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At least 343 records · Page 19Linked to original sources
PubMed1987

[Inter-organ neural communications in the innervation of bronchi and pulmonary circulation vessels].

By means of V.P. Vorobiov's preparation in complex of the thoracic cavity organs of persons at various age and sex in fetuses, sources of innervation of bronchi and vessels of the pulmonary circulation have been stated. They make the composition of the cardiac nerves getting off the superior, middle cervical, cervico-thoracic (stellate) and from 3 to 5 thoracic nodes of the sympathetic trunk, superior and inferior cardiac branches of the nervus vagus. Connection between the nerves of the bronchi and vessels of the pulmonary circulation with the cardiac and esophageal nerves and formation of interorganic nervous plexuses are demonstrated. Not always the diaphragmal nerve participates in the innervation of the bronchi and pulmonary vessels. In total preparations and flat sections, elective revealing of the nervous elements with Shiff reagent in M. G. Shubich and A. B. Khodos modification and Gomori thiocholine method, makes it possible to follow connections of the pulmonary veins nerves with the left atrium, intrapulmonary connection of the perivascular and peribronchial plexuses, as well as participation of nervous elements of the pulmonary trunk in innervation of the right ventricle walls. There are multiple vegetative communications participating in innervation of the bronchi and vessels of the pulmonary circulation. The relations of the pulmonary nerves with the nerves of other thoracic organs are very complex; this explains the nature of the repercussive reactions of the lungs after surgical interventions performed in the other organs of the thoracic cavity.

Animals↗
PubMed1990

Role of endothelium-derived relaxing factor during transition of pulmonary circulation at birth.

To examine the potential role of endothelium-derived relaxing factor (EDRF) in regulation of the perinatal pulmonary circulation, we studied the hemodynamic effects of a selective inhibitor of EDRF production, nitro-L-arginine (L-NA), on pulmonary vascular tone and dilator reactivity in the late-gestation ovine fetus and on the pulmonary vasodilation that normally occurs at birth. L-NA infusion decreased pulmonary blood flow from 78 +/- 8 to 65 +/- 6 ml/min (P less than 0.01) and increased pulmonary artery pressure from 48 +/- 2 to 54 +/- 3 mmHg (P less than 0.002, n = 8 animals). To study the selectivity of L-NA on vasodilator responses to endothelium-dependent (acetylcholine) and -independent (atrial natriuretic factor) stimuli, we measured responses to brief infusions of each dilator before and after L-NA treatment. Acetylcholine increased pulmonary blood flow during the control period but not after L-NA treatment. In contrast, L-NA had little effect on the vasodilator response to atrial natriuretic factor. To study the role of EDRF in the transition of the pulmonary circulation from fetal to neonatal conditions, we infused L-NA into the left pulmonary artery immediately before cesarean-section delivery. In comparison with control animals, the rise in pulmonary blood flow at 1 h after delivery was reduced in the L-NA-treated animals (331 +/- 28 in control vs. 185 +/- 16 ml/min in treated, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Prostaglandins, related compounds, and the perinatal pulmonary circulation.

It is clear that prostaglandins and related compounds are important in the physiology and pathophysiology of the perinatal pulmonary circulation. This article focuses on what is known about prostaglandin-related compounds (PRC) in the pulmonary circulation of the developing and newly born mammal. Also included is a discussion of the effects of PRC on the ductus arteriosus and on the systemic circulation.

Animals↗
PubMed1994

Effects of neuropeptide Y on lung vascular permeability in the pulmonary circulation of rats.

The effects of neuropeptides on the capillary filtration coefficient in the vessels of the pulmonary circulation were examined, using isolated lung perfusion preparations from rats. Neuropeptide Y and neurokinin A elevated the filtration coefficient, and calcitonin gene related peptide diminished it. Neurotensin and substance P did not affect the value at concentrations less than 10(-7) M. The number of extravasated carbon particle deposits subsequent to tracheal application of neuropeptide Y during spontaneous respiration increased in a dose-dependent manner. From these results, we conclude that neuropeptide Y may increase vascular permeability in the pulmonary circulation.

Animals↗
PubMed1995

Analysis of responses to ANG IV: effects of PD-123319 and DuP-753 in the pulmonary circulation of the rat.

Pulmonary vasoconstrictor responses to angiotensin (ANG) IV, the 3-8 amino acid fragment of ANG II, were compared with responses to ANG I, ANG II, and ANG III and to other vasoactive peptides in the isolated blood perfused rat lung. In terms of relative activity, ANG IV was similar in potency to bradykinin and serotonin but was approximately 100-fold less potent than ANG I, ANG II, and ANG III. PD-123319, an AT2-receptor antagonist, enhanced pressor responses to the four angiotensin peptides and to bradykinin but did not significantly change the pressor response to serotonin or to ventilatory hypoxia. DuP-753, an AT1-receptor antagonist, significantly decreased pressor responses to the four angiotensin peptides and enhanced the pressor responses to bradykinin but not to serotonin. Captopril and enalaprilat increased the pressor response to ANG IV. Meclofenamate and N omega-nitro-L-arginine methyl ester shifted the dose-response curve for ANG IV to the left in a manner similar to that observed with ANG II and ANG III. These data show that ANG IV has significant vasoconstrictor activity and suggest that responses are mediated by the activation of AT1 receptors and that vasopressor responses of the angiotensin peptides may be modulated by activation of AT2 receptors. These results also suggest that responses to ANG IV are modulated by the release of vasodilator prostaglandins and nitric oxide and that AT2 receptors have little, if any, role in mediating or modulating the pressor response to ventilatory hypoxia.

Angiotensin II↗
PubMed1990

Organ-specific disposition of group B streptococci in piglets: evidence for a direct interaction with target cells in the pulmonary circulation.

Despite the serious pulmonary manifestations of early onset group B streptococcal (GBS) sepsis, it is not known whether the organism distributes into lung tissue and whether adverse pulmonary hemodynamic abnormalities relate to an interaction between the organism and target cells in the pulmonary vascular bed. Accordingly, this study evaluated the distribution and fate of GBS in the lung, liver, and spleen of anesthetized infant piglets and in isolated, salt solution-perfused piglet lung preparations. GBS were radiolabeled with 111Indium-oxine and infused at a dose of 10(8) organisms/kg/min for 15 min into anesthetized piglets ranging in age from 5-10 d. Forty-five min after termination of the infusion, animals were killed and specimens of lung, liver, spleen, and blood were excised and the relative deposition and viability of GBS were determined. Most of the recovered bacteria were detected in the lung (53.2 +/- 3.9%) followed by the liver (41.4 +/- 2.0%) and spleen (2.2 +/- 0.38%). GBS detected in the blood was estimated to be only 3.2 +/- 1.0% of the infused dose. Viability of GBS was least in the lung (21.4 +/- 2.6%) relative to the liver (45.7 +/- 11.2%) and spleen (83.4 +/- 19.5%). After a 60-min GBS infusion, transmission electron microscopy localized the organism within pulmonary intravascular macrophages in the lung; there was no evidence for bacterial interaction with either neutrophils or endothelial cells. In the liver, GBS was found exclusively in Kupffer cells. In isolated piglet lungs perfused at a constant flow rate with blood-free physiologic salt solution, GBS (10(6) to 10(8) organisms/mL) provoked concentration-dependent increases in pulmonary vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Relationship between pulmonary circulation and respiratory mechanics in patients artificial pulmonary ventilation].

Thirty-four patients in the early postoperative period after surgery on the lungs and mediastinum and 23 patients after cardiopulmonary bypass surgery have been examined. 187 studies of central hemodynamics and pulmonary function during cardiopulmonary bypass have been performed to investigate the correlation between pulmonary hemodynamics and parameters of respiratory mechanics in the early postoperative period after thoracic surgery. The studies have revealed reverse dependence of lung and chest compliance (C) on pulmonary artery diastolic pressure (PAPdiast) (r = -0.61, p < 0.05) in patients after thoracic surgery with clinical signs of cardiopulmonary failure. When analogous studies were performed in patients with intact lungs after aortocoronary bypass, C/PAPdiast correlation was more close (r = 0.880, p < 0.05). At the same time there is a correlation between C and extracellular fluid volume (r = -0.7). The above correlations to a great extent predetermine the pathogenesis of respiratory failure in the postoperative period.

Humans↗
PubMed2002

L-selectin is required for fMLP- but not C5a-induced margination of neutrophils in pulmonary circulation.

To study the role of L-selectin in neutrophil (PMN) margination and sequestration in the pulmonary microcirculation, maximally active concentrations of C5a (900 pmol/g) and N-formylmethionyl-leucyl-phenylalanine (fMLP; 0.34 pmol/g) were injected into the jugular vein of wild-type or L-selectin-deficient C57BL/6 mice. In wild-type mice administered C5a or fMLP, 92 +/- 1% and 34 +/- 9%, respectively, of peripheral blood PMN were trapped mostly in the pulmonary circulation as determined by immunohistochemistry and myeloperoxidase activity. In wild-type mice treated with F(ab')(2) fragments of the L-selectin monoclonal antibody MEL-14 or in L-selectin-deficient mice, C5a-induced neutropenia was not significantly reduced, but the decrease in peripheral PMN in response to fMLP was completely abolished, indicating that L-selectin is necessary for fMLP- but not C5a-induced pulmonary margination. Immunostained lung sections of fMLP- or C5a-treated mice showed sequestered neutrophils in alveolar capillaries with no evidence of neutrophil aggregates. We conclude that chemoattractant-induced PMN margination in the pulmonary circulation can occur by two separate mechanisms, one of which requires L-selectin.

Animals↗
PubMed2005

[Right ventricular function and pulmonary circulation hemodynamics in patients with vibration disease].

AIM: To study contractile and diastolic function of the right ventricle, mechanic activity of the right heart, hemodynamics of the pulmonary circulation in patients with vibration disease (VD). MATERIAL AND METHODS: The study group consisted of patients in contact with vibration (15 subjects without VD symptoms, 44 patients with VD of the first degree and 10 patients with VD of the second degree). 20 control males had no contact with vibration. RESULTS: VD patients developed right ventricular (RIO dysfunction: disturbed diastolic function, hypodynamic syndrome of the first degree accompanied with reduced ejection fraction, stroke output and cardiac index. In VD, RV dysfunction appears in parallel with left ventricular dysfunction due to high pressure in pulmonary circulation and interventricular interaction. CONCLUSION: VD-specific features of the lesser circulation and RV function give rise to formation of heart failure. Thus, early diagnostic and prophylactic measures should be taken in subjects in contact with vibration.

Disease Progression↗
PubMed2003

Paracrine role of soluble guanylate cyclase and type III nitric oxide synthase in ovine fetal pulmonary circulation: a double labeling immunohistochemical study.

Endothelial nitric oxide synthase (eNOS) or NOS-III in the endothelium catalyzes production of nitric oxide (NO). Nitric oxide diffuses freely into vascular smooth muscle, where it activates soluble guanylate cyclase (sGC) to produce guanosine 3',5'-cyclic monophosphate (cGMP) and causes vasorelaxation. The NO/cGMP pathway is an important signaling pathway in the control of perinatal pulmonary circulation. An exact colocalization of NOS-III in the pulmonary endothelium and sGC in the vascular smooth muscle was demonstrated using a double immunolabeling technique. The sGC immunoreactivity was higher in resistant pulmonary vessels and veins than in conduit arteries, whereas NOS-III immunoreactivity was higher in conduit arteries than in veins. These results demonstrated anatomically in situ a paracrine role of NOS-III and sGC in the regulation of fetal pulmonary circulation and suggested a heterogeneous distribution of NOS-III and sGC within fetal ovine pulmonary vasculature. Our results provided an anatomic basis that supported previous functional studies on perinatal control of pulmonary circulation.

Animals↗
PubMed2001

The active molecular form of plasma adrenomedullin is extracted in the pulmonary circulation in patients with mitral stenosis: possible role of adrenomedullin in pulmonary hypertension.

Adrenomedullin (AM), a novel hypotensive peptide, preferentially dilates pulmonary vessels rather than systemic vessels. This suggests the possibility that AM is a circulating hormone which participates in regulation of the pulmonary circulation. A recent study revealed that two molecular forms of AM, i.e. a mature, active form of AM (AM-m) and an intermediate, inactive, glycine-extended form of AM (AM-Gly), circulate in human plasma. In the present study we investigated the production and clearance sites and pathophysiological significance of the two molecular forms of AM in the pulmonary circulation in patients with mitral stenosis. We measured the plasma levels of AM-m and total AM (AM-T; AM-m+AM-Gly) using a recently developed specific immunoradiometric assay, and thus calculated plasma AM-Gly levels, in blood samples obtained from the femoral vein, pulmonary artery, left atrium and aorta of 28 consecutive patients with mitral stenosis (20 females and eight males; age 53+/-10 years). Patients with mitral stenosis had significantly higher venous concentrations of AM-T, AM-Gly and AM-m than age-matched normal controls (AM-T, 15.9+/-2.5 and 10.6+/-2.1 pmol/l respectively; AM-Gly, 14.0+/-2.1 and 9.8+/-1.9 pmol/l respectively; AM-m, 1.9+/-0.6 and 1.1+/-0.3 pmol/l respectively; each P<0.001). There was a significant decrease in the concentrations of AM-m and AM-T between the pulmonary artery and the left atrium (AM-T, 16.1+/-2.7 and 14.0+/-2.4 pmol/l respectively; AM-m, 2.0+/-0.6 and 0.7+/-0.2 pmol/l respectively; each P<0.001); however, there were no differences in plasma AM-Gly levels between the pulmonary artery and the left atrium (14.1+/-2.3 and 13.5+/-2.3 pmol/l respectively). The venous concentrations of AM-m, AM-Gly and AM-T showed similar correlations with mean pulmonary artery pressure (AM-T, r=0.67; AM-Gly, r=0.63; AM-m, r=0.59; each P<0.001) and total pulmonary vascular resistance (AM-T, r=0.77; AM-Gly, r=0.70; AM-m, r=0.75; each P<0.001). These results suggest that the plasma concentration of AM-m is increased in parallel with those of AM-Gly and AM-T, and that the main site for clearance of AM-m from the plasma is the lung; the extracted AM-m in the lungs may help to attenuate the increased pulmonary arterial resistance in secondary pulmonary hypertension due to mitral stenosis.

Adrenomedullin↗
PubMed1986

Evaluation of alpha-1 and alpha-2 adrenoceptor-mediated vasoconstriction in the in situ, autoperfused, pulmonary circulation of the anesthetized dog.

Alpha-1 and alpha-2 adrenoceptor-mediated vasoconstriction was studied in the in situ, autoperfused pulmonary circulation of the open-chest anesthetized dog utilizing selective alpha adrenoceptor agonists and antagonists. Animals were pretreated with propranolol (1 mg/kg i.v.) to eliminate beta adrenoceptor-mediated effects in the pulmonary circulation. Blood was withdrawn from the right femoral artery and transferred, via a peristaltic pump, to the pulmonary arterial branch supplying the left diaphragmatic lobe of the lung. The flow rate of the pump was set so that the perfusion pressure in the lobe was equal to resting diastolic pulmonary artery pressure (10 +/- 1 mm Hg). Under conditions of constant left atrial pressure and pulmonary blood flow, intralobar administration of alpha adrenoceptor agonists elicited increases in perfusion pressure of the lobe, reflecting changes in pulmonary vascular resistance. Intralobar administration of the selective alpha-1 adrenoceptor agonist methoxamine and the selective alpha-2 adrenoceptor agonist B-HT 933 elicited dose-dependent increases in lobar perfusion pressure, as did the nonselective alpha adrenoceptor agonist norepinephrine. Prazosin (100 micrograms/kg i.v.), a selective alpha-1 adrenoceptor antagonist, inhibited pulmonary vasopressor responses to methoxamine and norepinephrine without altering significantly the response to B-HT 933. Rauwolscine (100 micrograms/kg i.v.), a selective alpha-2 adrenoceptor antagonist, inhibited the response to B-HT 933 and norepinephrine with little effect on methoxamine. Intralobar administration of tyramine to evoke the release of endogenous norepinephrine resulted in dose-dependent increases in lobar perfusion pressure. The response to tyramine was inhibited selectively by prazosin with little effect of rauwolscine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗