Newborn intrapulmonary veins are more reactive than arteries in normal and hypertensive piglets

1999 ◽  
Vol 277 (5) ◽  
pp. L887-L892 ◽  
Author(s):  
F. I. Arrigoni ◽  
A. A. Hislop ◽  
S. G. Haworth ◽  
J. A. Mitchell

The reactivity of pulmonary veins during adaptation from pre- to postnatal life is not well characterized. With an in vitro organ bath technique, the responses to the contractile and relaxant agonists U-46619 (10−10 to 3 × 10−6 M) and acetylcholine (10−9 to 10−4 M) were compared in adjacent conduit pulmonary vein and artery rings from 66 piglets aged 1 wk preterm to 14 days of postnatal life and from adult tissue. Five additional piglets were made hypertensive by exposure to chronic hypoxia for 3 days after birth. Both arteries and veins showed smaller contractile and relaxant responses before birth than after. By 5 min after birth, the contraction by arteries and relaxation by veins had increased ( P < 0.05). By 3 days of age, arterial relaxation increased, but in all animals, venous relaxation exceeded that in arteries ( P < 0.05). Veins contracted more than arteries in animals aged 3–14 days. Neonatal hypoxia diminished the responses to both agonists in the veins ( P < 0.05), whereas the response in the arteries remained similar to that in the normal newborn. We speculate that veins may be more important in postnatal adaptation than previously suggested.

2007 ◽  
Vol 18 (10) ◽  
pp. 1067-1075 ◽  
Author(s):  
EUGENE PATTERSON ◽  
WARREN M. JACKMAN ◽  
KAREN J. BECKMAN ◽  
RALPH LAZZARA ◽  
DEBORAH LOCKWOOD ◽  
...  

1994 ◽  
Vol 267 (1) ◽  
pp. H139-H147 ◽  
Author(s):  
T. M. Zellers ◽  
J. McCormick ◽  
Y. Wu

Endothelin-1 causes vasodilation of the intact porcine pulmonary vascular bed. To determine the cause of this vasodilation, we investigated the interactions of endothelin-1 (ET-1), endothelium-derived nitric oxide (EDNO), and prostacyclin in isolated small porcine pulmonary arteries and veins under in vitro conditions. ET-1 caused concentration-dependent contractions in arteries and veins, augmented by the nitric oxide synthase (NOS) inhibitor, N omega-nitro-L-arginine, in pulmonary veins. BQ-123 (ETA-receptor antagonist) depressed the ET-1-induced contractions. Sarafotoxin S6C, an ETB-receptor agonist, caused contractions of pulmonary veins only. Endothelium-dependent relaxations to bradykinin and ET-1 were greater in pulmonary veins compared with arteries, inhibited by N omega-nitro-L-arginine, and reversed by L-arginine. BQ-123 augmented ET-1-induced arterial relaxation. ET-3 and sarafotoxin S6C, ETB-receptor agonists, caused comparable endothelium-dependent relaxations in arteries and veins. ET-1 caused a fourfold greater increase in prostacyclin release in pulmonary veins compared with arteries. We conclude that ET-1 is a potent vasoconstrictor of porcine pulmonary vessels and stimulates the release of EDNO and prostacyclin, which oppose the contractions to the peptide. The release of these endothelium-derived vasodilators appears greater in pulmonary veins.


1978 ◽  
Vol 56 (5) ◽  
pp. 812-817 ◽  
Author(s):  
C. J. Hanna ◽  
P. Eyre

Horses suffer from a respiratory condition, similar to human allergic asthma, that is characterized by severe dyspnea, wheezing, coughing, and mucus production. Mediator substances released during the allergic reaction may contract airways and pulmonary vasculature. Nothing is known of the effects of autacoids and other vasoactive substances on equine pulmonary vessels. Therefore, spiral strips of equine pulmonary vein were prepared in vitro and the effects of histamine (H), 5-hydroxytryptamine (5HT), bradykinin (Bk), carbachol (Carb), and phenylephrine (Phen) were studied. The order of contractile effectiveness for the agonists on the vein was found to be 5HT > H> Bk > Phen > Carb, although H consistently produced the greatest maximal effects. H1-receptors appeared to mediate H contractions while H2-receptors had no measurable effect. 5HT responses were mediated directly by 'D-type' smooth muscle receptors. Bk produced contractions but of a lesser magnitude than either H or 5HT. Varying degrees of tachyphylaxis were observed for each agent. α-Adrenergic receptor stimulation by Phen initiated low-magnitude contractions whereas Carb exhibited virtually no activity on the pulmonary vein. Contractile responses of pulmonary veins to various spasmogens may contribute to the equine asthmatic response by raising vascular hydrostatic pressure, thereby enhancing edema formation.


1993 ◽  
Vol 264 (6) ◽  
pp. H2162-H2167 ◽  
Author(s):  
R. H. Steinhorn ◽  
F. C. Morin ◽  
S. F. Gugino ◽  
E. C. Giese ◽  
J. A. Russell

Despite evidence for an important role for endothelium-derived relaxing factor (EDRF) in transitional circulation, previous in vitro studies of newborn pulmonary arteries have demonstrated diminished EDRF activity when compared with arteries from older animals. We studied pulmonary arteries and veins isolated from early newborn and juvenile sheep using standard tissue bath techniques. Incubation of vessels with the nitric oxide synthase inhibitor N omega-nitro-L-arginine (L-NNA) constricted veins but not arteries from both age groups. Further studies using preconstricted vessels revealed that arteries relaxed to acetylcholine (ACh), with significantly greater responses observed in juvenile arteries. Veins from both age groups contracted to ACh. Pretreatment with prostaglandin inhibitors (indomethacin and SQ 29,548) diminished ACh relaxations in pulmonary arteries from both age groups, greatly enhanced relaxations to ACh in newborn pulmonary veins, and depressed contractions in juvenile pulmonary veins. Removal of endothelium mechanically or functionally with prostaglandin inhibitors and L-NNA eliminated relaxations to ACh in pulmonary arteries from both age groups and resulted in contractions in veins. We conclude that isolated pulmonary veins from newborn sheep exhibit both baseline and stimulated release of EDRF, and we speculate that these venous responses may be important in the transitional pulmonary circulation.


1971 ◽  
Vol 25 (02) ◽  
pp. 354-378 ◽  
Author(s):  
R Gottlob ◽  
L Stockinger ◽  
U Pötting ◽  
G Schattenmann

SummaryIn vitro whole blood clots of various ages, experimental thrombi produced in the jugular vein of rabbits and human thrombi from arteries and veins were examined in semi-thin sections and by means of electron microscopy.In all types of clots examined a typical course of retraction was found. Retraction starts with a dense excentrical focus which grows into a densification ring. After 24 hours the entire clot becomes almost homogeneously dense; later a secondary swelling sets in.Shortly after coagulation the erythrocytes on the rim of the clot are bi-concave discs. They then assume the shape of crenate spheres, turn into smooth spheres and finally become indented ghosts which have lost the largest part of their contents. In the inner zone, which makes up the bulk of the clot, we observed bi-concave discs prior to retraction. After retraction we see no crenations but irregularly shaped erythrocytes. Once the secondary swelling sets in, the cross-section becomes polygonal and later spherical. After extensive hemolysis we observe the “retiform thrombus” made up of ghosts.Experimental and clinical thrombi present the same morphology but are differentiated from in vitro clots by: earlier hemolysis, immigration of leukocytes, formation of a rim layer consisting of fibrin and thrombocytes, and the symptoms of organization. Such symptoms of organization which definitely will prevent lysis with streptokinase were found relatively late in experimental and clinical thrombi. Capillary buds and capillary loops were never found in clinical thrombi prior to the third month.The morphological findings agree with earlier physical and enzymatic investigations. The observation that phenomena of reorganization occur relatively late and frequently only in the rim areas of large thrombi explains why lytic therapy is possible in some of the chronic obliterations.


Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 855
Author(s):  
Paola Serrano Martinez ◽  
Lorena Giuranno ◽  
Marc Vooijs ◽  
Robert P. Coppes

Radiotherapy is involved in the treatment of many cancers, but damage induced to the surrounding normal tissue is often inevitable. Evidence suggests that the maintenance of homeostasis and regeneration of the normal tissue is driven by specific adult tissue stem/progenitor cells. These tasks involve the input from several signaling pathways. Irradiation also targets these stem/progenitor cells, triggering a cellular response aimed at achieving tissue regeneration. Here we discuss the currently used in vitro and in vivo models and the involved specific tissue stem/progenitor cell signaling pathways to study the response to irradiation. The combination of the use of complex in vitro models that offer high in vivo resemblance and lineage tracing models, which address organ complexity constitute potential tools for the study of the stem/progenitor cellular response post-irradiation. The Notch, Wnt, Hippo, Hedgehog, and autophagy signaling pathways have been found as crucial for driving stem/progenitor radiation-induced tissue regeneration. We review how these signaling pathways drive the response of solid tissue-specific stem/progenitor cells to radiotherapy and the used models to address this.


2021 ◽  
Vol 22 (15) ◽  
pp. 7774
Author(s):  
Sevil Korkmaz-Icöz ◽  
Cenk Kocer ◽  
Alex A. Sayour ◽  
Patricia Kraft ◽  
Mona I. Benker ◽  
...  

Vascular ischemia/reperfusion injury (IRI) contributes to graft failure and adverse clinical outcomes following coronary artery bypass grafting. Sodium-glucose-cotransporter (SGLT)-2-inhibitors have been shown to protect against myocardial IRI, irrespective of diabetes. We hypothesized that adding canagliflozin (CANA) (an SGLT-2-inhibitor) to saline protects vascular grafts from IRI. Aortic rings from non-diabetic rats were isolated and immediately mounted in organ bath chambers (control, n = 9–10 rats) or underwent cold ischemic preservation in saline, supplemented either with a DMSO vehicle (IR, n = 8–10 rats) or 50µM CANA (IR + CANA, n = 9–11 rats). Vascular function was measured, the expression of 88 genes using PCR-array was analyzed, and feature selection using machine learning was applied. Impaired maximal vasorelaxation to acetylcholine in the IR-group compared to controls was significantly ameliorated by CANA (IR 31.7 ± 3.2% vs. IR + CANA 51.9 ± 2.5%, p < 0.05). IR altered the expression of 17 genes. Ccl2, Ccl3, Ccl4, CxCr4, Fos, Icam1, Il10, Il1a and Il1b have been found to have the highest interaction. Compared to controls, IR significantly upregulated the mRNA expressions of Il1a and Il6, which were reduced by 1.5- and 1.75-fold with CANA, respectively. CANA significantly prevented the upregulation of Cd40, downregulated NoxO1 gene expression, decreased ICAM-1 and nitrotyrosine, and increased PECAM-1 immunoreactivity. CANA alleviates endothelial dysfunction following IRI.


Author(s):  
Alan G Dawson ◽  
Cathy J Richards ◽  
Leonidas Hadjinikolaou ◽  
Apostolos Nakas

Abstract Metastatic renal cell carcinoma with involvement through the pulmonary veins to the left atrium is very rare. We report the case of a 70-year-old male with metastatic renal cell carcinoma to the right lower lobe of the lung abutting the inferior pulmonary vein with extension to the left atrium without pre-operative evidence. Surgical resection was achieved through a posterolateral thoracotomy. Lung masses that abut the pulmonary veins should prompt further investigation with a pre-operative transoesophageal echocardiogram to minimize unexpected intraoperative findings.


1877 ◽  
Vol 25 (171-178) ◽  
pp. 174-176 ◽  

In a former communication we incidentally mentioned that in a rabbit killed by the injection of cobra-poison into the jugular vein we had observed the pulmonary vein pulsating after all motion had ceased in the cavities of the heart. We have since observed the same phenomenon three or four times under conditions which show that this pulsation is not due to the action of the cobra-poison with which the animal in which we first observed it had been killed. The following example will show the changes in rhythm observed in these pulsations. A cat was chloroformed, and the vagi exposed and irritated by an interrupted current. Artificial respiration was kept up by air containing chloroform vapour, and the thorax was then opened, and a solution of atropia injected directly into the heart by means of a Wood’s syringe. The vagi were again irritated, but without any effect being produced on the heart, the inhibitory apparatus in it being evidently paralyzed by the atropia. A solution of glycerine extract of physostigma was now injected into the heart in a similar way. The vagi were now irritated again, and the heart stood still, the effect of the atropia having been counteracted by the physostigma. After the irritation ceased the heart again commenced to pulsate.


1983 ◽  
Vol 3 (3) ◽  
pp. 354-361 ◽  
Author(s):  
E. Müller-Schweinitzer ◽  
P. Neumann

PN 200–110 [4-(2, 1, 3-benzoxadiazol - 4 -) - 1,4-dihydro - 2,6 - dimethyl - pyridine - 3,5 - dicarboxylic acid methyl 1-methylethyl ester], a new dihydropyridine derivative, was investigated by recording isometric tension on spiral strips from human and canine arteries in tissue baths at 37°C. Responses to increasing concentrations of CaCl2 were investigated in calcium-free depolarizing solution (60 mmol/L KCl in equimolar replacement for NaCl, 50 mmol/L TRIZMA buffer, pH 7.4). Comparison of those concentrations that reduced the vasoconstrictor response to 1.6 mmol/L CaCl2 by 50% revealed the following order of potencies on both human and canine arteries: PN 200–110 > nimodipine > nifedipine. Responses to 5-hydroxytryptamine (5-HT) and blood were investigated in Krebs–Henseleit solution (NaHCO3 buffer). On canine arteries, PN 200–110 antagonized responses to 5-HT when used at 10–30 pmol/L; it was ∼70 times more potent on basilar than on mesenteric arteries, whereas both nifedipine and nimodipine were, respectively, ∼10 and 6 times more potent on basilar than on mesenteric arteries. When canine basilar arteries were constricted by the addition of blood to the organ bath, each of the investigated dihydropyridine derivatives elicited concentration-dependent relaxation, producing the following order of potencies: PN 200–110 > nifedipine = nimodipine. On human anterior cerebral arteries, the blood-induced contractions were counteracted in the following rank order: PN 200–110 = nimodipine > nifedipine. The results suggest that due to its potent calcium-blocking activity on cerebral arteries, PN 200–110 might be of value for the prevention and treatment of cerebrovascular spasms following subarachnoid hemorrhage.


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