The development of oxygenators in extra corporeal circulation

The objective of this paper is to present one of the most important components of the extracorporeal circulation circuit, the oxygenator. In addition, the manufacture materials, the function and superiority of modern oxygenators are presented in order to stress their advantages over the older types. The future of oxygenators and the tendency to develop small intravascular artificial lungs are also discussed. A bibliographic study of the history and first reports of extracorporeal blood oxygenation has been performed in an attempt to describe the function of these initial oxygenators and to analyze the disadvantages which led to the development and to the exclusive of the membrane oxygenators. Since the establishment of the current knowledge that the artificial membrane of the modern oxygenators is the best material to oxygenate blood and remove carbon dioxide during extracorporeal circulation, further research concerning the oxygenator’s membrane was necessary to solve particular problems, such as plasma leak. Technologic advantages in the oxygenator’s membrane made possible the safe use of the oxygenator for 28 days in the extracorporeal membrane oxygenation (ECMO) circuits. The different materials used for the construction of the oxygenators are discussed with details. The incorporation in the oxygenator of additional devices, such as the heat exchanger, the arterial filter and blood reservoir to develop one compact construction is considered to be one more upgrade of the oxygenator’s technology. Accidents and safety precautions of the oxygenators are also discussed especially that of the thrombosis of the device. The necessity for more detailed and accurate monitoring of the oxygenator in real time during cardiac surgery is discussed. The latter holistic approach to the operation of the oxygenator and of the components which incorporate in the device offers specific advantages, while modification of the surface in contact with the blood ameliorates the inflammatory response.

Blood reservoir function in patients with Fontan circulation and asplenia syndrome

Splanchnic circulation constitutes a major portion of the vasculature capacitance and plays an important role in maintaining blood perfusion. Because patients with asplenia syndrome lack this vascular bed as a blood reservoir, they may have a unique blood volume and distribution, which may be related to their vulnerability to the haemodynamic changes often observed in clinical practice. During cardiac catheterisation, the mean circulatory filling pressure was calculated with the Valsalva manoeuvre in 19 patients with Fontan circulation, including 5 patients with asplenia syndrome. We also measured the cardiac output index and circulatory blood volume by using a dye dilution technique. The blood volume and the mean circulatory filling pressure and the venous capacitance in patients with asplenia syndrome were similar to those in the remaining patients with Fontan circulation (85 ± 14 versus 77 ± 18 ml/kg, p = 0.43, 31 ± 8 versus 27 ± 5 mmHg, p = 0.19, 2.8 ± 0.6 versus 2.9 ± 0.9 ml/kg/mmHg, p = 0.86). Unexpectedly, our data indicated that patients with asplenia syndrome, who lack splanchnic capacitance circulation, have blood volume and venous capacitance comparable to those in patients with splanchnic circulation. These data suggest that (1) there is a blood reservoir other than the spleen even in patients with asplenia; (2) considering the large blood pool of the spleen, the presence of a symmetrical liver may represent the possible organ functioning as a blood reservoir in asplenia syndrome; and (3) if this is indeed the case, there may be a higher risk of hepatic congestion in patients with Fontan circulation with asplenia syndrome than in those without.

Myogenic responses and compliance of mesenteric and splenic vasculature in the rat

In the rat, the spleen is a major site of fluid efflux out of the blood. By contrast, the mesenteric vasculature serves as a blood reservoir. We proposed that the compliance and myogenic responses of these vascular beds would reflect their different functional demands. Mesenteric and splenic arterioles (∼150–200 μm) and venules (<250 μm) from rats anesthetized with pentobarbital sodium were mounted in a pressurized myograph. Mesenteric arterial diameter decreased from 146 ± 6 to 133 ± 6 μm on raising intraluminal pressures from 80 to 120 mmHg. This response was enhanced in the presence of N ω-nitro-l-arginine methyl ester (l-NAME; 139 ± 6 to 112 ± 7 μm). There was no such myogenic response in the splenic arterioles, except in the presence of l-NAME (194 ± 4 to 164 ± 4.2 μm). We propose that, whereas mesenteric arterioles exhibit myogenic responses, this is normally masked by NO-mediated dilation in the splenic vessels. The mesenteric venules were highly distensible (active, 184 ± 15 to 320 ± 30.9 μm; passive in Ca2+-free media, 209 ± 31 to 344 ± 27 μm; 4–8 mmHg) compared with the splenic vessels (active, 169 ± 11 to 184 ± 16 μm; passive, 187 ± 12 to 207 ± 17 μm). We conclude that, in response to an increase in perfusion pressure, mesenteric arterial diameter would decrease to limit the changes in flow and microvascular pressure. In addition, mesenteric venous capacitance would increase. By contrast, splenic arterial diameter would increase, while there would be little change in venous diameter. This would enhance the increase in intrasplenic microvascular pressure and increase fluid extravasation.

Skin vascular bed is a potential blood reservoir during heat stress

To determine the potential role of the skin vasculature as a blood reservoir, we measured venous compliance (Cv), resistance (Rv), and their product, the time constant of venous drainage (tau sk = RvCv), in skin flaps from the hindlimbs of 15 dogs anesthetized with pentobarbital sodium at different core temperatures (Tc, 37-42 degrees C), skin temperature (Ts, 25.3-50.0 degrees C), and during an infusion of papaverine (5%). The vasculature of the flap was isolated, and a double-occlusion technique was used to measure the static pressure in the venous compartment. The blood volume of the flap was altered by changing either flow or outflow pressure (Pv). The change in volume was estimated from the change in weight of the flap with a force transducer. At Tc = 37 degrees C, Rv was 2.27 +/- 0.81 mmHg.min.ml-1.100 g-1 (means +/- SD), Cv was 0.17 +/- 0.06 ml.mmHg-1.100 g-1, and tau sk was 28.0 +/- 8.8 s. Rv decreased with elevated Tc, Ts, and with papaverine. Cv increased with a rise in Tc and Ts. Increasing Tc and Ts did not change tau sk, but the papaverine infusion shortened it. The lowest tau sk (20 s) occurred during maximal vasodilatation. This long tau sk indicates that the skin could serve as a blood reservoir during heat stress.

Blood reservoir function of dog spleen, liver, and intestine

The reflex decrease in blood volume of the spleen, the liver, and the intestine of vagotomized dogs was measured by plethysmographic techniques during bilateral carotid occlusion and moderate and severe hemorrhage. The volume of blood mobilized from each organ during carotid occlusion and moderate hemorrhage was from 6 to 30% of their respective blood volumes and from 55 to 81% during severe hemorrhage. In each experimental situation the spleen exhibited the greatest ability to release blood and the intestine, the least. During moderate hemorrhage (9 ml/kg) the spleen yielded a volume equal to 35% of the blood lost, the liver 14% and the intestine 7%. Comparable figures for severe hemorrhage were 26, 13, and 5%, respectively. This order of ranking the component regions of the splanchnic circulation with regard to function as a blood reservoir may be specific for the dog

Hepatic venous compliance and role of liver as a blood reservoir

Changes in hepatic blood volume in response to rapid elevations in hepatic venous pressure were examined in cats using hepatic plethysmography. The liver was intact and received blood from an intact portal vein and hepatic artery. The hepatic blood volume increased in response to elevated venous pressure. Compliance of the hepatic capacitance vessels became greater as the distending venous pressure was increased over the range of venous pressures studied (0-9.4 mmHg). When hepatic venous pressure was elevated to 9.4 MMHg, the hepatic blood volume more than doubled. The liver serves as an important buffer for rapid changes in blood volume, the importance increasing with greater infused volumes of fluid. While overall venous compliance decreased at distending pressures in excess of 5-6 mmHg, the compliance of the hepatic capacitance vessels shows marked increases at pressures above this level. Expansions of the blood volume results in elevations of central venous pressure. Within a few minutes the hepatic capacitance vessels sequester a significant proportion of the added volume. As long as central venous pressure is raised, the liver demonstrates a secondary fluid buffering role by filtering large volumes of fluid across the vascular bed into the peritoneum.

INACTIVATION OF ARGININE-VASOPRESSIN BY THE ISOLATED PERFUSED RABBIT KIDNEY

SUMMARY The ability of the kidney to extract (inactivate and excrete) argininevasopressin (AVP) from the blood was studied in the isolated perfused rabbit kidney. AVP was added to the blood reservoir to give an initial approximate concentration of 100 μu./ml plasma and samples were taken simultaneously from the arterial and venous side at 5, 15, 30 and 45 min. The AVP concentration in the plasma samples was determined by bioassay in the water-loaded, ethanol-anaesthetized rat. The clearance (extraction ratio x renal plasma flow) of AVP from the blood was concentration-dependent. The average extraction ratio ranged from 0·25 at levels of 100 to 44 μu./ml plasma and 0·42 at levels of 44 to 19 μu./ml plasma. The excretion of AVP in the urine was 23% and 29% respectively of the calculated filtered load, in two isolated perfused kidneys, indicating tubular reabsorption and/or tissue inactivation of the filtered hormone.