The electromagnetic blood flowmeter

SUMMARY1. Hind limb blood flow was measured in lambs of from 91 days gestation (delivered by Caesarean section) to 1 month after birth (term is about 147 days), under chloralose anaesthesia. Vascular resistance/100 g wet wt. increased progressively with age. There was reflex femoral vascular tone from the earliest age studied, as shown by vasodilatation on cutting the sciatic nerve.2. On asphyxia by cord occlusion reflex femoral vasoconstriction began earlier and was somewhat greater in older foetal lambs. At all ages, and after denervation of the hind limb, there was vasodilatation after local ischaemia, and a vasoconstriction of delayed onset during asphyxia attributed to release of noradrenaline into the circulation. The vasoconstrictor effect of noradrenaline in immature lambs was at least as great as at term or in the new-born.3. Injections of minimal effective doses of cyanide were used to localize possible chemoreceptor sites in foetal lambs. Injection into the left atrium caused a rise of arterial pressure, femoral vasoconstriction and a complex change in heart rate (usually bradycardia) but rarely any respiratory movement. After atropine, cyanide caused a large tachycardia. All responses were much reduced or abolished by cervical vagotomy.4. Injection of the same doses of cyanide into a jugular vein, the right ventricle, pulmonary or common carotid arteries of foetal lambs caused

Section: Foetal Circulation 57supporting

confidence: 63%

Section: Foetal Circulation 57mentioning

confidence: 99%

Vasomotor responses in the hind limbs of foetal and new‐born lambs to asphyxia and aortic chemoreceptor stimulation

Dawes¹,

Lewis²,

Milligan³

et al. 1968

“…for a flow of 40 ml./min on the, most sensitive range. The stability of this gauge head is equal to that described previously (Wyatt, 1961) (Severinghaus & Bradley, 1958) using a Beckman 160 gas analyser. Alternatively blood samples (total 0-4 ml.)…”

Section: Methodsmentioning

confidence: 94%

“…The flow pulses in the left pulmonary artery were relatively much larger than the pressure pulses so that the flow pulses were not wholly damped. The electromagnetic flowmeter (Wyatt, 1961) was used with a small gauge head, which has an internal diameter of 2 mm and gives a full scale meter deflexion (equivalent to an output of 42 4tV r.m.s.) for a flow of 40 ml./min on the, most sensitive range.…”

Section: Methodsmentioning

confidence: 99%

Pulmonary vasoconstriction and changes in heart rate during asphyxia in immature foetal lambs

Campbell¹,

Dawes²,

Fishman³

et al. 1967

SUMMARY1. The effect of changing the composition of pulmonary arterial blood on the pulmonary vasoconstrictor response to asphyxia was studied in immature foetal lambs of 90 days gestation age.2. When normal foetal carotid arterial blood (withdrawn before asphyxia) was introduced during asphyxia, the pulmonary vasoconstriction was rapidly and wholly relieved as soon as this blood reached the lung. This did not happen when blood was used which had been withdrawn during asphyxia.3. Conversely introduction into a pulmonary artery of a foetal lamb during recovery, of arterial blood withdrawn during asphyxia, caused an immediate return of pulmonary vasoconstriction.4. These phenomena could not be explained by the generation of vasodilator agents such as bradykinin, acetylcholine, histamine or isoprenaline.5. During asphyxia injection of normal foetal arterial blood into the left atrium did not cause pulmonary vasodilatation, but did elicit a large increase in heart rate.6. Neither the pulmonary vasoconstriction during asphyxia, nor its relief by normal foetal arterial blood, nor the changes in heart rate were affected by previous bilateral vagotomy or administration of atropine or hexamethonium.7. It was concluded that, in immature foetal lambs, the effect of asphyxia in causing pulmonary vasoconstriction was mainly, if not exclusively, by a local action within the lungs, and that the bradycardia during asphyxia was mainly due to the fall in Po2 acting locally upon the heart.

“…1B). Over a small time interval the pressure trace approximates to a straight line and the rate of flow during this time interval is dP/dT x cross-sectional area of the tube in cm2 (P in cm H20 (Wyatt, 1961) measured flow on the arterial side. The circuit was initially filled with dextran.…”

Section: Isolated Perfumed Rat Lung8mentioning

confidence: 99%

Pulmonary vasodilator and vasoconstrictor actions of carbon dioxide

Barer¹,

Shaw²

1971

SUMMARY1. Three preparations were used to study the actions of CO2 on the pulmonary vasculature: isolated rat and cat lungs perfused at a constant flow rate with homologous blood and a lobe of cat lung perfused at a constant flow rate in vivo. In all three changes in pulmonary artery pressure (Ppa) reflected changes in pulmonary vascular resistance.2. In the isolated rat lung CO2 caused vasodilatation when vascular tone was high. The lung was first ventilated with N2 causing a rise in Ppa-CO2 caused vasodilatation during hypoxia whether the initial blood CO2 level was low or normal and in spite of a fall in blood pH which usually augments the constrictor action of N2.3. In the rat lung ventilation with CO2 from the control state usually caused weak vasoconstriction. Reducing blood pH with acids also caused weak vasoconstriction while alkali caused vasodilatation.4. The over-all effect of CO2 on the pulmonary vasculature depends on a balance between a vasoconstrictor action probably caused by carbonic acid and vasodilatation caused by some other property of the molecule. The dilator action is powerful in the isolated rat lung.5. By contrast, in both cat lung preparations, no direct evidence for a vasodilator action of CO2 was obtained. Ventilation with CO2 when vascular tone was raised by hypoxia, drugs or acids caused further vasoconstriction. From the control state CO2 caused strong vasoconstriction.6. Indirect evidence from other work suggests that a pulmonary vasodilator action of CO2 exists in the cat but is usually masked by the strong vasoconstrictor action of carbonic acid. In life the dilator mechanism may be important when pH changes caused by CO2 are minimized by renal compensation.PHY 213