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Results for “PULMONARY CIRCULATION”

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At least 613 records · Page 34Linked to original sources
PubMed1981

[Effect of consecutive administration of obsidan and novodrin on pulmonary circulation in anesthesized dogs].

It was established in experiments on mongrel anesthesized dogs that the beta-blocking agent obsidan (propranolol) in a dose of 0.5-1.0 mg/kg causes an increase in total pulmonary and pulmono-arteriole resistance, which correlates with the decrease in volume blood flow in the pulmonary arteries. The pressure in the pulmonary artery and the left atrium does not change substantially. Injection of 0.25-0.5 mg of novodrin increases the volume blood flow, causes no effect on pressure in the left atrium, and reduces total pulmonary resistance. The changes occurring in pulmonary circulation under the effect of beta-adrenergic agents depend on their primary action on cardiac activity whereas the increase in total pulmonary and pulmono-arteriole resistance depends on the secondary spasm of the pulmonary vessels.

Anesthesia, Inhalation↗
PubMed1995

[Effect of dopamine in dopaminergic doses on pulmonary circulation of dogs in normoxia and hypoxia].

PURPOSE: To study if dopamine in dopaminergic doses (1.5 and 4.0 micrograms/kg/min) had some effect on the pulmonary vasoconstriction mechanism, and if in those doses the drug had some action on systemic and pulmonary hemodynamic variables, as well as in the pulmonary gas exchange. METHODS: Seventeen normal mongrel dogs, anesthetized and paralized under mechanical ventilation were submitted to two different gas mixtures: room air (F1O2 = 0.2093 -10 dogs) and hypoxic mixture (F1O2 = 0.125 -7 dogs). Dopamine was infused in both groups during 15 min in the two doses 1.5 and 4.0 micrograms/km/min, separated by a period of 30 min. RESULTS: Pulmonary hemodynamics and gas exchange variables after infusion of dopamine at 1.5 and 4.0 micrograms/km/min in dogs in normoxia and hypoxia. [table: see text] CONCLUSION: Dopamine in the used doses had no action on the pulmonary circulation and on the hypoxic pulmonary vasoconstriction mechanism; pulmonary gas exchange was not affected by dopamine in both doses during normoxia and hypoxia; in the experimental model there was no evidence of dopaminergic receptors in the pulmonary vessels.

Animals↗
PubMed1999

Superoxide in the pulmonary circulation.

Superoxide formation in pulmonary tissue is modulated by cytokines, PO2, shear force, and disease states, and can be stimulated by drugs. Superoxide has diverse actions on pulmonary cells, including smooth muscle contraction, interaction with redox enzymes, cell proliferation, and gene transcription. In the lungs, there is an impressive array of specific defence mechanisms that destroy superoxide, especially superoxide dismutase (SOD) and metallothionein. Superoxide formation is increased in hyperoxia (e.g., oxygen therapy); however, superoxide-forming enzymes also can be up-regulated in hypoxia. Superoxide has been implicated in acute respiratory distress syndrome, lung ischaemia-reperfusion injury, and lung transplantation. Novel approaches to therapy have been explored, including SOD gene therapy and SOD targeting to the lung. In the future, new drugs interacting with superoxide may provide significant advances in the treatment of lung diseases.

Animals↗
PubMed2004

Effect of blood passage through the pulmonary circulation on fibrinolytic parameters.

The lung vasculature bed has a unique fibrinolytic potential, which has not yet been completely elucidated. We investigated the effect of blood passage through the pulmonary circulation on the values of fibrinolytic parameters in plasma. Forty-seven patients (16 women, 31 men, mean age 54 years, range 21-67 years) who had undergone elective cardiac catheterization were included in the study. The blood samples were taken simultaneously from the right atrium and the left ventricle. The following fibrinolytic parameters were measured: tissue-type plasminogen (t-PA) antigen and activity, plasminogen activator inhibitor-1 (PAI-1) antigen and activity, and euglobulin clot lysis time (ECLT). No difference was found between the samples obtained from the right atrium and the left ventricle with respect to t-PA antigen: 8.1 (6.7-11.3) vs 8.4 (5.9-11.0) ng/ml; t-PA activity: 92 (5-680) vs 62 (32-696) IU/ml; PAI-1 antigen: 8.4 (5.5-14.3) vs 8.7 (6.2-13.1) ng/ml; and ECLT: 5.5 (4.1-9.1) vs 5.6 (4.1-8.5) 1 000/min. In contrast, PAI activity decreased significantly: 7.9 (5.8-10.3) vs 7.4 (6.0-10.4) IU/ml, P < 0.01. Patients with and without pulmonary hypertension did not differ in any of measured parameters, either in the right atrium or in the left ventricle. These results show that under basal conditions fibrinolytic activity which is not attributed to t-PA is elevated in lung vasculature. Further, basal fibrinolytic activity in the lungs is not influenced by pulmonary hypertension.

Blood Coagulation Tests↗
PubMed1984

The responses of the systemic and pulmonary circulations to intravenously administered clonidine in anaesthetized dogs.

We have studied the immediate (0 to 30 min) effects of an i.v. bolus of clonidine (0.5, 1, 3, 5, 7, 10, and 15 micrograms/kg of b.w.) on systemic and pulmonary haemodynamics in anaesthetized (morphine, pentobarbital), artificially ventilated, normotensive beagle dogs. Clonidine initially raised and then decreased aortic pressures in a dose-dependent manner except in the case of dose 10 micrograms/kg when only a rise was observed. The effects on pulmonary arterial pressures were less consistent, and only at doses 3 to 5 micrograms/kg was the clear diphasic response pattern recognized. Heart rate and cardiac output decreased. Systemic vascular and pulmonary arterial resistances increased with the greatest increase soon after administration of the drug administration. Right atrial and pulmonary arterial wedge pressures increased. Additionally, we explored the effects of atropine with and without clonidine, which were increase in heart rate, cardiac output and aortic pressures but a decrease in right atrial and pulmonary arterial wedge pressures. It was concluded that clonidine induces a dose-dependent vasoconstriction in both systemic and pulmonary circulations, and pressure changes, thus, depend on peripheral vasomotion and flow. Atropine restores heart rate and also partially flow, but cannot abolish clonidine induced vasoconstriction.

Animals↗
PubMed1979

[Regional neurovasomotor reactions of pulmonary circulation].

In experiments on anaesthetized cats with intact chest regional blood volume and flow in the lungs at horizontal and vertical body positions and under vagus and sympathetic nerve stimulation were studied using regional lung electroplethysmography. The regions of the lungs bearing more significant hydrostatic and hemodynamic load turn more labile to neurogen stimuli. The parasympathetic vasomotor reaction of the basal lung regions increases while the apical region reaction decreases at a vertical body position. The results obtained suggest the occurrence of regionally differentiated mechanisms of vasomotor control in the pulmonary circulation, directed to compensation of postural changes in pulmonary hemodynamics.

Animals↗
PubMed1988

Alteration of fate of vasoactive autacoids in pulmonary circulation following monocrotaline-induced lung vascular injury in rats.

1. To learn how pulmonary vascular injury alters the ability of the lung to metabolize vasoactive autacoids, lung vascular lesions were produced in rats by a single subcutaneous injection of monocrotaline (90 mg kg-1), and the blood pressure responses to angiotensin I (AI), angiotensin II (AII), bradykinin, prostaglandin E2 (PGE2) and substance P were examined. Vasoactive agents were given intravenously or intra-arterially. 2. On histological examination of the lung at 3 weeks after monocrotaline treatment, degeneration or necrotization of endothelial cells was evident. 3. The conversion of AI to AII was only slightly depressed by monocrotaline treatment. On the other hand, the depressor response to intravenously injected bradykinin was enhanced in monocrotaline-treated rats. When the rats were pretreated with indomethacin the depressor response to intravenous bradykinin was the same for both control and monocrotaline-treated groups which suggests that endogenous prostaglandins are involved in the enhancement of the response to bradykinin. 4. In monocrotaline-treated rats the depressor response to intravenous PGE2 was significantly enhanced depending on the period following the treatment, while that to the intra-arterial injection did not differ from control. 5. The data suggest that monocrotaline-induced lung injury impairs the metabolism of PGE2 during pulmonary circulation but has little effect on the conversion of AI to AII and the degradation of bradykinin in rats.

Angiotensin I↗
PubMed1994

[The effect of high blood viscosity, caused by secondary polycythemia, on pulmonary circulation and gas exchange in patients with chronic cor pulmonale].

Blood viscosity, pressure of pulmonary artery, pulmonary functions, arterial and mixed venous oxygen content, cardiac output, oxygen transport capacity, oxygen consumption, ejection fraction have been examined at 25 patients with or without hypoxic cor pulmonale with or without secondary polycythaemia. Although secondary polycythaemia occurs in patients with hypoxic cor pulmonale as a compensatory process to increase the oxygen carrying capacity of the blood theoretically but as our findings: 1. The rise of haematocrit causes rise in blood viscosity significantly. 2. Polycythaemia secondary over 0.50 l/l of haematocrit contributes the rise of pressure in pulmonary artery. 3. The systemic oxygen carrying capacity is increasing with the rise of haematocrit up to 0.45 l/l but decreasing over 0.50 l/l. 4. Oxygen consumption is decreasing parallel with the rise of haematocrit. 5. Pulmonary functions, cardiac output do not change by the rise of haematocrit.

Blood Viscosity↗
PubMedDate not supplied

The role of eicosanoids and endothelium-dependent factors in regulation of the fetal pulmonary circulation.

A complex interaction of mechanical, hormonal, vasoactive, morphological and gaseous factors is responsible for the transitional period and maintenance of these changes in the newborn period. Vasoactive eicosanoids, formed at multiple sites in the lungs exert multiple effects on the perinatal pulmonary circulation. By direct, as well as indirect interaction with other systems, eicosanoids appear to have a role in the rearrangement of the circulation at birth. At this time PGE1, acetylcholine, bradykinin, and endothelin appears to work, at least in part, to cause fetal pulmonary vasodilation via the release of EDRF. Products of the lipoxygenase pathway are powerful vasoconstrictors, but may not be important in regulation of high fetal pulmonary vascular tone or the pulmonary pressor response to hypoxia.

Animals↗