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At least 523 records · Page 29Linked to original sources
PubMed1979

[Effects of dopamine, noradrenaline and isoproterenol on pulmonary circulation in anesthetized dogs].

Experiments were performed on 19 anaesthetized open-chest dog instrumented with polyethylene catheters inserted: into the aorta, in pulmonary artery and in left atrium and with an electromagnetic flow-transducer placed around the ascending aorta in order to record : systemic arterial and pulmonary pressures, mean left auricular pressure and phasic aortic flow. Heart rate, stroke volume, total systemic and pulmonary resistance, cardiac work were moreover calculated. Each dog was given intravenously by slow infusione : Dopamine (micrograms 5--10--20/kg/min/ 5 min), Isoproterenol (microgram 0.125--0.25--0.5/kg/min/5 min) and Norepinephrine (microgram 0.25--0.5--1 /kg/min/5 min). Results obtained on systemic hemodynamics agree with those reported by many other investigators. On pulmonary circulation : Isoproterenol, at the tested doses, elicited vasodilator effects, Norepinephrine increased total pulmonary resistance but not pulmonary vascular resistance, while Dopamine did not modify or slightly reduced vascular pulmonary tone.

Animals↗
PubMed1994

Endothelin-1 causes accumulation of leukocytes in the pulmonary circulation.

We previously reported that the endothelin-1 (ET-1)-induced increase in microvascular permeability in isolated rat lungs required leukocytes in the perfusate. The present study examines whether intravenous administration of ET-1 in rats causes an inflammatory reaction in the lungs. Histological examination of the lung specimens 2 hr following ET-1 infusion showed adhesion of leukocytes to the vascular endothelium in pulmonary vessels and sequestration of leukocytes in the pulmonary capillaries. Microscopic examination of the bronchoalveolar lavage fluid revealed that leukocytes had migrated into the alveoli. Simultaneously a depletion of peripheral blood leukocytes was observed. These effects were reversible by 24 hr. Monitoring of systemic hemodynamic effects showed a continued reduced cardiac stroke volume and increasing heart rate after 2 hr. In isolated rat lungs, ET-1 caused a rapid increase in pulmonary artery pressure, pulmonary microvascular pressure, and edema formation. Compared with Krebs-albumin-perfused lungs, blood-perfusion accelerated the edemagenic effect of ET-1. ET-1 plays a role in the regulation of leukocyte-endothelial cell interactions in the pulmonary circulation. This has potential importance for the edemagenic effect of ET-1.

Animals↗
PubMed1992

Echocardiographic proof of pulmonary hypertension with irreversible increased resistance in the pulmonary circulation as a complication after placement of a ventriculo-atrial shunt for internal hydrocephalus.

Increased resistance in the pulmonary vessels in children with ventriculo-atrial shunts is a rare and often unrecognized permanent complication. We report 2 children in whom this diagnosis was detected by two-dimensional echocardiography. The first patient received a ventriculo-atrial shunt at age 9 days for congenital internal hydrocephalus. At 17 months it had to be replaced because of infection of the efferent catheter limb. At 22 months at a routine follow-up the echocardiographic diagnosis of pulmonary hypertension was made. Invasive studies confirmed the presence of irreversible increased resistance in the pulmonary circulation. The second patient received a ventriculo-atrial shunt at age 13 months because of a cerebral cyst. After repeated catheter infections, at 28 months a ventriculo-peritoneal shunt was placed. At age 4 years the diagnosis of pulmonary hypertension was made by routine echocardiography. This finding was confirmed by invasive studies. The left pulmonary artery was completely occluded. Both patients had developed microemboli, caused or aggravated by catheter sepsis, in the second case probably through contiguous clot growth up to complete occlusion of the left pulmonary artery. Therapeutic measures seemed not to be indicated. Two-dimensional echocardiography proved to be a reliable method for diagnosing increased resistance and pulmonary hypertension. We recommend routine echocardiography for follow-up in all children with ventriculo-atrial shunts.

Cerebrospinal Fluid Shunts↗
PubMed1997

Risk factors for early degeneration of allografts in pulmonary circulation.

OBJECTIVE: The aim of this study was to define risk factors for early degeneration of allografts in pulmonary circulation and to recommend some guidelines to minimize them. METHODS: Between January 1988 and March 1995, 202 patients with various types of congenital heart disease received cryopreserved allograft conduits for reconstruction of their right ventricular outflow tract. We report on 63 patients receiving allografts ranging from 9-24 mm size within the first 2 years of life. RESULTS: Survivors have been followed for 4-67 months. Survival at 5 years, including hospital mortality, was 66%. Two patients died at reoperation. Of the patients 19.6% (9/46) had early structural deterioration (SD) of their vascular allografts at a mean of 15.2 months after implantation. Seven of these have already been reoperated with allograft exchange. Freedom of reoperation was 66% at 5 years. Infants showed 48% freedom of reoperation at 5 years compared to 90% in the 1-2 years age group, while freedom of SD was 59% in infants at 48 months compared to 87% in the 1-2 years age group. Of allografts with SD in the infant group 66% had an allograft size of < 14 mm. In aortic allografts freedom of SD was 62% compared to 93% in pulmonary allografts. Freedom of allograft wall calcification was 46% at 18 months in all patients. In the statistical analysis, only infant age (P = 0.03) and aortic allograft (P = 0.02) were shown to be significant risk factors for early SD. CONCLUSION: The use of pulmonary allografts, avoidance of relatively short and small conduits of < 14 mm in diameter, might improve the durability of allografts in infants and small children.

Bioprosthesis↗
PubMed1997

Comparison between three- and four-element Windkessel models to characterize vascular properties of pulmonary circulation.

In 11 anaesthetised pigs the accuracy of the three-element (WK3) and the four-element (WK4) Windkessel models to describe hemodynamic properties of the pulmonary circulation was compared during six different experimental conditions increasing pulmonary arterial pressure: increase in left atrial pressure, increase in alveolar pressure, increase in pulmonary blood flow, endotoxin shock, mechanical obstruction of left pulmonary artery or histamine infusion. Our results showed that WK4 fitted better the data than did WK3 because values of 1-R2 decreased from 6 percent (WK3) to 1.4 percent (WK4) when WK4 was used (P < 0.0005). 1-R2 was an adequate marker of the accuracy of the linear regression used to solve equations of both models. Compliance values estimated by WK4 were decreased by 5% comparatively to WK3 (P = 0.008). However, this difference can be considered as not physiologically relevant. Values of characteristic resistance corresponding to R1 + (L/R2C) in WK4 and to R1 in WK3 were not different (P = 0.22). The relative changes in R1, R2, and C observed due to the different experimental conditions were comparable regardless of the model. In conclusion, the conversion of WK3 in WK4 by adding an inductance, whose physiological meaning is not clear, resulted in an increased statistical accuracy of the model, but did not seem to have relevant influence on parameters or their evolution during experimental conditions.

Animals↗
PubMed1995

[Effects of long term oxygen therapy in patients with idiopathic pulmonary fibrosis. I. Effect on the course of the primary disease and on pulmonary circulation].

The study was performed in 18 patients (15 F and 3-M) aged 35-57 yers (mean 46 +/- 7) diagnosed as idiopathic lung fibrosis. Ten patients (group A) recived standard treatment (prednisone 10-15 mg/day) and supplementary home oxygen therapy (mean 16.4 h/day) for a period of 4 years. During exacerbations antibiotics, theophylline and expectorants were prescribed. Eight patients (group B) receiving the same treatment without home oxygen, served as controls. At study entry lung function test (TLC, VL, Dlco), blood gases, hematocrit, hemodynamic parameters of the pulmonary circulation and thermodilution cardiac output were measured in all patients. The measurements were repeated after 4 years of follow-up. At follow-up examination no differences in pulmonary function parameters were shown between the groups. Mean pulmonary artery pressure and pulmonary vascular resistance were significantly lower in patients receiving home oxygen therapy (group A) as compared with those treated pharmacologically only (group B). Best effects of oxygen therapy were observed in patient with lower pulmonary artery pressures at study entry.

Adult↗
PubMed1993

Functional and structural adaptation of the yak pulmonary circulation to residence at high altitude.

The high-altitude (HA) native yak (Bos grunniens) has successfully adapted to chronic hypoxia (CH) despite being in the same genus as domestic cows, which are known for their great hypoxic pulmonary vasoconstrictor responses (HPVRs), muscular pulmonary arteries, and development of severe pulmonary hypertension on exposure to CH. To determine possible mechanisms by which the pulmonary circulation may adapt to CH, yak pulmonary vascular reactivity to both vasoconstrictor and vasodilator stimuli and yak pulmonary artery structure were assessed. Hypoxia caused a small but significant HPVR, and norepinephrine infusion caused a greater rise in pulmonary arterial pressure (Ppa) than did hypoxia. Acetylcholine, an endothelium-dependent vasodilator, had no effect on Ppa but lowered pulmonary resistance (Rp) by causing an increase in cardiac output. Sodium nitroprusside, an endothelium-independent vasodilator, decreased both Ppa and Rp significantly. Yak small pulmonary arteries had a 4.1 +/- 0.1% medial thickness, with vessels < or = 100 microns devoid of smooth muscle. Yak pulmonary artery endothelial cells were much longer, wider, and rounder in appearance than those of domestic cows. Thus the yak has successfully adapted to HA conditions by maintaining both a blunted HPVR and thin-walled pulmonary vessels. Differences in both endothelial cell morphology and response to acetylcholine between the yak and those reported in the domestic cow suggest the adaptation to HA may include changes not only in the amount of pulmonary vascular smooth muscle but in endothelial cell function and structure as well.

Acclimatization↗
PubMed1994

Autoradiographic localization of dopamine D1-like receptors in the rabbit pulmonary circulation.

The pharmacological characteristics and the anatomical localization of dopamine D1-like receptors were studied in sections of rabbit lung using [3H]SCH 23390 as a ligand. [3H]SCH 23390 was bound to sections of rabbit lung in a manner consistent with the labelling of dopamine D1-like receptors. The binding was time-, temperature-, and concentration-dependent belonging to a single class of high affinity sites. The dissociation constant value (Kd) was 2.05 nM, whereas the maximum density of binding sites (Bmax) averaged 85 +/- 4 fmol/mg tissue. The pharmacological profile of [3H]SCH 23390 binding to sections of rabbit lung is consistent with the labelling of dopamine D1 receptors. Light microscope autoradiography revealed the development of silver grains which correspond to [3H]SCH 23390 binding sites within the tunica intima and the tunica media of large intrapulmonary artery branches. The presence of silver grains was also observed in the tunica media, but not in the tunica intima of medium-sized pulmonary artery branches. No silver grains were observed in small-sized pulmonary artery branches or in the pulmonary veins. Dopamine D1-like receptors localized in the rabbit pulmonary circulation probably mediate vasodilatation. Further work is necessary to clarify the functional significance of the non-homogeneous distribution of dopamine D1-like receptor sites in the pulmonary circulation.

Animals↗
PubMed1990

Interactions between alveolar hypercapnia and epoprostenol on the pulmonary circulation: clinical and pharmacological implications.

Hypoxic vasoconstriction has been the subject of many studies, but little is known about the interaction of hypercapnia and the pulmonary circulation. We performed two haemodynamic studies on each of three patients with pulmonary vascular disease secondary to congenital heart disease. On the first occasion ventilation was inadequate due to technical problems, and the patients were therefore hypercapnic (arterial pCO2 greater than 5.3 kPa). On the second occasion, they were normocapnic. Pulmonary vascular resistance was measured on each occasion while the patients were breathing 100% oxygen (alveolar hyperoxia) and while epoprostenol (prostacyclin) was infused at doses of 5-20 ng/kg/min. Pulmonary vascular resistance was elevated in the presence of hypercapnia and, despite oxygen and epoprostenol, could not be reduced to the levels observed in the normocapnic study. We conclude that hypercapnia causes significant vasoconstriction in infants; and that epoprostenol is a relatively ineffective pulmonary vasodilator in infants who are hypercapnic due to inadequate ventilation. Where possible, respiratory acidosis should be corrected before using oxygen or epoprostenol as a pulmonary vasodilator.

Carbon Dioxide↗
PubMed1983

Effect of streptozotocin-induced diabetes on the metabolism of ADP, AMP and adenosine in the pulmonary circulation of rat isolated lung.

The uptake and metabolism of radioactive ADP, AMP and adenosine was investigated in the pulmonary circulation of lungs taken from rats with streptozotocin-induced diabetes. Between 0.26 and 500 mumol/l ADP was extensively hydrolysed to AMP equally in control and diabetic lungs. At 1 mmol/l there was less ADP breakdown in diabetic lungs. Hydrolysis of AMP to adenosine was also less in diabetic lungs at 10 mumol/l and 1 mmol/l substrate concentration, but adenosine metabolism and uptake at these concentrations was not affected by diabetes. The results indicate that formation of the anti-aggregatory adenosine and, to a lesser extent, breakdown of the pro-aggregatory ADP were decreased in diabetic lungs and may contribute to the platelet hyperreactivity associated with diabetes.

Adenosine↗
PubMed1996

Alteration of segmental vascular resistance in the pulmonary circulation of diabetic rats.

Numerous studies have shown that altered plasma glucose and (or) insulin have profound effects on the pulmonary circulation. Recently, we documented diminished pressor responses to the synthetic thromboxane analogue U-46619 (9,11-dideoxy-9 alpha, 11 alpha-methanoepoxy prostaglandin F2 alpha) following short-term streptozotocin-induced diabetes in rats. However, these earlier studies examined the effects of diabetes on resistance changes across the entire pulmonary vasculature and made no effort to localize the site(s) of any abnormalities. Thus, in the present study we examined segmental pulmonary vascular resistances using the double-occlusion method in isolated, perfused rat lungs 2 weeks after streptozotocin-induced diabetes. Under baseline conditions, total pulmonary vascular resistance (TPVR) did not differ in lungs isolated from control and diabetic animals (0.66 +/- 0.03 vs. 0.85 +/- 0.05 mmHg.mL-1.min-1, respectively (1 mmHg = 133.3 Pa)). However, control animals demonstrated greater arterial (Ra) than venous (Rv) contribution to TPVR (0.43 +/- 0.02 vs. 0.23 +/- 0.02 mmHg.mL-1.min-1, respectively). This relationship was reversed in diabetic animals (Ra = 0.30 +/- 0.02 mmHg.mL-1.min-1; Rv = 0.54 +/- 0.04 mmHg.mL-1.min-1). Following constriction with U-46619 this pattern persisted, although the absolute vasoconstrictor response to the agent was similar in each segment. Likewise, this pattern of resistance was unaffected following dilation of the pulmonary vascular bed with arginine vasopressin. These findings illustrate that pulmonary segmental vascular resistances are altered and, more specifically, that pulmonary venous resistance is selectively increased, 2 weeks following the induction of diabetes.

Animals↗
PubMed1986

Comparison of computed tomographic lung density with haemodynamic data of the pulmonary circulation.

Computed tomographic (CT) lung density measurements were prospectively correlated with pulmonary haemodynamic data in 33 patients with chronic heart disease. Cardiac catheterisation and five specific computed tomographic scans (three at nearly total lung capacity, one at functional residual capacity, and one at residual volume) were performed. There was a significant correlation between anterior lung density and mean pulmonary artery pressure (r = 0.86), pulmonary vascular resistance (r = 0.80), and pulmonary artery wedge pressure (r = 0.65). Lung density, as measured by CT, thus provides a valuable estimate of pulmonary arterial pressure and pulmonary vascular resistance, but is affected by other pathological conditions, such as emphysema and congestional or post-inflammatory fibrosis.

Adult↗
PubMed1975

Release of adenosine by hypoxic canine lung tissue and its possible role in pulmonary circulation.

Adenosine is a possible mediator of myocardial and skeletal muscle blood flow regulation. Whether adenosine plays a similar role in modulating the pulmonary pressor response to acute alveolar hypoxia is not known. Adenosine levels (nmol/g tissue) in lung in six dogs ventilated with 95% N2, and 5% CO2 for a period of 3 min increased nearly 10-fold. Inosine and hypoxanthine, adenosine enzymatic degradation products, sustained a 10- and 7-fold increase, respectively. These degradative products are mainly formed in the capillary endothelial cells that contain the degradative enzyme nucleoside phosphorylase as demonstrated by histochemical techniques. To determine the effect of ATP, ADP, AMP, and adenosine on the pulmonary circulation, the in situ left lower lobe of 10 dogs was perfused at either free flow or constant flow via its pulmonary artery. ATP and ADP increased lobar vascular resistance; AMP and adenosine decreased the resistance. During hypoxic ventilation, adenosine infusions (100 nmol/ml blood) entirely abolished the increase in vascular resistance that was due solely to hypoxia. Dipyridamole produced similar responses. These data indicate that adenosine is a pulmonary vasodilator and that it may modulate the pulmonary pressor response to acute alveolar hypoxia. The findings suggest that the use of adenosine or dipyridamole may be beneficial in patients with pathologic elevations of the pulmonary vascular resistance which are a result of an exaggerated pulmonary pressor response to hypoxia, as seen in high-altitude pulmonary edema or that following cerebral injury.

Adenosine↗
PubMed1975

[Vaso-active substances and pulmonary circulation].

This study reveals the main vaso-active substances which pass through the lung, by studying in each case the extra-pulmonary of pulmonary origin, the effects of the lung on these substances: capture, discharge, transformation, and the effects of these substances on the lung. Eight groups of substances are studied: mediators of the sympatho-adrenergic system, substances interfering with adrenergic agents, acetyl-choline, serotonin, angiotensin, histamine, kinins, and prostaglandins. The lung behaves either as a neutral organ, or a filtering organ, or a filtering organ, or a secreting organ for these substances. In this way it strangely resembles the kidney. The pulmonary circulation is not completely comprised of simple reaction. It is capable of internal adjustement and redistribution under the effect of these substances. Pulmonary edema probably will always remain difficult to their mechanism of production, in so far as can be estimated from the multitude of substances. It is still rather a delicate matter to distinguish between edema-generating phenomena and phenomena which are secondary to the edema itself.

Acetylcholine↗