Efflux of Prostaglandin-like Smooth-Muscle-Stimulating Activity in the Right Lymphatic Duct in Man

1974 ◽  
Vol 33 (2) ◽  
pp. 131-137 ◽  
Author(s):  
G. Arturson ◽  
A. Hallán ◽  
H. -E. Hansson ◽  
C. -E. Jonsson
1991 ◽  
Vol 11 (1) ◽  
pp. 161-164 ◽  
Author(s):  
Mária Faragó ◽  
Csaba Szabó ◽  
Eörs Dóra ◽  
Ildikó Horváth ◽  
Arisztid G. B. Kovách

To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10−8-10−5 M norepinephrine, were significantly potentiated at low Mg2+ (0.8 m M v. the normal, 1.2 m M). High (1.6 and 2.0 m M) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 108–10−5 M acetylcholine were inhibited by high (1.6 and 2.0 m M) Mg2+. Lowering of the Mg2+ concentration to 0.8 m M or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.


2000 ◽  
Vol 89 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Robert L. Coon ◽  
Patrick J. Mueller ◽  
Philip S. Clifford

The canine cervical trachea has been used for numerous studies regarding the neural control of tracheal smooth muscle. The purpose of the present study was to determine whether there is lateral dominance by either the left or right vagal innervation of the canine cervical trachea. In anesthetized dogs, pressure in the cuff of the endotracheal tube was used as an index of smooth muscle tone in the trachea. After establishment of tracheal tone, as indicated by increased cuff pressure, either the right or left vagus nerve was sectioned followed by section of the contralateral vagus. Sectioning the right vagus first resulted in total loss of tone in the cervical trachea, whereas sectioning the left vagus first produced either a partial or no decrease in tracheal tone. After bilateral section of the vagi, cuff pressure was recorded during electrical stimulation of the rostral end of the right or left vagus. At the maximum current strength used, stimulation of the left vagus produced tracheal constriction that averaged 28.5% of the response to stimulation of the right vagus (9.0 ± 1.8 and 31.6 ± 2.5 mmHg, respectively). In conclusion, the musculature of cervical trachea in the dog appears to be predominantly controlled by vagal efferents in the right vagus nerve.


1990 ◽  
Vol 68 (5) ◽  
pp. 608-613 ◽  
Author(s):  
Mudumbi V. Ramagopal ◽  
S. Jamal Mustafa

Adenosine relaxes the coronary arteries of various species through A2 receptors. The aim of the present investigation was to evaluate the relaxing effects of adenosine in relation to the role of calcium in bovine coronary arteries by studying the vasodilatory effect of adenosine in normal and calcium-free medium and on calcium-45 efflux into calcium-free medium. Acetylcholine (ACh) and norepinephrine (NE) were used to induce tone in coronary artery rings. Adenosine, 5′-(N-ethylcarboxamido)adenosine (NECA), and N6-(L-phenylisopropyl)adenosine (L-PIA) produced concentration-dependent relaxations of the coronary artery rings. Both in normal and calcium-free medium, the order of potency for adenosine analogs (NECA > L-PIA > adenosine) was similar and 8-phenyltheophylline antagonized the relaxation responses to adenosine and its analogs. Removal of extracellular calcium shifted the concentration–response curves to the right in a parallel fashion, slowed the rate of relaxation, and in NE contracted rings reduced the maximum responses for adenosine and its analogs. In calcium-free medium, adenosine was without an effect on calcium-45 efflux in the presence of ACh. However, adenosine inhibited the stimulated calcium-45 efflux induced by NE. The data suggest that the vasodilatory action of adenosine in bovine coronary smooth muscle has both extracellular calcium-dependent and -independent components.Key words: adenosine receptors, calcium, coronary circulation, vascular smooth muscle, acetylcholine, norepinephrine.


2018 ◽  
Vol 46 (6) ◽  
pp. 2423-2435
Author(s):  
Domna Dorotheou ◽  
Marie-Luce Bochaton-Piallat ◽  
Catherine Giannopoulou ◽  
Stavros Kiliaridis

Objective This study was performed to explore the expression of α-smooth muscle actin (α-SMA) in the periodontal ligament (PDL) of young and adult rats during post-emergent tooth eruption in opposed and unopposed teeth at two time points: 3 and 15 days after antagonist loss. Methods Four-week-old (n = 20) and 22-week-old (n = 20) male Wistar rats were used. The right maxillary molar crowns were cut down. PDL samples were isolated from the first mandibular molars at two time points: 3 and 15 days after cut-down of the right maxillary molars. Quantitative reverse-transcription polymerase chain reaction and immunohistochemical staining were performed to detect differences in α-SMA expression in the PDL tissues of unopposed versus opposed molars. Results α-SMA was upregulated in the PDL of the unopposed molars in the 3-day group of young rats. The region around the root apex of the unopposed molars in this group exhibited strong immunostaining for α-SMA. The expression level and immunoreactivity of α-SMA did not differ in both time points in young controls and among all the adult groups. Conclusion α-SMA-positive myofibroblasts are implicated in post-emergent tooth eruption of unopposed molars of young animals.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Naila Mahmut ◽  
Caroline Kinnear ◽  
Megan Thompson ◽  
Patrick Shannon ◽  
David Chitayat ◽  
...  

The RV in hypoplastic left heart syndrome (HLHS) and Tetralogy of Fallot (TOF) is exposed to hypoxia and abnormal load which may lead to RV dysfunction despite surgical repair. The ability of hypoxia to upregulate angiogenic signaling in the RV is not known. We measured vascular endothelial growth factor (VEGF) mediated regulation of cardiac progenitors in the RV of patients with HLHS and TOF. Methods: RV myocardial samples were obtained from 6 pts with HLHS (age 0.96±1.5 yrs), 6 pts with TOF (age 3.5±6.3 yrs) and 9 age-matched controls with structurally normal hearts (age 0.16±0.3 yrs) at surgery/transplant/autopsy. The following were measured: VEGF, thymosin β-4 (recruits progenitors), Nkx2.5 (myocyte precursor), Flk-1 (smooth muscle progenitor), CD34 (endothelial progenitor), and von willebrand factor (vWf) (endothelial marker). Results: (i) VEGF and thymosin β-4 expression was lower in HLHS vs controls. This was associated with reduced cardiac progenitors and lower myocardial capillary density vs controls (0.14±0.01 vs 0.55±0.16, p<0.05). (ii) VEGF expression was preserved but thymosin β-4 was reduced in RV in TOF. This was associated with preserved myocyte progenitors but reduction in endothelial and smooth muscle lineages and reduced capillary density vs controls (0.13±0.03 vs 0.55±0.16, p<0.05) (Figure 1 ). Conclusion: Hypoxia fails to induce an angiogenic response in the RV in cyanotic heart lesions. This may be due to reduced VEGF (HLHS) or impaired coupling of VEGF to thymosin β-4 (TOF). This maladaptation may contribute to post-operative RV dysfunction and lower RV regenerative capacity in later life. Figure 1: Reduced capillary density (red) in HLHS and TOF


1983 ◽  
Vol 54 (1) ◽  
pp. 215-224 ◽  
Author(s):  
S. G. Hendrix ◽  
N. M. Munoz ◽  
A. R. Leff

We studied the isometric response of bronchial smooth muscle in a single third-order bronchus of 24 dogs in situ. Length-tension studies were performed in six dogs by repeated injection of 10(-5) mol acetylcholine (ACh) into the right bronchoesophageal artery, and the resting tension (30.6 +/- 6.9 g/cm) and length (0.76 +/- 0.14 cm) permitting maximal contraction were determined. In eight other dogs, dose-related bronchial contraction was obtained with 10(-10) to 10(-5) mol intra-arterial (ia) ACh. Supramaximal electrical stimulation of the right cervical vagus nerve and bronchial parasympathetic ganglion stimulation with ia 1–1-dimethyl-4-phenylpiperazinium (DMPP) also caused bronchial contraction. The maximal response to ia ACh (28.5 +/- 1.7 g/cm), supramaximal electrical stimulation (15.2 +/- 1.1 g/cm), and ia DMPP (10.5 +/- 3.0 g/cm) was blocked by an ia dose of atropine (1–5 micrograms/kg) that did not alter the sympathetic relaxation response in the trachea. In four dogs, the bronchial response to sympathetic activation was studied by intravenous (iv) bolus injection of DMPP after cholinergic blockade with atropine. DMPP (25 micrograms/kg iv) caused 9.5 +/- 2.2 g/cm bronchial relaxation, which was blocked completely by 2–4 mg/kg iv propranolol. In six other dogs, hypoxia induced by ventilation with pure nitrogen caused bronchial contraction, which was blocked by vagotomy, atropine, and hexamethonium. We report a sensitive method for selective measurement of bronchial smooth muscle response in a single resistance bronchus. This preparation preserves regional innervation and circulation and permits selective physiological stimulation in situ.


2014 ◽  
Vol 138 (8) ◽  
pp. 1059-1066 ◽  
Author(s):  
Xianyong Gui ◽  
Yi Zhou ◽  
Leslie Eidus ◽  
Vincent Falck ◽  
Zu-hua Gao ◽  
...  

Context.—Pneumatosis cystoides intestinalis (PCI) is a condition with multiple gas-filled cysts within the bowel wall, associated with diverse background diseases. Its pathogenesis is still a mystery. Some previous observations scattered in the literature have suggested an association of the cystic spaces in PCI with the lymphatics. Objective.—To further investigate whether PCI results from the ballooning of gas-filled lymphatic channels. Design.—We did immunostaining of podoplanin, a mucoprotein preferentially expressed in lymphatic endothelial cells, in 13 cases (8 men, 5 women; age range, 18–80 years) of PCI. Ten cases were diagnosed in resected segments of bowel and 3 in biopsies. Pneumatosis was seen in the right side of the colon (9 cases), transverse colon (1 case), sigmoid colon (1 case), and small bowel (2 cases). In addition, immunostaining for CD31, calretinin, WT1, CD68, smooth muscle actin, desmin, vimentin, and cytokeratins was also performed for comparison and correlation. Results.—A strong immunopositivity of podoplanin was seen in a condensed linear structure in the pericystic interstitium in 100% of the cases, but was not seen in the overlying giant and flat cells that were all CD68-positive histiocytes. Meanwhile, the podoplanin-expressing structure was negative for calretinin and WT1, which ruled out the possible mesothelial origin. There were coexistent variable immunopositivity of smooth muscle actin, which suggests an admixture of myofibroblasts. These findings indicated that the PCI cases were gas-distended lymphatics with the lymphatic epithelium ruptured and embedded in the reactive histiocytes and giant cells. Conclusion.—Our findings support the lymphatic theory about the pathogenesis of PCI.


Angiology ◽  
2019 ◽  
Vol 71 (1) ◽  
pp. 62-69 ◽  
Author(s):  
Roberto Guerri-Guttenberg ◽  
Rocío Castilla ◽  
Gabriel Cao ◽  
Francisco Azzato ◽  
Giuseppe Ambrosio ◽  
...  

The prevalence of coronary intimal thickening (IT) was assessed in fetuses and pediatric population. We studied the coronary arteries of 63 hearts obtained from fetuses, infants, children, and adolescents, deceased from noncardiac disease or trauma. Histomorphometric analysis, planimetry, and immunohistochemical studies were conducted. Intimal thickening consisted of proliferation of smooth muscle cells and scarce monocytes embedded in amorphous deposits within the internal elastic membrane (IEM). Intermingled lesions of intimal hyperplasia and parietal nonstenotic plaques were also observed. Intimal thickening was found in 10% of 20 fetuses, in 33.3% of 18 infants, 73.3% of 15 children, and 100% of 10 adolescents. A significant correlation ( r = 0.671, P < 0.001) was found between the extent of IT and age. The IEM was duplicated or interrupted in 43% of patients, showing a positive correlation with the degree of IT ( P = 0.01). Intimal thickening was predominantly found near bifurcation sites in the left anterior descending coronary artery (55.6%) and in zones free of bifurcation in the right coronary artery (75%). In conclusion, the prevalence and extension of IT lesions are higher at older ages within a young population. Intimal thickening may be regarded as the first event occurring in coronary preatherosclerosis, preceding lipid deposition.


2005 ◽  
Vol 170 (7) ◽  
pp. 1135-1146 ◽  
Author(s):  
Yuichi Tomita ◽  
Keisuke Matsumura ◽  
Yoshio Wakamatsu ◽  
Yumi Matsuzaki ◽  
Isao Shibuya ◽  
...  

Arodent cardiac side population cell fraction formed clonal spheroids in serum-free medium, which expressed nestin, Musashi-1, and multi-drug resistance transporter gene 1, markers of undifferentiated neural precursor cells. These markers were lost following differentiation, and were replaced by the expression of neuron-, glial-, smooth muscle cell–, or cardiomyocyte-specific proteins. Cardiosphere-derived cells transplanted into chick embryos migrated to the truncus arteriosus and cardiac outflow tract and contributed to dorsal root ganglia, spinal nerves, and aortic smooth muscle cells. Lineage studies using double transgenic mice encoding protein 0–Cre/Floxed-EGFP revealed undifferentiated and differentiated neural crest-derived cells in the fetal myocardium. Undifferentiated cells expressed GATA-binding protein 4 and nestin, but not actinin, whereas the differentiated cells were identified as cardiomyocytes. These results suggest that cardiac neural crest-derived cells migrate into the heart, remain there as dormant multipotent stem cells—and under the right conditions—differentiate into cardiomyocytes and typical neural crest-derived cells, including neurons, glia, and smooth muscle.


2002 ◽  
Vol 80 (6) ◽  
pp. 507-514 ◽  
Author(s):  
G Baños ◽  
F Martínez ◽  
J I Grimaldo ◽  
M Franco

The contribution of adenosine receptors was evaluated in vascular relaxation in experimental hypothyroidism. Hypothyroid aortic rings contracted less than normal controls with noradrenaline, phenylephrine, and KCl; the difference was maintained after incubation with 1,3-dipropyl-8-p-sulfophenylxanthine (an A1 and A2 adenosine receptor blocker). The vascular relaxation induced by acetylcholine or carbachol was similar in normal and hypothyroid aortic rings. However, adenosine, N6-cyclopentyladenosine (an A1 adenosine receptor analogue), and 5'-N-ethylcarbox amidoadenosine (an A2 and A3 adenosine analogue) induced vasodilation that was larger in hypothyroid than in normal aortas. Nω-nitro-L-arginine methyl ester shifted the dose-response curves of adenosine, N6-cyclopentyladenosine, or 5'-N-ethylcarboxamidoadenosine to the right in both normal and hypothyroid vessels. The blocker 1,3-dipropyl-8-p-sulfophenylxanthine significantly reduced adenosine-induced relaxation in the hypothyroid but not in the normal aortic vessels. These results suggest that in hypothyroid aortas, a larger adenosine-mediated vasodilation is observed probably due to an increase in receptor number or sensitivity.Key words: adenosine receptors, nitric oxide, hypothyroidism, smooth muscle, rat aorta.


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