotid arteriovenous anastomoses. This effect seems to be of high predictive value for antimigraine activity. In the present experiments, we studied the effects of a new non-indole 5-HT1B/1D receptor agonist, alniditan, on systemic and carotid haemodynamics in anaesthetised pigs. In control animals, no significant changes in either systemic or carotid haemodynamics were observed after four consecutive i.v. injections of physiological saline (0.5 ml each, every 20 min; n = 4). On the other hand, i.v. doses of alniditan (3, 10, 30 and 100 microg kg(-1) in 0.5 ml saline, every 20 min; n = 6) dose-dependently decreased total carotid conductance (maximum change: -31 +/- 6%) by a selective vasoconstrictor action on arteriovenous anastomoses (maximum change: -72 +/- 5%); the nutrient vascular bed dilated in response to alniditan (maximum change: +103 +/- 39%). The dose of alniditan that decreased arteriovenous anastomotic conductance by 50% was 24 +/- 8 microg kg(-1) (64 +/- 20 nmol kg(-1)). Alniditan produced a slight bradycardia (maximum change: -4 +/- 1%) and a more pronounced hypotensive effect (maximum change: -23 +/- 5%). In six animals pre-treated with the potent and selective 5-HT1B/1D receptor antagonist, GR127935, the alniditan-induced changes in carotid haemodynamics were clearly antagonised, whereas the bradycardia and hypotension remained unaffected. These results suggest that alniditan selectively constricts porcine carotid arteriovenous anastomoses mainly via 5-HT1B/1D receptors and should be able to abort migraine headaches. The latter has indeed been confirmed in initial clinical studies in man.

Analgesics↗
PubMed1998

ATP-induced, P2U purinoceptor-mediated constriction of isolated, perfused mesenteric beds of the rat.

alpha,beta-Methylene ATP (alpha, beta-mATP), ATP and UTP dose dependently increased the perfusion pressure of rat mesenteric arteries with a potency order of alpha, beta-mATP >> ATP > UTP. In the veins, while alpha, beta-mATP did not affect the pressure, both ATP and UTP equi-potently increased it. The arterial ATP response was attenuated to some degree by suramin (100 microM), but markedly and to a similar extent by pyridoxal-phosphate-6-azophenyl-2',4-disulphonic acid (PPADS 30 microM) and alpha, beta-mATP (100 nmol). The venous response was not affected by PPADS or alpha, beta-mATP, but was slightly attenuated by suramin. Thus, ATP seems to elicit arterial constriction predominantly by stimulating P2X, but venous constriction by stimulating P2U purinoceptors.

Adenosine Triphosphate↗
PubMed1999

Aminoguanidine induces constrictive vascular remodeling and inhibits smooth muscle cell death after balloon injury.

We examined the effects of aminoguanidine, an inhibitor of inducible nitric oxide synthase, in the rat model of balloon injury. Arteries were assessed by histomorphometry, and vascular smooth muscle cell death and proliferation were examined 24 h and 14 days after balloon injury by in situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) of fragmented DNA and expression of proliferating cell nuclear antigen, respectively. Aminoguanidine decreased the luminal area 14 days after balloon injury (0.19+/-0.04 mm2 vs. 0.35+/-0.02 mmr2; P < 0.005), and this effect was attributable to reduction of the total vessel area, i.e., constrictive vascular remodeling (0.42+/-0.03 mm2 vs. 0.55+/-0.03 mm2; P < 0.005). At 24 h after injury, the percentage of TUNEL-positive cells in the medial layer was reduced by aminoguanidine (2.0+/-1.0% vs. 17.3+/-5.4%; P < 0.05), and the percentage of proliferating cells was increased (18.4+/-5.5% vs. 4.9+/-2.2%; P < 0.05). Aminoguanidine did not influence the density of VSMC nuclei in the injured artery wall, systemic blood pressure or endothelium-dependent vasorelaxation. We conclude, that in the rat model of balloon injury, aminoguanidine induces luminal loss by constrictive vascular remodeling in association with reduced early VSMC death and increased proliferation.

Angioplasty, Balloon↗
PubMed1984

Reduction of prostacyclin synthesis as a possible cause of transient flow reduction in a partially constricted canine coronary artery.

Coronary blood flow decreases cyclically in a partially occluded coronary artery of anesthetized dogs. Spontaneous aggregation and deaggregation of platelet plugs in the constricted artery have been indicated to be responsible for this phenomenon. A current hypothesis is that platelet aggregation may be determined by a balance between proaggregatory platelet product, thromboxane A2 (TXA2), and antiaggregatory substance, prostacyclin (PGI2). To elucidate the relationship between the cyclical reduction of coronary flow (CRCF) and metabolic alterations of TXA2 and PGI2, we attempted to determine the plasma levels of their stable catabolites, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), in the coronary circulation of 69 dogs. Of 40 cases, 20 cases exhibited CRCF accompanying a significant increase in TXB2 in the coronary sinus (CS) (P less than 0.05) and constant levels of 6-keto-PGF1 alpha in the CS and aorta (Ao). Another 20 cases did not exhibit CRCF that accompanied a marked increase in 6-keto-PGF1 alpha (P less than 0.05) with virtually no change in TXB2 in the CS and Ao. A higher dose of indomethacin (10 mg/kg, i.v.) was capable of evoking CRCF in cases not exhibiting CRCF spontaneously. Under these conditions, a significant decrease in 6-keto-PGF1 alpha was seen both in the CS and Ao compared with lower doses of indomethacin (1 to 3 mg/kg, P less than 0.01), that produced less pronounced reduction of 6-keto-PGF1 alpha without CRCF. Intravenous infusion of PGI2 (0.1 microgram/kg/min.) completely abolished spontaneously and indomethacin-induced CRCF with a marked elevation of 6-keto-PGF1 alpha in the CS and Ao. Although OKY-1580, a TXA2 synthetase inhibitor, relieved spontaneously-evoked CRCF with a marked increase in 6-keto-PGF1 alpha and a slight reduction of TXB2, indomethacin-induced CRCF was not abolished by this agent. These results are consistent with the hypothesis that the reduction of endogenous PGI2 synthesis in the vascular wall is related to the occurrence of CRCF after partial constriction of coronary artery and indomethacin.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Etiology of intestinal damage in gastroschisis. I: Effects of amniotic fluid exposure and bowel constriction in a fetal lamb model.

Gastroschisis is often complicated by damage to the herniated small bowel, resulting in motility and absorption disturbances and occasional intestinal necrosis and atresia. To study the pathophysiology of this process, a model of gastroschisis was developed in fetal lambs. At 80 days' gestation, the anterior abdominal wall was partially excised to create a small peritoneal cavity, and the small bowel was extruded through a Silastic ring to create a defect of uniform size. In one experimental group, a tie was placed around the herniated bowel at the level of the abdominal wall to provide gradual constriction as the fetus grew. In a second group, no tie was placed. Control animals had a simple laparotomy and no abdominal wall defect; some also had a constrictor placed around the base of the bowel. The animals were delivered near term, and the bowel was evaluated histologically and by an in-vitro bowel motility assay. Histologic examination showed normal ganglion cells in all groups and no evidence of ischemic injury. A fibrous peel was seen only in bowel exposed to amniotic fluid, with or without a constrictor. Lymphatic and venous dilation, smooth-muscle thickening, and focal mucosal blunting were seen in bowel subjected to chronic obstruction by a constrictor, regardless of whether it was exposed to amniotic fluid. Both constriction of the bowel and amniotic fluid exposure were associated with a decrease in motility; these two effects were independent and additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Muscles↗