Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PULMONARY CIRCULATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources

Compact mock loops of the systemic and pulmonary circulation for blood pump testing.

Mock loops are an important tool for in vitro investigations of artificial blood pumps. The simple windkessel, throttle, and atrium principle was used for the mock loop design presented. The components of the systemic and the pulmonary mock loop were designed according to calculated numerical simulation parameters. The loops offer a compact design and simple handling. For simulating biventricular assist or total artificial heart (TAH), both loops can be coupled correspondingly. The numerical simulation and the first results with the loops show very good similarity to physiological data of systemic and pulmonary circulation. The measurements of pump characteristics are significant for quantitative comparison of different pump sizes and types, or driving systems.

Blood Circulation↗

[Scintigraphy in the evaluation of postoperative disorders of pulmonary circulation in cancer of the breast and genitalia].

Altogether 60 patients with genital tumors and breast cancer were examined on the 3rd-7th day after operation using ON-110 gamma-camera (USA). Perfusion pulmonary scintigraphy with labeled MMA was performed in all the patients. In 66% of the examinees pulmonary blood flow disorders localized mainly in the lower part of the lungs, were noted, and in breast cancer patients--on the tumor lesion side, too. Perfusion pulmonary scintigraphy was shown to be an informative method of diagnosis of postoperative changes of the capillary pulmonary circulation which were clinically undetectable.

Adult↗

BQ123, an ETA receptor antagonist, attenuates endothelin-1-induced vasoconstriction in rat pulmonary circulation.

Endothelin-1 (ET-1) is a potent endogenous vasoactive peptide whose role in regulation of vascular tone is unclear. BQ123 is a recently described ETA receptor antagonist which may be useful in further investigation of the physiologic and pathophysiologic significance of ET-1. To test its efficacy in the pulmonary circulation, the vascular response to exogenous ET-1 with and without BQ123 was assessed in rat pulmonary artery (PA) rings and salt-perfused lungs. In both main and distal (250-350 microns ID) PA rings, BQ123 significantly attenuated ET-1-induced contractility, but was more effective in the larger vessels. Likewise, BQ123 significantly blunted ET-1-induced vasoconstriction in perfused lungs by > 80%. In addition, it had no effect on ET-3-mediated or U46619-mediated vasoconstriction, nor did it influence ET-1-induced vasodilation. Development of ET-1-associated hydrostatic edema was also unaffected by BQ123. We conclude that BQ123 effectively attenuates ET-1-induced vasoconstriction in both PA rings and in isolated perfused lungs. The absence of effect of BQ123 on ET-3 vasoconstriction, ET-1 vasodilation, or ET-1- and ET-3-induced hydrostatic edema formation suggests that these processes may be transduced through a non-ETA receptor.

Amino Acid Sequence↗

Pulmonary circulation and loss of microspheres from the lung following acute pulmonary venous occlusion.

The pulmonary vein from right upper lobe was ligated in 15 rats while 15 others served as controls. Prior to occlusion, 15 mum microspheres were injected into the superior caval vein. Another population of 15 mum microspheres was similarly given 1 min, 10 min or 30 min after ligation. All rats were killed 5 min after the second microsphere injection. The weight of the ligated lobe was 63% higher than that of the controls. This was probably due to acute vascular congestion since no significant oedema developed. Increased weight caused a reduction in the number of preocclusion microspheres per gram of tissue in the ligated lobe. In addition a gradual loss of preocclusion microspheres took place following pulmonary venous ligation. After 35 min of ligation, 30% of the preocclusion spheres had disappeared from the ligated lobe. Postocclusion flow through the pulmonary artery into right upper lobe was estimated by microspheres from the second injection, and averaged 5% of normal flow. Following acute venous occlusion, a rapid dilatation of the bronchopulmonary communicating system probably takes place. By reversal of the flow in this system, blood and microspheres can be drained into the bronchial venous circulation. In spite of methodological problems caused by acute congestion and loss of microspheres after pulmonary venous occlusion, we consider the microsphere method to be useful for further studies of collateral lung circulation.

Animals↗

Doppler echocardiographic assessment of pulmonary circulation in severe respiratory failure of the neonate: an aid for extracorporeal lung support indications.

Extracorporeal lung support (ECLS) for newborns with acute respiratory failure has achieved increased popularity over the last decade. However, precise criteria for its implementation remain controversial. The aim of this study was to assess the value of Doppler echocardiography (DE) in 31 neonates with PaO2 of < or = 50 mmHg, FIO2 of 1, and optimal ventilation. Treatment included mechanical ventilation, paralysis, volume loading, vasopressors, and tolazoline. Markers indicative of ECLS (failure of maximal medical therapy, assessed by AaDO2 of more than 610 mm Hg beyond 8 hours and/or an oxygenation index (OI = mean airway pressure x FIO2%/postductal PaO2) of more than 40 beyond 4 to 6 hours) were present in 23 (group 1) and absent in eight (group 2). Shunt direction and systolic pulmonary arterial pressure (sPAP) calculated from tricuspid insufficiency velocity were assessed using DE. At the time of admission, sPAP was significantly higher in group 1 (62.1 v 43.7 mm Hg). On day 1, group 1 differed from group 2 in maximum sPAP value (73.2 v 44.4 mm Hg), PaCO2 (56.1 v 40 mm Hg), right-to-left shunting (85% v 25% of the patients), and pulmonary-to-systemic-pressure systolic ratio (sPAP:sSAP) (1.29 v 0.75). Patients with an sPAP:sSAP ratio of more than 1 and patients with high sPAP associated with high PaCO2 on day 1, all later (average, 10 hours later) fulfilled ECLS criteria; this suggests that DE assessment of pulmonary circulation may yield early and predictive markers of impending ECLS indication. Further confirmation of these results would help avoid unnecessary delays in ECLS implementation in newborns with severe respiratory failure.

Echocardiography, Doppler↗

Maturational changes in endothelium-derived relaxations in newborn piglet pulmonary circulation.

It is accepted knowledge that the endothelium can profoundly affect vascular tone through the release of vasoactive substances. The maturational changes in the role of the endothelium-derived relaxing factor (EDRF) and ATP-dependent K+ channels in the neonatal pulmonary circulation were investigated in isolated perfused lungs from 1- and 7-day-old piglets. The EDRF inhibitor, N omega-nitro-L-arginine (L-NNA), had potent dose-dependent constrictor effects on the pulmonary vasculature with normal and raised tone. The constrictor effect of L-NNA was greater (P < 0.05) in the 1-day-old than in the 7-day-old lungs and was significantly (P < 0.005) attenuated by pretreatment with the EDRF precursor, L-arginine. Furthermore, we studied the possibility of developmental changes in the sensitivity of smooth muscle cells to EDRF by testing sodium nitroprusside, nitric oxide, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP). All caused a decrease in perfusion pressure, but only sodium nitroprusside elicited a greater (P < 0.01) effect in the 1-day-old. Endothelin-1 (ET-1) and bradykinin (BK) elicited dilator responses that were significantly (P < 0.05) reduced in the presence of L-NNA. Interestingly, the dilator response to ET-1 was more marked (P < 0.001) in the younger group, whereas no age difference was noted with BK. Finally, lemakalim, a K+ channel activator, caused a vasodilation of equal magnitude at both ages. In summary, EDRF and ATP-dependent K+ channels appear to play a role in the control of the newborn piglet pulmonary vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

[Status of the venous system and pulmonary circulation at early stages of development of arterial hypertension (clinico-experimental comparisons)].

The study was undertaken to examine 116 patients with borderline arterial hypertension (BAH), 67 normotensives without a family history of hypertensive disease (HD), and 29 normotensive relatives with HD. The hemodynamics of systemic and pulmonary circulations were investigated. For comparison, the functional activity of the portal vein was studied in spontaneously hypertensive rats of different age. High systolic pressure in the pulmonary artery and predominant hyperkinetic central hemodynamics were observed in the normotensives with a family history of HD and patients with BAH. The findings are in good agreement with experimental evidence for a higher functional activity of the venous system in early essential hypertension.

Adolescent↗

Effects of dotarizine on peripheral and pulmonary circulation and cardiac dynamics in dogs.

The cardiovascular effects of dotarizine in 10-min intravenous infusions were studied in thiopental-anesthetized dogs. The effects of dotarizine 0.024 mg/kg/min almost paralleled those of saline controls; 0.079 mg/kg/min dotarizine significantly raised the stroke index and ejection fraction, and, at a rate of 0.25 mg/kg/min, further effects appeared and were dose-dependent. Dotarizine produced arterial dilation in both systemic and pulmonary circulation: the total peripheral resistance dropped, and femoral artery flow rose; aortic and pulmonary artery mean and diastolic pressures declined, and systolic pressures remained almost stable. A trend of bradycardia and pulmonary artery pressure reduction persisted for 30 min. As compared with the reduced total peripheral resistance, aortic pressure fell only moderately because of rising cardiac output due to a higher ejection fraction and stroke volume. Cardiac preload tended to decline; contractility tended to increase. Cardiac performance remained stable while myocardial oxygen consumption tended to fall, as did the pressure-rate product and the tension time index. Dotarizine exerted direct cardiovascular effects similar to those of the 5-HT2-receptor antagonist ketanserin and, more generally, to calcium channel blockers rather than to alpha-adrenoceptor blockers.

Animals↗

[Effects of serotoninergic block on reactivity of systemic and pulmonary circulation in hypertensive patients].

The aim of this study was to verify the possible role of serotonin on vascular basal tone and over-reactivity in systemic and pulmonary circuits in hypertensive patients. We studied 15 hypertensive (G1) and 10 normotensive (G2) subjects. Right-side pressure and intravascular-arterial pressure measurements were obtained in baseline conditions and during alpha-adrenergic activation by cold-pressor-test (CPT), before and after intravenous injection of ketanserin 10 mg (K), an S2-receptor antagonist. Systemic and pulmonary pressures and resistances were higher in G1 than in G2 in the steady state. K induced a significant reduction of both pressures and resistances in G1, no change in systemic response to CPT in the 2 groups and a significant reduction in the pulmonary vascular reactivity to adrenergic stimulus only in G1. These data confirm the vasodilator action of serotonin-blockade. The observation of vasodilatation in pulmonary circulation is not in favor of its dependence on vascular endothelium damage. In fact the arterial endothelium lesions due to hypertension are present only in the systemic circuit. Concerning result of CPT: 1) serotonin doesn't seem responsible for vascular over-reactivity in hypertension, unchanged by K; 2) the particular pattern of pulmonary vascular contractility in G1 may be interpreted as resulting from an elective depressive action of S2-blockade, depending on a different distribution of S1 and S2 receptors in the two circuits.

Adult↗

Role of the pulmonary circulation in the distribution of human fetal cardiac output during the second half of pregnancy.

BACKGROUND: By using Doppler echocardiography, we determined the normal distribution of human fetal combined cardiac output (CCO) from the left and right ventricles. We also established weight-indexed pulmonary and systemic vascular resistances (Rpi and Rsi, respectively) and changes during the second half of pregnancy. METHODS AND RESULTS: Blood flows at the aortic and pulmonary valve annuli (LVCO and RVCO, respectively), right and left pulmonary arteries (QP), and ductus arteriosus (QDA) were calculated in 63 normal fetuses. Foramen ovale blood flow (QFO = LVCO-QP) was estimated. From 20 to 30 weeks of gestation, the proportion of QP of the CCO increased (from 13% to 25%, P < .001), while the proportion of QFO decreased (from 34% to 18%, P < .001). After 30 weeks, the proportions of QP and QFO were unchanged. At 38 weeks, the proportion of RVCO (60%) was higher (P < .05) than that of LVCO (40%). The proportion of QDA did not change significantly. The correlation between RVCO calculated from blood flow through the pulmonary valve and from QDA and QP was good (r = .97, P < .0001). RPi (P < .001) decreased from 20 to 30 weeks of gestation. From 30 to 38 weeks, RPi increased (P < .0001). Rsi increased (P < .001) from 20 to 38 weeks. The ratio of RPi to RSi decreased (P < .01) from 20 to 30 weeks and later remained unchanged. CONCLUSIONS: The human fetal pulmonary circulation has an important role in the distribution of cardiac output.

Blood Pressure↗

Altered reactivity to acetylcholine in the pulmonary circulation after cardiopulmonary bypass is part of reperfusion injury.

STUDY OBJECTIVE: To investigate whether a time sequence of acetylcholine (ACH) reactivity indicative of endothelial reperfusion injury could be demonstrated in the pulmonary circulation in patients after cardiopulmonary bypass (CPB). DESIGN: Prospective study. SETTING: Operating theater and intensive care unit of a university hospital. PATIENTS: 10 ASA physical status III and IV patients with ischemic or valvular heart disease. INTERVENTIONS: Pulmonary vascular resistance index (PVRI) was measured before and during an infusion of ACH. This procedure was done after induction of anesthesia but before surgery, immediately after weaning from bypass, and at 1 to 1.5 and 4 hours after CPB. MEASUREMENTS AND MAIN RESULTS: ACH caused a decrease in PVRI before (p < 0.01) and directly after CPB (p < 0.05) but not at 1 to 1.5 or 4 hours after bypass. CONCLUSIONS: The maintained reactivity to ACH directly after CPB, followed by no reaction at 1 to 1.5 and 4 hours, was in agreement with experimental findings and indicates endothelial reperfusion injury caused by the period with no blood flow through the pulmonary artery during CPB and subsequent reperfusion.

Acetylcholine↗

[Studies on dose-dependent effect of ouabain on right ventricular function and pulmonary circulation].

The clinical utility of digitalis glycoside for the treatment of cor pulmonale induced by chronic pulmonary disease has not been clarified. In the present study, a rational use of this drug for the treatment of cor pulmonale was investigated especially concerning it's dose. In normal open-chested anesthetized dogs, the effect of ouabain was studied with special reference to pulmonary vascular resistance and right ventricular myocardial contractility by changing dose of 0.01 mg/kg, 0.02 mg/kg and 0.03 mg/kg. Pulmonary vascular resistance was increased extremely when the dogs were treated with 0.03 mg/kg, but not changed remarkably with 0.02 mg/kg and 0.01 mg/kg. On the other hand, right ventricular myocardial contractility was increased equally in dogs treated with 0.03 mg/kg and 0.02 mg/kg but slightly in dogs treated with 0.01 mg/kg. From these data, the existence of the optimum therapeutic dose of ouabain for cor pulmonale which increases myocardial contractility enough but has no significant pulmonary vasoconstrictive effect may be suggested. Then this dose of ouabain was given to acute experimental pulmonary hypertensive dogs (mean PA pressure 40-50 mmHg) due to recurrent miliary pulmonary embolization. The other group of pulmonary embolization was not treated with ouabain. Pulmonary vascular resistance was not increased in both groups, but myocardial contractility and cardiac output were increased significantly only in the ouabain treated group. In conclusion, though the dose-response relationship was observed in increasing myocardial contractility and pulmonary vasoconstriction by ouabain, the dose which increases myocardial contractility was less than that which evokes pulmonary vasoconstriction in normal and pulmonary hypertensive dogs.

Animals↗

Duroquinone reduction during passage through the pulmonary circulation.

The lungs can substantially influence the redox status of redox-active plasma constituents. Our objective was to examine aspects of the kinetics and mechanisms that determine pulmonary disposition of redox-active compounds during passage through the pulmonary circulation. Experiments were carried out on rat and mouse lungs with 2,3,5,6-tetramethyl-1,4-benzoquinone [duroquinone (DQ)] as a model amphipathic quinone reductase substrate. We measured DQ and durohydroquinone (DQH2) concentrations in the lung venous effluent after injecting, or while infusing, DQ or DQH2 into the pulmonary arterial inflow. The maximum net rates of DQ reduction to DQH2 in the rat and mouse lungs were approximately 4.9 and 2.5 micromol. min(-1).g dry lung wt(-1), respectively. The net rate was apparently the result of freely permeating access of DQ and DQH2 to tissue sites of redox reactions, dominated by dicumarol-sensitive DQ reduction to DQH2 and cyanide-sensitive DQH2 reoxidation back to DQ. The dicumarol sensitivity along with immunodetectable expression of NAD(P)H-quinone oxidoreductase 1 (NQO1) in the rat lung tissue suggest cytoplasmic NQO1 as the dominant site of DQ reduction. The effect of cyanide on DQH2 oxidation suggests that the dominant site of oxidation is complex III of the mitochondrial electron transport chain. If one envisions DQ as a model compound for examining the disposition of amphipathic NQO1 substrates in the lungs, the results are consistent with a role for lung NQO1 in determining the redox status of such compounds in the circulation. For DQ, the effect is conversion of a redox-cycling, oxygen-activating quinone into a stable hydroquinone.

Animals↗

[Status of pulmonary circulation and the presence of regurgitant wave from the left ventricle in primary dilated cardiomyopathy].

The purpose of the study was to analyse relationships between the presence and magnitude of a regurgitant wave from the left ventricle to the left atrium and the state of the pulmonary circulation in patients with primary dilated cardiomyopathy. The study population consisted of 97 patients divided into three subgroups I--41 patients without the regurgitant wave, II--31 patients with the first-degree regurgitant wave, III--25 patients with the second-degree regurgitant wave. Diagnosis was based upon non invasive studies, cardiac catheterization and left ventriculography. Average values of the left ventricular systolic and end-diastolic pressures were similar in all subgroups, whereas the cardiac index was the lowest in the subgroup of patients with a large regurgitant wave to the left atrium. There were no differences in mean values of the pulmonary artery pressures, total pulmonary resistance and pulmonary vascular resistance between the patients without the regurgitant wave (subgroup II). In contrast the patients with a large regurgitant wave (subgroup III) showed statistically significantly higher pulmonary artery pressures, higher total pulmonary resistance and pulmonary vascular resistance. In 64% of the patients of this subgroup the left atrium was said to be large. The results of the present study indicate that even not a large regurgitant wave (second-degree) from the left ventricle to the left atrium leads to secondary pulmonary hypertension in patients with primary dilated cardiomyopathy.

Adolescent↗