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At least 487 records · Page 27Linked to original sources
PubMed1996

[Absence of unilateral pulmonary circulation, detected by perfusion scintigraphy of the lung, and its clinical significance].

Single acute shortage of pulmonary circulation may cause a life threatening condition, its definitive lack--in consequence of developmental trouble--decreased loading and inclination to infections. It's recognition is most easy by non invasive isotope perfusion pulmonary scintigraphy. Frequency, diagnostic difficulties are a little bit known in Hungary, therefore retrospective investigations were performed by the authors. Examining 961 perfusion pulmonary scintigraphic material of a four year (1990-1994) period-among them that of 52 children-in 8 cases total perfusion-lack of one lung-side was found. Surveyng history of 5 children and 3 adults, besides conventional physical and X-ray suspicion-sings, attention is drawn to signs of non-invasive perfusion and aerosol inhalation pulmonary scintigraphy which are more suitable to demonstrate deviations. In the background of severe circulatory trouble there have been found in one infant grave bronchial stenosis, in 4 children--with different age--arteria pulmonalis agenesia at right, and in 1 young adult (with Fallot-tetralogy), ateria pulmonalis agenesia at left. One of the other adults had bronchial carcinoma, and the other massive pulmonary embolisation. In their diagnostic schedule besides isotope investigations, importance of cardiologic echo-examinations, and the bronchoscopy has been stressed respectively. Catheterisation of the heart is important only in selected cases.

Adolescent↗
PubMedDate not supplied

Significance of endothelial prostacyclin and nitric oxide in peripheral and pulmonary circulation.

BACKGROUND: Vasoprotective function of endothelial cells is associated, among others, with biosynthesis and release of nitric oxide (NO), prostacyclin (PGI2), prostaglandin E2 (PGE2), carbon monoxide (CO) and plasminogen activator (t-PA). These endothelial mediators calm down activated platelets and leukocytes, prevent the occurrence of parietal thrombotic events, promote thrombolysis, maintain tissue perfusion and protect vascular wall against acute damage and against chronic remodeling. Endothelial dysfunction in patients suffering from atherosclerosis or diabetes type 2 is associated not only with suppression in release of the above mediators but also with deleterious discharge of prostaglandin endoperoxides (PGH2, PGG2), superoxide anion (O2-, peroxynitrite (ONOO-), and plasminogen activator inhibitor (PAI-1). We looked for mechanisms of protective endothelial function, with a special respect to the differences between peripheral and pulmonary circulation. METHODS: Cultured endothelial cells of bovine aorta (BAEC) were used to study physiological and pharmacological mechanisms of increasing free cytoplasmic calcium [Ca2+]i. A porphyrinic sensor quantified the release of NO from BAEC. In cultured human umbilical vein endothelial cells (HUVEC) we looked for induction by bradykinin (Bk) of mRNAs for a number of enzymes. In blood perfused rat lungs we studied protective role of NO against injury inferred by lipopolysaccharide on pulmonary microcirculation that was accomplished by thromboxane A2 (TXA2), platelet activating factor (PAF), cysteinyl-leukotrienes (cyst-LTs) and the complement system. In vivo we analyzed the influence of Bk, perindopril and quinapril ('tissue type' angiotensin converting enzyme inhibitors, ACE-Is) on endothelial function in entire circulation of anaesthetized rats using a thrombolytic bioassay and EIA for 6-keto-PGF1 alpha and t-PA antigen. RESULTS: In BAEC Bk via kinin B2 receptors raised in a concentration-dependent manner (1 pM-10 nM) free cytoplasmic calcium ions [Ca2+]i, that triggered the release of NO from BAEC. Calcium ionophore (A23187, 1-100 nM) as well as receptor agonists such as adenosine diphosphate (ADP, 10 nM-1 microM), adrenaline (Adr, 1-10 microM) or acetylcholine (Ach, 10-100 microM) produced a similar rise in endothelial [Ca2+]i as did Bk at a nanomolar concentration. 'Tissue type' ACE-Is, e.g. quinapril or perindopril acted through accumulation of endogenous Bk. However, the potency of ACE-I to change endothelial function is by several orders of magnitude lower than that for exogenous Bk. In vivo the major difference between thrombolytic actions by quinapril or perindopril on one hand, and by exogenous Bk on the other was longevity of thrombolysis by ACE I and a distinct hypotensive action of exogenous Bk. Still, the long-lasting isolated thrombolytic effect of ACE I was mediated entirely by endogenous BK as evidenced by the preventive action of icatibant, a kinin B2 receptor antagonist. Moreover, in vivo the immediate thrombolysis by ACE-I was mediated by PGI2 rather than by NO or t-PA, as shown by pharmacological analysis, and by direct blood assays of 6-keto-PGF1 alpha and t-PA antigen. Bradykinin as a mediator of pleiotropic endothelial action of several cardiovascular drugs (e.g. ACE-I) may complete its mission not only through B2 receptor and [Ca2+]i--mediated release of PGI2 or NO. Here, we describe a new route of the Bk action. Bk mediated induction of the [Ca2+]i-independent, so called 'inducible', endothelial isoenzymes required for generation of CO, PGI2 and PGE2. After 4 hours of incubation of HUVEC with Bk (10 nM) it induced mRNAs for haemooxygenase 1 (HO-1), cyclooxygenase 2 (COX-2), prostaglandin E synthase (PGE-S) whereas mRNA for nitric oxide synthase 2 (NOS-2) was weakly affected. We proved also that unlike in peripheral circulation, in pulmonary circulation only NO but not PGI2 would play a protective role. In the blood-perfused lung, endotoxaemia liberates lipids, such as TXA2, PAF and cyst-LTs. These toxic lipids along with the activated complement mediate pulmonary damage. Pulmonary endothelial nitric oxide is the only local protector against lung injury evoked by the phagocytised bacterial lipopolysaccharide. SUMMARY: Summing up, in peripheral circulation endogenous Bk is the most efficient activator of protective endothelial function. For instance, thrombolytic action of 'tissue type' ACE-I depends on the Bk-released PGI2. Acting as an agonist of endothelial B2 kinin receptors Bk rises [Ca2+]i with a subsequent activation of constitutive COX 1 and NOS-3. This is followed by an immediate release of PGI2 and NO. Moreover, acting as 'microcytokine' Bk induces mRNAs for HO-1, COX-2 and PGE S, the isoenzymes responsible for a delayed endothelial biosynthesis of CO, PGI2 and PGE2. (ABSTRACT TRUNCATED)

6-Ketoprostaglandin F1 alpha↗
PubMed1985

[Collateral pulmonary circulation in Fallot's tetralogy].

An angiographic study of 231 patients with tetralogy of Fallot (TOF) in both neonatal and adult age groups (0 to 49 years) was in this condition. Cases of pulmonary atresia with ventricular septal defect were excluded. Two types of collateral pulmonary circulation were observed: the most common form is the result of distal intrapulmonary anastomosis between systemic parietal, mammary and bronchial vessels with the pulmonary arteries. This type of collateral circulation represents an evolutive stage of TOF and is directly related to age and to the degree of hypoxia; the other, oa rare and probably congenital form (1.7 p. 100 of cases) observed even in young children, consisting of proximal anastomoses between systemic vessels arising from the aorta (1 to 3 vessels) and the pulmonary arterial tree. The rare forms of TOF with single pulmonary arteries acquired after palliative or congenital anastomoses (1.4 p. 100) have both types of collateral circulation. Preoperative diagnosis of the collateral pulmonary circulation requires opacification of the aorta especially of the descending thoracic segment and its branches, completed in cases of an absent pulmonary artery by wedged pulmonary venous opacification. The haemodynamic effects of this collateral circulation on the pulmonary bed to a variable degree of histological change. This may partially explain some of the poor surgical results of repair of TOF and, in view of recent progress in cardiopulmonary bypass techniques in children, incite to earlier surgical correction of this condition.

Adolescent↗
PubMed2005

Deletion of the eNOS gene has a greater impact on the pulmonary circulation of male than female mice.

Nitric oxide is involved in development and postnatal adaptation of the pulmonary circulation. This study aimed to determine whether genetic deletion of nitric oxide synthase (NOS) would lead to maldevelopment of the pulmonary arteries in fetal life, compromise adaptation to extrauterine life, and be associated with a pulmonary hypertensive phenotype in adult life and if any abnormalities were detected, were they sex dependent. Morphometric analyses were made on lung tissue from male and female fetal, newborn, 14-day-old, and adult endothelial NOS-deficient (eNOS-/-) or inducible NOS-deficient (iNOS-/-) and wild-type mice. Hemodynamic studies were carried out on adult mice with deletion of either eNOS or iNOS genes. We found that in eNOS-/- mice, lung development was normal in fetal, newborn, and adult lungs. Pulmonary arterial muscularity was greater than normal in both male and female eNOS-/- during fetal life and at birth, but the abnormality persisted only in male mice. Right ventricular hypertrophy was present in 14-day-old and adult male eNOS-/- but not in female mice. Adult male eNOS-/- mice had higher mean right ventricular and systemic pressures than female eNOS-/- mice (P < 0.05). Thus deletion of the eNOS gene was associated with structural evidence of pulmonary hypertension in both sexes during fetal life, but pulmonary hypertension persisted only in the male. In neither sex did iNOS or neuronal NOS appear to compensate for the eNOS deletion. Adult iNOS-/- mice did not have structural or hemodynamic evidence of pulmonary hypertension. Possible compensatory mechanisms are discussed.

Actins↗
PubMed1980

[Problems of early detection of latent pulmonary hypertension--the value of ergometric tests and the correlation between pulmonary circulation and parameters of lung function (author's transl)].

The possibility of early detection of pulmonary hypertension is rather late according to the large capacity of the lung vessels in the condition of rest. Consequently the parameters of the pulmonary circulation were measured in 89 healthy subjects and 261 men suffering from silicosis in rest and bicycle exercise by means of the microcatheter technique and statistically compared with other parameters of lung function. In conclusion it can be said there is a statistical correlation between pressure at rest and during exercise conditions, but this is not available in an individual case. Furthermore the pressure values of persons suffering from silicosis are higher than those of the healthy group at rest and the pressure rise is higher in the ill group during exercise. Statistically there is a slight correlation between the pressure behavior and the FEV1, Rtot, PO2, DCO and of minor importance to VC, RC and FRC.

Blood Pressure↗
PubMed1996

Galenicae Quaestiones Disputatae Duae: rete mirabile and pulmonary circulation.

The author discusses two points of Galenic medicine that have long interested medical historians: why did Galen describe a non-existent arterial rete mirabile at the base of the human brain and was Galen the first to discover the pulmonary circulation. After reviewing the evidence, it is concluded that Galen mistook the venous rete mirabile at the base of the human brain for an arterial one and that he indeed described the passage of blood from the right to the left ventricle although he did not discover the pulmonary circulation.

Blood Circulation↗
PubMed2006

Vascular impedance analysis in human pulmonary circulation.

Vascular impedance is determined by morphometry and mechanical properties of the vascular system, as well as the rheology of the blood. The interactions between all these factors are complicated and difficult to investigate solely by experiments. A mathematical model representing the entire system of human pulmonary circulation was constructed based on experimentally measured morphometric and elasticity data of the vessels. The model consisted of 16 orders of arteries and 15 orders of veins. The pulmonary arteries and veins were considered as elastic tubes and their impedance was calculated based on Womersley's theory. The flow in capillaries was described by the "sheet-flow" theory. The model yielded an impedance modulus spectrum that fell steeply from a high value at 0 Hz to a minimum around 1.5 Hz. At about 4 Hz, it reached a second high and then oscillated around a relatively small value at higher frequencies. Characteristic impedance was 27.9 dyn-sec/cm5. Influence of variations in vessel geometry and elasticity on impedance spectra was analyzed. Simulation results showed good agreement with experimental measurements.

Blood Flow Velocity↗
PubMed1975

Influence of lung resection on pulmonary circulation and lung function at rest and on exercise.

Since June 1972, preoperative evaluation of the pulmonary hemodynamics and lung function tests at rest and on exercise were done in patients undergoing thoracotomy with lung resection. 49 patients have been investigated postoperatively, 28 patients had pre- and postoperative rightsided heart catheterization. 80% of the patients were feeling well and more than 50% were working again. The pulmonary hemodynamics showed postoperatively already at rest an increase of the pulmonary artery pressures, the cardiac index reached on exercise no longer the preoperative values and there was an increase of PCV pressures on exercise compared to preoperative. Stroke volume, heart rate, AV difference for oxygen, oxygen uptake, PaO2, V, VD/VT, AadO2, and diffusing capacity for CO steady state on exercise showed no statistical significant changes. The extent of lung resection showed no different influence on the pulmonary circulation for the time period investigated.

Adult↗
PubMed2001

Potential genetic contributions to control of the pulmonary circulation and ventilation at high altitude.

This review examines evidence that genetic factors may be important determinants of response of the pulmonary circulation and ventilation at high altitude. Early observations of cattle at high altitude with brisket disease-pulmonary hypertension with right heart failure-found that the disorder ran in families. Subsequent studies confirmed a genetic determination of the pulmonary vasoconstrictor response to hypoxia by selective breeding of cattle for high and low responses. Clear interspecies and interstrain differences in the hypoxic pulmonary pressor response also underscore a major role for genetic influence in animals. In humans, differences in pulmonary hemodynamics are also evident among discrete populations living at altitude in the Andes, Himalayas, and North America suggesting an evolutionary, genetic influence on the response of the lung circulation to the hypoxia of altitude. Ventilation is increased by the hypoxia of high altitude. The strength of the ventilatory response to hypoxia shows considerable variation among individuals at low altitude. Family clusters of high and low responses and greater concordance among identical than fraternal twins suggest a strong genetic modulation of the human hypoxic ventilatory response. Similar effects are seen in interstrain differences among inbred strains of rats and mice. Differences among diverse altitude populations support the possible influence of genetic variation in the hypoxic response on ventilation and adaptation at altitude. Mechanisms linking genetic influences to variation in the hypoxic pulmonary pressor and ventilatory responses are unknown, but could reflect effects on hypoxic sensor, mediator or effector limbs of the response.

Adaptation, Physiological↗
PubMed1999

Vascular inflammation inhibits gene transfer to the pulmonary circulation in vivo.

We report gene transfer to the normal and injured murine pulmonary circulation via systemic (intravascular) and airway (intratracheal) delivery of novel polycationic liposomes (imidazolium chloride, imidazolinium chloride-cholesterol, and ethyl phosphocholine). With use of the reporter genes chloramphenicol acetyltransferase (CAT) or human placental alkaline phosphatase (hpAP), intravascular injection of lipid-DNA complexes resulted in gene expression primarily in the lung, with lesser expression in the heart (11% of lung, P < 0.05) and spleen (8% of lung, P < 0.05). Histochemical staining for the hpAP reporter gene showed localized transgene expression in the microvascular endothelium. Monocrotaline (80 mg/kg body wt sc) treatment produced endovascular inflammation and reduced lung CAT activity (2 days postintravascular transfection) by 75 +/- 8 and 86 +/- 6% at 7 and 21 days, respectively, after monocrotaline (P < 0. 05). Despite the apparent decrease in functional CAT protein, Southern blot analysis suggested maintained plasmid delivery, whereas quantitative PCR (TaqMan) showed decreased CAT mRNA levels in monocrotaline mice. In contrast, intratracheal delivery of lipid-DNA complexes showed enhanced CAT expression in monocrotaline mice. Transfection in alternate pulmonary vascular disorders was studied by inducing hypoxic pulmonary hypertension (4 wk at barometric pressure of 410 mmHg). Efficiency and duration of gene transfer, assessed by CAT activity, were similar in pulmonary hypertensive and normal lungs. We conclude that imidazolinium-derived polycationic liposomes provide a means of relatively selective and efficient gene transfer to the normal and injured murine microvascular circulation, although translation of transgene mRNA may be reduced by preexisting endothelial injury.

Animals↗
PubMed2002

Responses of the bronchial and pulmonary circulations to short-term nitric oxide inhalation before and after endotoxaemia in the pig.

The physiological responses of the bronchial circulation to acute lung injury and endotoxin shock are largely unexplored territory. This study was carried out to study the responsiveness of the bronchial circulation to nitric oxide (NO) inhalation before and after endotoxaemia, in comparison with the pulmonary circulation, as well as to study changes in bronchial blood flow during endotoxaemia. Six anaesthetized pigs (pre-treated with the cortisol-synthesis inhibitor metyrapone) received an infusion of 10 microg/kg endotoxin during 2 h. Absolute bronchial blood flow was measured via an ultrasonic flow probe around the bronchial artery. The pigs received increasing doses of inhaled NO over 5 min each (0, 0.2, 2 and 20 ppm) before and after 4 h of endotoxaemia. The increase in bronchial vascular conductance during 5 min of inhalation of 20 ppm NO before endotoxin shock was significantly higher (area under curve (AUC) 474.2 +/- 84.5% change) than after endotoxin shock (AUC 118.2 +/- 40.4%, P < 0.05 Mann-Whitney U-test). The reduction of the pulmonary arterial pressure by 20 ppm NO was not different. A short rebound effect of the pulmonary arterial pressure occurred after discontinuation of inhaled NO before endotoxaemia (AUC values above baseline 54.4 +/- 19.7% change), and was virtually abolished after endotoxaemia (AUC 6.1 +/- 4.0%, P = 0.052, Mann-Whitney U-test). Our results indicate that the responsiveness of the bronchial circulation to inhalation of increasing doses of inhaled NO during endotoxin shock clearly differ from the responsiveness of the pulmonary circulation. The reduced responsiveness of the bronchial circulation is probably related to decreased driving pressure for the bronchial blood flow. The absence of the short rebound effect on pulmonary arterial pressure (PAP) after induction of shock could be related to maximum constriction of the pulmonary vessels at 4 h.

Administration, Inhalation↗