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Results for “PULMONARY CIRCULATION”

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At least 739 records · Page 41Linked to original sources
PubMed1988

Pathophysiological aspects of predominant preload lowering on pulmonary circulation, gas exchange, and the biventricular function in patients with chronic obstructive lung disease.

A group of 21 patients with various degrees of chronic obstructive pulmonary disease underwent radionuclide ventriculography with hemodynamic monitoring to assess the extent to which pulmonary artery pressures and pulmonary vascular resistance can be lowered by the vasodilator molsidomine. Molsidomine (N-carboxy-3-morpholino-sydnonimin-ethylester) is similar to nitroglycerin in its mode of action. After hemodynamic and radionuclide data acquisition, at rest and during submaximal exercise in the steady state, 2 mg molsidomine was injected intravenously. Rest and exercise measurements were repeated 45 min after molsidomine injection. In patients with mild to moderate disease (group 1), pulmonary artery resting pressures decreased by 12% (p less than 0.05) at rest by 22% (p less than 0.01) during exercise after the administration of the drug. Total pulmonary resistance during exercise decreased significantly (p less than 0.01) as a result of marked decrease of pulmonary artery pressure (PAP) compared with a minimal decrease in cardiac index (CI). In patients with severe disease (group 2), only the resting values of PAP decreased while the relationship between pressure and flow was unchanged. During the exercise period, the preload parameters of the right and left ventricles decreased by an average of 30%. With regard to gas exchange, only the arterial PO2 at rest decreased slightly but significantly (p less than 0.05) after molsidomine, while the coefficient of oxygen delivery was not affected by the drug. However, in four patients arterial PO2 was markedly reduced by the drug. Right ventricular ejection fraction increased significantly (p less than 0.01) both at rest and during exercise in group 1 and during exercise in group 2 after administration of molsidomine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Effects of high-dose corticosteroids on the pulmonary circulation.

A major controversy in the treatment of the Adult Respiratory Distress Syndrome (ARDS) is the role of steroids, which may attenuate permeability as well as pulmonary vascular resistance (PVR). Empirically methylprednisolone (MP) in high doses (30 mg/kg) has been "the steroid of choice" in clinical practice. By autoradiography MP has been shown to penetrate more easily into lung tissue than other steroids tested. MP prevented the late phase increase in lung vascular permeability to endotoxin in sheep, whereas the inhibition of the pulmonary hypertensive response was far less pronounced. In human septic ARDS MP reduced both PVR and the increased vascular permeability. However, a few patients characterized by more severe ARDS did not respond to MP. There is some evidence that steroids may modulate both pre- and postcapillary vasomotion in the lungs. MP was found to inhibit pulmonary venoconstriction as well as pulmonary erythrocyte sludging in canine hemorrhagic shock. Oleic acid induced edema also appears to be attenuated by MP. This effect is partly due to a lowering of hydrostatic pressure in the lung capillaries, because MP blocks the downstream resistance increase. Hypoxic pulmonary vasoconstriction has predominantly a precapillary localisation. MP inhibits hypoxic vasoconstriction in a dose-dependent fashion in isolated rat lungs, but does not cause a general dampening of vascular reactivity, as the pulmonary constrictor response to angiotensin II is unchanged. However, MP inhibits histamine-induced vasoconstriction in isolated canine lung lobes. The increased vascular resistance in atelectatic lungs is also inhibited by MP. Corticosteroids may alter the reaction of the pulmonary vasculature to various stimuli or agents by influencing the release of mediators, for instance, the cyclooxygenase and lipoxygenase products of arachidonic acid, modulate the action of mediators, reducing the activation of leukocytes and/or platelets, or changing the state of the pulmonary vascular muscle cells. Which mechanisms are active in the various situations are at present objects of pure speculation. However, in most situations with ARDS a reduction in pulmonary arterial pressure and PVR may be regarded as beneficial.

Airway Resistance↗
PubMed1980

Pulmonary circulation in juvenile hypertension.

In 28 juvenile hypertensives (mean age 24 years) central haemodynamics was investigated at rest and during exercise. Hypertensives had significantly higher diastolic pulmonary artery pressure at rest than controls. Pulmonary diastolic pressure increased in parallel with cardiac output during exercise in hypertensives, in controls there was no relationship of pulmonary wedge pressure to cardiac output. Patients with diastolic pulmonary artery pressure higher than 12 mmHg at rest, or higher than controls during exercise, showed also signs of left ventricular hypertrophy on the ECG and/or X-ray. Those who were hyperkinetic and had systemic blood pressure greater than or equal to 150/90 at rest, had also significantly higher mean pulmonary artery pressure at rest. A correlation between total pulmonary, as well as pulmonary vascular and systemic resistances has been found at rest and during exercise in hypertensives; in controls, there was a correlation between the total pulmonary, as well as pulmonary vascular, and systemic resistances at rest; during exercise there was a correlation between total pulmonary, as well as postcapillary pulmonary and systemic resistances.

Adolescent↗
PubMed1990

Changes in the pulmonary circulation during birth-related events.

At birth, pulmonary vascular resistance decreases dramatically, allowing pulmonary blood flow to increase and oxygen exchange to occur in the lungs. To determine the extent to which ventilation of the fetus's lungs, oxygenation of the lungs, and umbilical cord occlusion can account for this decrease in resistance, we studied 16 chronically instrumented, near-term sheep fetuses in utero. We performed the experiment in a sequential fashion: we first studied the effects of ventilation alone (without oxygenation) on pulmonary vascular resistance and blood flow, and then determined the additive effects of oxygenation and cord occlusion. We calculated pulmonary vascular resistance from measurements of vascular pressures and measurements of pulmonary blood flow obtained by injecting radionuclide-labeled microspheres. We found that ventilation alone caused a large but variable increase in pulmonary blood flow, to 401% of control, no change in pulmonary arterial pressure, and a doubling of left atrial pressure. Thus, pulmonary vascular resistance fell dramatically, to 34% of control. Oxygenation caused a modest further increase in pulmonary blood flow and a decrease in mean pulmonary arterial pressure, so resistance fell to 10% of control. Umbilical cord occlusion caused no further changes in pressure, flow, or resistance. Unexpectedly, the fetuses' pulmonary blood flow responses to ventilation fell into two groups: the mean increase was maximal in eight of the 16 fetuses but was only 20% of the cumulative increase in the other eight. We found no differences between the two groups of fetuses to explain their different responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Possible mechanisms of oxygen sensing in the pulmonary circulation.

Oxygen tension is known to control the pulmonary vascular tone. We reviewed three hypotheses that try to explain the mechanism whereby hypoxia is sensed in the lung tissue. The first hypothesis concerns the role of the oxygen binding hemoprotein cytochrome P-450. Studies using various inhibitors and activators of cytochrome P-450 show that this enzyme affects pulmonary vascular tone. The data are, however, contradictory. The second hypothesis postulates that hypoxia reduces the synthesis of vasodilator oxygen radicals in the lung. This hypothesis is quite well supported by experimental data. The third hypothesis, similarly widely documented, states that slowing of the respiratory chain and altered cellular energetics is crucial for sensing of hypoxia. In this case, however, it is not exactly clear how changes in cellular energetics are connected with vascular tone. The possibility exists that changes in both the cytochrome P-450 activity and in the rate of electrons flow in the respiratory chain may alter the amount of oxygen radicals in the cells and, similarly as in the "oxygen radicals" hypothesis, govern calcium channels through the control of the redox status of these channels.

Oxidation-Reduction↗
PubMedDate not supplied

[Effect of acute blood loss on catecholamine balance in the pulmonary circulation in anesthetized rats].

The contribution of pulmonary inactivation of catecholamines (CA) in the formation of their level in circulating blood during the development of a posthemorrhagic reaction was studied. Pulmonary CA inactivation was evaluated according to the arteriovenous difference (right ventricle and carotid artery) in epinephrine (E) and norepinephrine (NE) whose concentration was determined by the method of highly-effective liquid chromatography with electrochemical detection. Reciprocal phase changes in the dynamics of the arteriovenous difference in NE and E and levels of the corresponding CA in arterial blood plasma were discovered during the development of the posthemorrhagic reaction. Pulmonary inactivation of CA increased by the 2nd minute, then dropped below the initial level with subsequent restoration. The NE level in the arterial blood plasma was marked by a strictly contrary dynamics, while the concentration of E reached maximum when inactivation of E in the lungs was minimal (5th minute). The mechanisms and physiological significance of the discovered phenomenon are discussed.

Acute Disease↗