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At least 1,189 records · Page 66Linked to original sources
PubMed2006

Major differences in the pulmonary circulation between birds and mammals.

The lungs of domestic chickens were perfused with blood or dextran/saline and the pulmonary artery pressure (P(a)) and venous pressure (P(v)) were varied in relation to air capillary pressure (P(A)). In Zone 3 conditions, pulmonary vascular resistance (PVR) was virtually unchanged with increases in either P(a) or P(v). This is very different behavior from mammals where the same interventions greatly reduce PVR. In Zone 2 conditions blood flow was essentially independent of P(v) as in mammalian lungs but all the capillaries appeared to be open, apparently incompatible with a Starling resistor mechanism. In Zone 1 the capillaries were open even when P(A) exceeded P(a) by over 30 cm H(2)O which is very different behavior from that of the mammalian lung. We conclude that the air capillaries that surround the blood capillaries provide rigid support in both compression and expansion of the vessels. The work suggests a pathogenesis for pulmonary hypertension syndrome in chickens which costs the broiler industry $1 billion per year.

Animals↗
PubMed1973

The removal of noradrenaline in the pulmonary circulation of rat isolated lungs.

1. Removal of noradrenaline by isolated lungs of the rat, perfused via the pulmonary artery with Krebs bicarbonate solution has been studied.2. A constant removal (40.2%) was observed over a concentration range of 2-50 ng noradrenaline/ml (12-300 nM). At 100 ng/ml (600 nM), the removal is significantly reduced to 33.5%.3. The removal of noradrenaline was inhibited by cocaine (1 muM), but not by normetanephrine (5 muM), metaraminol (10 muM), phenoxybenzamine (10 muM) and 5-hydroxytryptamine (110 and 560 nM).4. We conclude that the removal of noradrenaline in the lungs does not involve an uptake process comparable with those previously described for this amine. The uptake process for noradrenaline in the lung is similar to that for 5-hydroxytryptamine and may be unique to this tissue.

Animals↗
PubMed1989

The response of the pulmonary circulation to exercise during normoxia and hypoxia following pneumonectomy in the adult sheep.

Pneumonectomy approximately halves the available pulmonary vascular bed. It is unknown whether the remaining lung has sufficient vascular reserve to cope with increased blood flow under stressful conditions without demonstrating abnormal pulmonary hemodynamics. To investigate this question, unanesthetized ewes with vascular catheters had hemodynamics assessed before and after a left pneumonectomy. Subsequently, on different days, the sheep were exercised on a treadmill under normoxic and hypobaric hypoxic (430 mmHg) (1 mmHg = 133.3 Pa) conditions. Pneumonectomy itself increased mean pulmonary arterial pressure by 4 mmHg. During normoxic or hypoxic exercise, the pneumonectomized sheep demonstrated a pulmonary hemodynamic response similar to normal sheep with two lungs. The pressure-flow relation for the right lung suggested the vascular reserve of the lung was not exceeded during exercise in the pneumonectomized sheep. Eighteen to 70 days after pneumonectomy there was no evidence of right ventricular hypertrophy, but there were small increases in the number of muscularized vessels less than 50 microns diameter and in the amount of muscle in normally muscularized pulmonary arteries. This study demonstrates that pneumonectomy slightly increases mean pulmonary arterial pressure. However, there is sufficient vascular reserve in the remaining lung to permit a normal hemodynamic response to exercise-induced increased blood flow even under hypoxic conditions.

Animals↗
PubMed1991

Loss of endothelium-dependent relaxant activity in the pulmonary circulation of rats exposed to chronic hypoxia.

To determine whether exposure to chronic hypoxia and subsequent development of pulmonary hypertension induces alterations of endothelium-dependent relaxation in rat pulmonary vascular bed, we studied isolated lung preparations from rats exposed to either room air (controls) or hypoxia (H) during 1 wk (1W-H), 3 wk (3W-H), or 3W-H followed by 48 h recovery to room air (3WH + R). In lungs pretreated with meclofenamate (3 microM), the endothelium-dependent vasodilator responses to acetylcholine (10(-9)-10(-6) M) and ionophore A23187 (10(-9)-10(-7) M) were examined during conditions of increased tone by U46619 (50 pmol/min). Acetylcholine or A23187 produced dose-dependent vasodilation in control lungs, this response was reduced in group 1W-H (P less than 0.02), abolished in group 3W-H (P less than 0.001), and restored in group 3WH + R. In contrast, the endothelium-independent vasodilator agent sodium nitroprusside remained fully active in group 3W-H. The pressor response to 300 pM endothelin was greater in group 3W-H than in controls (6.8 +/- 0.5 mmHg vs. 1.6 +/- 0.2 mmHg, P less than 0.001) but was not potentiated by the endothelium-dependent relaxing factor (EDRF) antagonists: hydroquinone (10(-4) M); methylene blue (10(-4) M); and pyrogallol (3 x 10(-5) M) as it was in controls. It was similar to controls in group 3W-H + R. Our results demonstrate that hypoxia-induced pulmonary hypertension is associated with a loss of EDRF activity in pulmonary vessels, with a rapid recovery on return to a normoxic environment.

Acetylcholine↗
PubMed1979

[Haemodynamics of the systemic and pulmonary circulation during surgery of hip fractures in spinal anaesthesia in elderly persons (author's transl)].

The haemodynamics of the pulmonary and systemic circulation during anaesthesia and surgical treatment of a hip fracture were investigated in 26 patients (mean age 73 +/- 4.5 years). After induction of spinal anaesthesia the mean arterial pressure, right atrial pressure, pulmonary capillary wedge pressure and systemic vascular resistance were significantly reduced. The cardiac index remained constant due to mild tachycardia. During the operation no significant variations of the haemodynamic parameters were observed. Implantation of methylmethacrylate in 10 patients was followed by a significant increase of the mean pulmonary pressure and pulmonary vascular resistance. The PaO2 DECREASED. 15 minutes after implantation the original values were again reached.

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