An apparatus for artificial circulation in laboratory animals

An artificial circulation apparatus consisting of two membrane pneumatic adaptive diaphragmatic-type pumps and artificial film-type lungs and principle of its operation are described. The apparatus permits maintaining volume blood flow to 800 ml/min during organism resuscitation after endured clinical death including prolonged one as well.     

The effect of deep hypothermia on the human pulmonary circulation

ObjectiveAcute rises in pulmonary artery pressures following complex cardiac surgery are associated with high morbidity and mortality. We hypothesised that periods of deep hypothermia predispose to elevated pulmonary pressures upon rewarming. We investigated the effect of this hypothermic preconditioning on isolated human pulmonary arteries and isolated perfused lungs.MethodsIsometric tension was measured in human pulmonary artery rings (n=24). We assessed the constriction and dilation of these arteries at 37 °C and 17 °C. Isolated perfused human lung models consisted of lobes ventilated via a bronchial cannula and perfused with Krebs via a pulmonary artery cannula. Bronchial and pulmonary artery pressures were recorded. We investigated the effect of temperature using a heat exchanger.ResultsRewarming from 17 °C to 37 °C caused a 1.3 fold increase in resting tension (p<0.05). Arteries constricted 8.6 times greater to 30 nM KCl, constricted 17 times greater to 1 nM Endothelin-1 and dilated 30.3 times greater to 100 μM SNP at 37 °C than at 17 °C (p<0.005). No difference was observed in the responses of arteries originally maintained at 37 °C compared to those arteries maintained at 17 °C and rewarmed to 37 °C. Hypothermia blunted the increase in pulmonary artery pressures to stimulants such as potassium chloride as well as to H-R but did not precondition arteries to higher pulmonary artery pressures upon re-warming.ConclusionsDeep hypothermia reduces the responsiveness of human pulmonary arteries but does not, however, precondition an exaggerated response to vasoactive agents upon re-warming.     

Effect of temporary hypovolemia on the early central pooling of the blood circulation following resuscitation and the survival of animals experiencing clinical death

The experiments were conducted on cats under pentobarbitone sodium anesthesia (40 mg/kg). The effect of 30-min hypovolemia (Wiggerse's model, 13.3 kPa or 100 mm Hg) on the cardiac output, its main fractions and the survival of animals recovered after clinical death (5 min) were studied. Hypovolemia was induced after cardiac contractions were recovered. In experimental (19 cats) and control (23 cats) studies clinical death was caused by arterial blood loss. The animals had been previously subject to hemorrhagic hypotension (according to Wiggerse, 6.7 kPa or 50 mm Hg, for 30 minutes). Temporary exclusion of part of blood volume from the circulation was found to abolish the phase of cardiac output increase in the postresuscitation period, attenuate the reaction of blood circulation centralization, improve the course of reparative processes and increase the survival of animals recovered after clinical death.     

Ultrastructure of coronary microvessels in conditions of heart reperfusion following prolonged ischemia while applying various methods of artificial hypothermia

It has been found out that in children with Roger's disease corrected in the conditions of two fundamentally different procedures of anesthetic management, myocardial reperfusion after cardiac arrest under artificial hypothermic circulation is accompanied by obstruction of more than 30% of coronary bed microvessels with hydropic endothelial cells or their cystiform fragments. The content of necrotic cells increases, while the "working" cells demonstrate a decrease in myocropinocytotic transport characteristics. Circulatory arrest under perfusionless hypothermia and immersion reperfusion do not result in a dramatic change of general morphology of microvessels as compared to the control group, while a heterogenic response of the structures responsible for transendothelial transfer of macromolecules provides the basis for recovery of the endothelium structure and function, as a patient's temperature reaches a standard value.     

Ultrastructure of coronary microvessels during heart reperfusion after prolonged ischemia under conditions of various forms of artificial hypothermia

It has been found that, in children with Roger’s disease corrected under conditions of two fundamentally different procedures of anesthetic management, myocardial reperfusion after cardiac arrest under artificial hypothermic circulation is accompanied with obstruction of more than 70% of coronary bed microvessels, one-third of them being blocked with hydropic endothelial cells or their cystiform fragments. It hampers or even totally prevents their functioning in the postoperative period. The content of necrotic cells increases, while the three “working” cell types demonstrate a decrease in myocropinocytotic transport. Circulatory arrest during perfusionless hypothermia and immersion reperfusion do not result in a dramatic change of general morphology of microvessels as compared to the control group maintaining the endothelial cell population unaltered. Ultrastructural organization of endothelial microvessels displayed no features of intracellular regeneration. However, a heterogenic response of the structures responsible for transendothelial transfer of macromolecules provides the basis for the recovery of endothelium structure and function, as a patient’s temperature reaches the standard value.