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At least 325 records · Page 18Linked to original sources
PubMed1997

Acute and chronic influences of obstructive sleep apnoea on the pulmonary circulation.

Obstructive sleep apnoea (OSA) produces immediate effects on pulmonary haemodynamics during sleep in all subjects. In addition, in some subjects, OSA is accompanied by chronic abnormalities of the pulmonary circulation. During sleep, pressure in the main pulmonary artery oscillates within each apnoea, in synchrony with intrathoracic pressure changes; in addition, it may increase progressively as a consequence of prolonged severe hypoxaemia. Pulmonary capillary wedge pressure may increase during inspiratory efforts, possibly reflecting a mechanical limitation of left ventricular function. Cardiac output decreases at apnoea resolution as an effect of a decreased right ventricular stroke volume, despite increased cardiac frequency. During wakefulness, postcapillary pulmonary hypertension occurs on exercise in many OSA patients, whilst pulmonary hypertension at rest is precapillary and occurs in patients with an altered daytime respiratory function. Development of right ventricular hypertrophy and a decrease in right ventricular ejection fraction appear to be related to the severity of respiratory alterations during sleep, whilst an overt right heart failure requires an altered daytime respiratory function. Long-term treatment of the obstructive sleep apnoea syndrome is more effective in increasing right ventricular ejection fraction than in decreasing pulmonary artery pressure during wakefulness.

Cardiac Output↗
PubMed1977

The role of adrenergic receptor blockade in serotonin-induced changes in the pulmonary circulation.

1. In dogs i.v. injection of serotonin caused a rise in pulmonary artery pressure and pulmonary arteriocapillary resistance that persisted even after alpha- and beta-adrenergic receptor blockade; pulmonary venous resistance also increased, but this was abolished by pretreatment with either propranolol or phenoxybenzamine. 2. The injection of serotonin into the ascending aorta produced an immediate rise in systemic, pulmonary arterial and pulmonary venous pressures and pulmonary venous resistance. After phenoxybenzmine, the rise in systemic and pulmonary arterial pressures remained unchanged, but previously observed increases in pulmonary venous pressure and resistance were blocked. In contrast, propranolol failed to abolish the rise in pulmonary venous resistance after serotonin injection into the ascending aorta. 3. These results confirm the observation that the vasoconstrictor effect attributed to intravenously injected serotonin on the arterial side of the pulmonary circulation is independent of the known sympathetic pathways. The data suggest that the pulmonary venoconstriction induced by intravenous serotonin is of reflex origin, abolished by alpha and beta receptor blockade, whereas the efferent arm of the reflex pulmonary venoconstriction following injection of serotonin into the ascending aorta is mediated via alpha-adrenergic receptors.

Animals↗
PubMed1999

The pulmonary circulation of homozygous or heterozygous eNOS-null mice is hyperresponsive to mild hypoxia.

Acute hypoxic vasoconstriction and development of hypoxic pulmonary hypertension (PHTN) are unique properties of the pulmonary circulation. The pulmonary endothelium produces vasoactive factors, including nitric oxide (NO), that modify these phenomena. We tested the hypothesis that NO produced by endothelial nitric oxide synthase (eNOS) modulates pulmonary vascular responses to hypoxia using mice with targeted disruption of the eNOS gene (eNOS-/-). Marked PHTN was found in eNOS-/- mice raised in mild hypoxia when compared with either controls or eNOS-/- mice raised in conditions simulating sea level. We found an approximate twofold increase in partially and fully muscularized distal pulmonary arteries in eNOS-/- mice compared with controls. Consistent with vasoconstriction being the primary mechanism of PHTN, however, acute inhalation of 25 ppm NO resulted in normalization of RV pressure in eNOS-/- mice. In addition to studies of eNOS-/- mice, the dose-effect of eNOS was tested using heterozygous eNOS+/- mice. Although the lungs of eNOS+/- mice had 50% of normal eNOS protein, the response to hypoxia was indistinguishable from that of eNOS-/- mice. We conclude that eNOS-derived NO is an important modulator of the pulmonary vascular response to chronic hypoxia and that more than 50% of eNOS expression is required to maintain normal pulmonary vascular tone.

Administration, Inhalation↗
PubMed2004

Endogenous nitric oxide and pulmonary circulation response to hypoxia in high-altitude adapted Tibetan sheep.

Nitric oxide (NO) is important for the pulmonary circulation response to acute and chronic hypoxia. We examined effects of endogenous nitric oxide synthase (NOS) inhibition on pulmonary vascular tone in response to hypoxia in Tibetan sheep dwelling at 3,000 m above sea level using a pressure chamber. Unanaesthetized male sheep living at 2,300 m above sea level ( n=7) were prepared for vascular monitoring. Pulmonary artery ( P(pa)), pulmonary artery wedge ( P(cwp)) and systemic artery pressures together with cardiac output (CO) were measured, and pulmonary vascular resistance (PVR) was calculated as ( P(pa)- P(cwp))/CO. A non-selective NOS inhibitor, N(omega)-nitro- l-arginine (NLA; 20 mg kg(-1)), and a selective NOS inhibitor, ONO-1714 (0.1 mg kg(-1)), were used and measurements were made at 0 m, 2,300 m, and 4,500 m, with and without the NOS inhibitors. After NLA, P(pa) increased slightly and CO decreased in animals at baseline (2,300 m). The increased PVR after NLA at 4,500 m was greater than that at 2,300 m ( P<0.05). Selective NOS inhibition increased PVR at baseline, but not at 4,500 m. The enhanced pulmonary vasoconstriction after NO inhibition at basal and hypoxic conditions suggests a modulating role of NOS bioactivity in the pulmonary circulation and that augmented endothelial NOS plays a counterregulatory role in the pulmonary vasoconstrictor response to acute hypoxia in high-altitude adapted Tibetan sheep.

Acclimatization↗
PubMed2006

Pulmonary circulation: contrast-enhanced 3.0-T MR angiography--initial results.

PURPOSE: To prospectively evaluate the technical feasibility of both high-spatial-resolution and time-resolved contrast material-enhanced magnetic resonance (MR) angiography of the pulmonary circulation at 3.0 T. MATERIALS AND METHODS: All examinations were HIPAA compliant. After institutional review board approval and written informed consent, time-resolved and high-spatial-resolution three-dimensional contrast-enhanced MR angiography of the pulmonary circulation was performed with a 3.0-T MR system in 31 adults (13 men, 18 women; age range, 29-87 years old): 22 volunteers and nine patients (two with mediastinal masses, seven with pulmonary arterial hypertension [PAH]). The image quality of pulmonary arterial branches and parenchymal enhancement conspicuity were evaluated independently by two radiologists. The signal-to-noise ratio and quantitative analysis of perfusion parameters was performed. Statistical analysis of data was performed by using Wilcoxon rank sum test and two-sample Student t test, and interobserver variability was tested with kappa coefficient. RESULTS: Visualization up to fourth-order pulmonary arterial branches was observed on time-resolved MR angiograms and that up to fifth-order branches was observed on high-spatial-resolution MR angiograms, with diagnostic-quality blood vessel definition and good interobserver agreement. Evaluation of parenchymal enhancement and semiquantitative analysis of perfusion parameters yielded dynamic information in all subjects. Comparative analysis of definition scores for fourth- and fifth-order pulmonary arterial branches, parenchymal enhancement, the time lag between the pulmonary arterial and parenchymal enhancement, and all of the calculated perfusion indices in patients with PAH showed statistically significant differences from volunteers (P < .05). CONCLUSION: Three-dimensional contrast-enhanced MR angiography of the pulmonary circulation was feasible at 3.0 T and provided high vascular morphologic detail and dynamic functional information. Clearly detectable abnormalities were present in patients with PAH.

Adult↗
PubMed1988

Thermal recovery after passage of the pulmonary circulation assessed by deconvolution.

For indicator-dilution studies, complete thermal recovery after passage of heat through the pulmonary circulation would be desirable. However, the results in the literature obtained by extrapolation techniques are inconsistent. To overcome problems of the extrapolation approach, transport functions of the pulmonary circulation (including the left heart) were computed by deconvolution of pulmonary arterial and aortic pairs of thermodilution curves after central venous indicator injection (10 ml of an ice-cold blood indocyanine green dye mixture). Thermal recovery was determined as the finite integral of the transport function. Thirteen mongrel dogs under piritramid-N2O anesthesia were examined under base-line conditions, in orthostasis to alter the distribution of pulmonary blood flow (9 dogs), and in oleic acid edema (8 dogs). Using the deconvolution approach, thermal recovery was 0.97 +/- 0.04 under base-line conditions, 0.96 +/- 0.03 in orthostasis, and 0.96 +/- 0.05 in pulmonary edema. Thermal recovery determined from extrapolated dilution curves was greater than 100% in all groups, a physically impossible finding. It is concluded that thermal recovery is incomplete but insensitive with respect to the distribution of blood flow and to the size of the extravascular compartment. Monoexponential extrapolation is unsuited for the determination of thermal recovery.

Animals↗
PubMed1975

Reversal of pulmonary circulation.

The preliminary results and the technique of total reversal of the pulmonary circulation (RPC) are presented. Total RPC is technically feasible and not incompatible with life. It affords a new experimental model for in vivo study of pulmonary pathophysiology. The influence of this reversal on blood oxygenation, on pulmonary vascular resistance, and on established pulmonary hypertension, as well as its reaction to hypoxia and acidosis, needs further investigation. RPC may have clinical implications in essential pulmonary hypertension and congenital pulmonary vascular anomalies.

Angiography↗
PubMed1993

Dilator effect of endothelins in pulmonary circulation: changes associated with chronic hypoxia.

To investigate dilator effects of endothelins (ETs) on the pulmonary circulation and possible changes induced by chronic hypoxia, we examined vascular responses to ET-1 and ET-3 as well as ET binding to receptor subtypes ETA and ETB in the lungs from rats exposed to either room air (controls), hypoxia (10% O2) for 3 wk (3 WH), or 3 WH followed by recovery to room air (3 WH+R). In controls, both ETA and ETB receptor binding was present in smooth muscle of airways and vessels. Infusion of ET-1 or ET-3 (3-100 pM) to isolated perfused lungs preconstricted by U-46619 produced dose-dependent vasodilation with a greater potency of ET-3 (P < 0.01). The vasodilator responses to ET-1 and ET-3 were potentiated by the cyclooxygenase blocker meclofenamate (3 x 10(-6) M) or by the thromboxane synthetase inhibitor R-68070. In meclofenamate-treated lungs, the vasodilator responses to ET-1 and ET-3 remained unaffected by the inhibitor of nitric oxide synthesis, NG-monomethyl-L-arginine (5 x 10(-4) M) or by the guanylate cyclase inhibitor, methylene blue (10(-4) M). Conversely, the K+ channel blockers glibenclamide (10(-4) M) and tetraethylammonium (10(-4) M) attenuated the vasodilator responses to both ET-1 and ET-3. The selective ETA receptor antagonist BQ-123 did not alter ET-induced vasodilation, whereas it attenuated ET-induced vasoconstriction. Vasodilation to both ET-1 and ET-3 was abolished in lungs from 3 WH rats (P < 0.01) but was fully restored in lungs from 3 WH+R rats. Pulmonary vasodilation induced by the K+ channel opener pinacidil, which was suppressed by glibenclamide, did not differ between controls and 3 WH rat lungs. We found no change in ETA and ETB receptor binding from pulmonary vessels in H rat lungs compared with controls. In conclusion, endothelin-induced pulmonary vasodilation which may involve activation of K+ channels is abolished during chronic hypoxia. This abolition does not appear to be related to alterations in ET-receptor subtypes or to unresponsiveness of K+ channels in the pulmonary circulation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Hemodynamic effects of 15-microm-diameter microspheres on the rat pulmonary circulation.

The microsphere method has been used extensively to measure regional blood flow in large laboratory animals. A fundamental premise of the method is that microspheres do not alter regional flow or vascular tone. Whereas this assumption is accepted in large animals, it may not be valid in the pulmonary circulation of smaller animals. Three studies were performed to determine the hemodynamic effects of microspheres on the rat pulmonary circulation. Increasing numbers of 15-microm-diameter microspheres were injected into a fully dilated, isolated-lung preparation. Vascular resistance increased 0.8% for every 100,000 microspheres injected. Microspheres were also injected into an isolated-lung preparation in which vascular tone was increased with hypoxia. Microspheres did not induce vasodilatation, as reported in other vascular beds. Fluorescent microspheres were injected via tail veins into awake rats, and the spatial locations of the microspheres were determined. Regional distributions remained highly correlated when microspheres of one color were injected after microspheres of another color. This indicates that the initial injection did not alter regional perfusion. We conclude that, when used in appropriate numbers, 15-microm-diameter microspheres do not alter regional flow or vascular tone in the rat pulmonary circulation.

Adenosine↗
PubMed1992

Pulmonary circulation in hypoxia.

Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance is seen in normal subjects during hypoxic breathing at sea level, in acclimatized lowlanders and in high altitude natives. Hypoxic pulmonary hypertension in all these circumstances is most generally moderate, except in high altitude natives at exercise. However, in the absence of high altitude pulmonary edema (HAPE) or chronic mountain sickness, a right heart failure that would be the human counterpart of brisket disease described in cattle, apparently never occurs. In adult patients with HAPE, reported mean pulmonary artery pressures (Ppa) measured during a right heart catheterization range from 22 to 63 mmHg with an average of 39 mmHg. Recent echo-Doppler estimates of systolic Ppa in patients with a HAPE are at an average of 53 mmHg, only moderately higher than in healthy subjects exposed to comparable normobaric or hypobaric hypoxia. Subjects with a previous HAPE often present with an enhanced pulmonary vascular reactivity to hypoxia compared to controls when tested at sea level, but the overlap is great. Non invasive echo-Doppler pulmonary hemodynamic studies at sea level have not been reported to reliably discriminate subjects susceptible to HAPE.

Altitude Sickness↗
PubMed1990

[Methodology and assessment of diagnosis of the hemodynamics of pulmonary circulation].

As to the examination of pulmonary haemodynamics the microheartcatheterization for sounding the right ventricle and the pulmonary artery should be found more acceptance in numerous pulmological and cardiological laboratories for verifying pulmonary hypertension, in preliminary examinations for vitium cordis, in intensive medical care for the continuous registration of haemodynamic parameters or to obtain expert opinion in connection with an occupational disease. Feasible measuring technique and method are put forward for making comparable evaluations. Reference values of haemodynamic parameters at rest and during bicycle exercise in sitting and lying position and regressions calculated on oxygen consumption and on age dependence are set forth. Critical suggestions on obtaining variables are given.

Cardiac Catheterization↗
PubMed1989

Effect of dopamine, ibopamine, and epinine on alpha- and beta-adrenoceptors in canine pulmonary circulation.

Dopamine has been widely utilized in the treatment of acute congestive heart failure, ibopamine, the diisobutyrate ester of N-methyldopamine (epinine), is a novel inotropic agent that, unlike-dopamine, is orally active. In clinical studies at doses that produce favorable hemodynamic responses, ibopamine and dopamine can evoke a slight and transient increase in pulmonary artery pressure and pulmonary capillary wedge pressure, an effect that is no longer apparent 1 h after administration. We have previously demonstrated in anesthetized dogs that this effect is due to stimulation of alpha-adrenoceptors in the pulmonary circulation by dopamine and ibopamine, as well as by the active form of ibopamine, epinine. The aim of the present investigation was to determine how dopamine, ibopamine, and epinine interact with beta-adrenoceptors in the canine pulmonary circulation, since this activity may serve to offset the alpha-adrenoceptor-mediated pulmonary vasoconstrictor responses. Intraarterial injection of dopamine, ibopamine, and epinine resulted in dose-dependent pulmonary vasoconstrictor responses with a maximum increase of approximately 50-60% above resting pulmonary vascular tone. When animals were pretreated with propranolol (1 mg/kg iv) to block beta-adrenoceptors, pulmonary vasoconstrictor responses to dopamine were unchanged, whereas pulmonary vasopressor responses to ibopamine and epinine were significantly potentiated, especially for epinine. Upon intraduodenal administration of a therapeutically effective dose of ibopamine (i.e. 36 mg/kg) to normal dogs, virtually no pulmonary pressor response was observed. However, administration of this same dose of ibopamine to dogs pretreated with propranolol (1 mg/kg iv) resulted in a marked pulmonary pressor response. These data indicate that epinine, and therefore the parent compound ibopamine, have the capacity to stimulate beta 2-adrenoceptors in the pulmonary circulation to a far greater degree than dopamine, and that this activity serves to offset, at least in part, the alpha-adrenoceptor-mediated pulmonary vasoconstriction that occurs in response to ibopamine.

Animals↗