The impairment of renal activity in cases of shock or haemorhage is primarily the result of hypoxia. With it there is a sharp decrease in haemorenal functions, prolonged and continuing inhibition of the processes of active and passive reabsorption and secretion in the renal tubules. Wide spread damage to the parenchymatous structure of the kidneys, moreover, may occur in this pathological state. The renal insufficiency can sometimes be the direct cause of death.
Complications in renal function undoubtedly render the treatment of terminal states more difficult and drag out the course of the postreanimation period. In that connection the functional state of the excretory system during dying and resuscitation becomes a problem of great importance.
It has now been established that a cause of the impairment of renal function is a decrease in the flow of blood to the kidneys. Dynamic studies of blood supply to the kidneys during dying and subsequent resuscitation showed that the state of renal blood flow during bleeding depends on the initial state of the renal vessels. When vascular tone is high, renal blood flow drops much more rapidly than when it is low. During resuscitation venous reflux is renewed as soon as intra-arterial transfusion is begun, and before cardiac activity is restored. But renal blood flow only becomes normal after restoration of the activity of the divisions of the higher nervous system.
In the early postreanimation period there is a gradual increase in renal blood flow, as a rule, independently of variations in arterial blood pressure. As the diencephalon functions have been restored, however, renal blood flow increases or decreases according to the changes in arterial blood pressure, and its effect on renal blood flow only begins to lessen with activation of the function of the diencephalon. In Vanchakov’s opinion, this phasic character of the alterations in renal blood flow is predetermined by the different sensitivity of the renal vessels to biologically active compounds during the various stages of reanimation.
We carried out experiments in our Laboratory to determine the haemorenal parameters, the functional state of the renal nephron, and the state of certain regulatory mechanisms of urine excretion in the early and late restorative periods after clinical death due to acute exsanguination. The investigations showed that the excretory function of the kidneys ceased 90 seconds to four minutes after bleeding began, at an arterial pressure of 20 to 40 mm Hg, as a result of the sharp reduction in filtrational capacity. In the early restorative period, however, the state of the system did not depend solely on haemodynamic factors.
In spite of the rapid rise in arterial pressure, excretion of urine only began after the corneal reflexes had been restored. In the first 60 minutes of the renewal of renal blood flow, however, glomerular filtration and depuration of urea were still greatly reduced. Along with the impairment of renal blood flow and filtration, disturbances of nephron function like reduction of reabsorption and secretion in the renal tubules were also noted in this period, and an increase in membrane permeability.
In later moments in the restorative period the osmotic clearance and haemorenal parameters are still low. But sodium clearance is sharply increased. The animals’ urine continues to contain much protein and sugar. Only on the fourteenth day do excretion of sodium and osmotically active compounds and volumetric renal circulation begin to change in the same way, these values oscillating in the direction of increase. Subsequently the activity of the functions under study decreases. Renal circulation becomes normal, judging from the clearance of endogenous creatine, after three or four months, and nephron function between the fifteenth and thirtieth days. The period of normalization greatly depends on the state of the higher sectors of the central nervous system.
In investigating the influence of adrenalin and osmotically active compounds on haemorenal factors in the early restorative period, we found that adrenalin caused a drop in renal activity in these conditions as in the initial state. Osmotic substances also caused an increase in volumetrie renal blood flow, but this happened with considerable delay and to a lesser degree than in the initial state.
These findings suggest considerable depression of the osmoreceptors involved in urine excretion.
As to the mechanism of these disturbances in renal activity, they can be assumed to be the result of paralytic dilatation of the pores of the glomerular membrane owing to severe hypoxia, which leads to its heightened permeability and sharp inhibition of reabsorption in the renal tubules. Active reabsorption is the first function affected, as is indicated by the increase in sodium excretion and the appearance of sugar in the urine.
It has thus been established that clinical death causes severe damage to renal functions. This is of very real practical importance and indicates that, when treating patients who have survived clinical death, it is necessary to pay close attention to the condition of the kidneys.