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At least 1,027 records · Page 57Linked to original sources
PubMed1998

Role of carotid body in pressure response of pulmonary circulation in rats.

We investigated how signals arising from peripheral chemoreceptors could affect pulmonary vasculature in rats. Effects of the hypoxic exposure (10%) on mean pulmonary arterial pressure (mPAP), abdominal aortic flow (Q) and the estimated total pulmonary vascular resistance (mPAP/Q) were determined in anesthetized, artificially ventilated, carotid sinus nerve intact or chemodenervated rats. The pressor response of PAP to hypoxia seen in intact rats changed to the depressor response after chemodenervation. Hypoxia elicited a decrease in Q and an increase in mPAP/Q in both intact and chemodenervated rats. Selective carotid body stimulation by the intra-carotid injection of sodium cyanide (NaCN) in normoxia elicited an immediate but transient increase in PAP and Q before and after bilateral vagotomy. The peak change in PAP slightly preceded that in Q. These responses to NaCN were completely abolished by chemodenervation. These results indicate that the immediate chemoreflex contributes to the short-term regulation of pulmonary vasculature in rats.

Animals↗
PubMed1985

Relation of arachidonate metabolites to abnormal control of the pulmonary circulation in a child.

To evaluate the role of arachidonate metabolites in regulating pulmonary vascular tone, we performed multiple studies on a 17-month-old girl with idiopathic pulmonary hypertension, systemic arterial hypoxemia (due to ventilation-perfusion mismatching), and an elevated thromboxane A2 (TXA2) to prostacyclin (PGI2) ratio due to increased TXA2 (measured as their stable metabolites, TXB2 and 6-keto-PGF1 alpha, respectively). Intravenous infusions of PGI2 reduced mean pulmonary arterial pressure (from 80 to 47 mmHg), increased cardiac output (from 3.43 to 3.97 L/min), increased systemic arterial oxygen saturation (from 60 to 72 percent), and decreased the TXB2 to 6-keto-PGF1 alpha ratio (from 5.9 to 0.2); mean systemic arterial pressure was unchanged. Pharmacologically decreasing the TXB2 to 6-keto-PGF1 alpha ratio with administration of nifedipine or diltiazem also reduced pulmonary hypertension and increased systemic arterial oxygen saturation in this patient. Nifedipine and diltiazem decreased the ratio by decreasing TXB2. Prostacyclin decreased the ratio by increasing 6-keto-PGF1 alpha. These studies support the hypothesis that the balance between TXA2 and PGI2 is an important influence on pulmonary vascular tone.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Scintigraphic evaluation of regional pulmonary circulation and ventilation abnormalities in mitral valvular disease and congestive heart failure.

Regional pulmonary mean transit time, MTT (RV-Lung) was measured by radionuclide angiography using 99mTc-pertechnetate or 99mTc-HSA. In 8 normal subjects, MTT (RV-Lung) in upper (U) and lower (L) lung fields averaged 2.48 and 2.81 sec, respectively. In MS and CHF groups, MTT (RV-Lung) in L was markedly prolonged (5.04 and 5.10 sec, respectively) and after appropriate medical or surgical treatment, MTT in L markedly reduced. Pulmonary ventilation perfusion scintigraphy with 133Xe was performed in 18 patients with MS. Both Vu/L and Ou/L increased in accordance with the severity of disease, however, Vu/L had never exceeded unity. The estimation of regional MTT in the lung field is to be useful way in evaluating the severity of pulmonary circulatory disturbance in MS or in congestive heart failure.

Adolescent↗
PubMed1990

Pulmonary endocrine cells and the pulmonary circulation in various species in the Himalaya.

The numbers, morphology and distribution of pulmonary endocrine cells in goats, sheep, and the yak and its interbreeds were demonstrated by means of the peroxidase-antiperoxidase technique using a polyclonal antiserum to neuron-specific enolase. The animals came from two different locations and altitudes, Srinagar, Kashmir at 1250 m and Sakti in Ladakh, 4500 m. The presence of immuno-reactive cells was demonstrated in all animals but was related to species and not to the altitude of residence.

Altitude↗
PubMed1993

Chronic EDRF inhibition and hypoxia: effects on pulmonary circulation and systemic blood pressure.

It has been suggested that chronic hypoxic pulmonary hypertension results from chronic hypoxic inhibition of endothelium-derived relaxing factor (EDRF) synthesis. We tested this hypothesis by studying whether chronic EDRF inhibition by N omega-nitro-L-arginine methyl ester (L-NAME) would induce pulmonary hypertension similar to that found in chronic hypoxia. L-NAME (1.85 mM) was given for 3 wk in drinking water to rats living in normoxia or hypoxia. Unlike chronic hypoxia, chronic L-NAME treatment did not increase pulmonary arterial pressure. Cardiac output was reduced and mean systemic arterial pressure was increased by chronic L-NAME treatment. The vascular pressure-flow relationship in isolated lungs was shifted toward higher pressures by chronic hypoxia and, to a lesser degree, by L-NAME intake. In isolated lungs, vasoconstriction in response to angiotensin II and acute hypoxia and vasodilation in response to sodium nitroprusside were increased by chronic L-NAME treatment in normoxia and chronic hypoxia. Chronic hypoxia, but not L-NAME, induced hypertensive pulmonary vascular remodeling. Chronic supplementation with the EDRF precursor L-arginine did not have any significant effect on chronic hypoxic pulmonary hypertension. We conclude that the chronic EDRF deficiency state, induced by L-NAME, does not mimic chronic hypoxic pulmonary hypertension in our model. In addition, EDRF proved to be less important for basal tone regulation in the pulmonary than in the systemic circulation.

Animals↗
PubMed1983

The effects of pulmonary circulation pulsatility on the impedance cardiogram.

To study the effects of pulmonary blood flow on the impedance cardiogram, the pattern of pulmonary blood flow was alternated from pulsatile to non pulsatile, or the reverse, using our extracorporeal bypass-method on anaesthetized dogs. The thoracic impedance cardiogram was recorded from band electrodes placed around the neck and upper abdomen. During nonpulsatile pulmonary blood flow, the height of the diastolic phase of the delta Z wave was lower than that during pulsatile pulmonary blood flow. The area under the impedance curve decreased during nonpulsatile pulmonary blood flow. This appeared to be more obvious as the pulmonary arterial flow was reduced. The results suggest that the pulmonary blood flow might have substantial effects on the impedance cardiogram.

Animals↗
PubMed1995

Interacting roles of nitric oxide and ATP in the pulmonary circulation of the rat.

1. The potentiating effect of NG-nitro-L-arginine methyl ester, (L-NAME) a nitric oxide synthesis inhibitor, on responses of the rat pulmonary vascular pressure (PVP) to purinoceptor agonists was examined. 2. At a constant flow of 23 ml min-1 the PVP was 22.4 +/- 2.5 mmHg (n = 15), and treatment with 100 microM L-NAME for 15 min was without effect on the PVP. After the tone was raised with 28 nmol 9,11-dideoxy-11 alpha, 9 alpha-epoxymethano-prostaglandin F2 alpha (U-46619), the PVP was 29.4 +/- 3.3 mmHg and treatment with 100 microM L-NAME was still without effect on the PVP. It appears that there is a graded release of nitric oxide in response to different levels of steady shear stress and in our experimental model the threshold for detection was not reached under basal conditions. 3. In contrast, when the circulation was challenged with 30 s step, additive increases in flow between 11 and 50 ml min-1 (n = 8), treatment with 100 microM L-NAME produced a significant (P < 0.05) increase in PVP suggesting that changes in flow-derived forces evoke the release of nitric oxide. This was evident for flow rates above 30 ml min-1. 4. In preparations in which tone was raised with U-46619, a dose of 1 x 10(-8) mol ATP or 2-meSATP evoked a drop in PVP while alpha,beta-meATP produced an increase in PVP under constant flow of 23 ml min-1. After treatment with 100 microM L-NAME, all three purinoceptor agonists evoked an increase in PVP. The increase in Pvp evoked by alpha, beta-meATP was not affected by L-NAME. These results suggest that P2Y-purinoceptor stimulation evokes the release of nitric oxide to produce vasodilatation.5. Under conditions of constant flow and basal pressure, 100 microM L-NAME significantly (P<0.05)potentiated the increase in Pvp evoked by 1 x 10-6 mol ATP, although the increase evoked by 1 x 10-8 mol (alpha,beta-meATP, which was of similar magnitude, was not affected. These results indicate that a blockade of evoked nitric oxide release is responsible for the potentiation of the increase in Pvp evoked by ATP.6. This study shows that, while nitric oxide does not appear to be released in the pulmonary circulation of the rat under constant flow conditions, nitric oxide release evoked by purinoceptor agonists attenuates increases in pulmonary vascular pressure.

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