Renal blood flow in dogs during diffusion respiration

1959 ◽  
Vol 14 (3) ◽  
pp. 405-410 ◽  
Author(s):  
Joseph E. Stone ◽  
Richard L. Irwin ◽  
Charles D. Wood ◽  
William B. Draper ◽  
Richard W. Whitehead

Two series of experiments were performed with appropriate controls on dogs in which respiratory arrest was produced and maintained by the injection of an overdose of thiopental or by administration of decamethonium, respectively. Renal blood flow was measured by a modification of the method of Selkurt ( Methods in Medical Research, vol. 1). A marked fall in renal blood flow coincident with apnea and anuria was found to occur consistently with diffusion respiration under thiopental. Both the renal ischemia and the anuria were preventable by renal denervation (pharmacological block). During diffusion respiration experiments in which decamethonium was used to cause and maintain apnea, a marked decline in renal blood flow or urine secretion did not occur during the first 15 minutes of apnea. It is concluded that the prompt onset of anuria in diffusion respiration under thiopental is due to a central synergism between thiopental and endogenous carbon dioxide. Further, it is reasoned that the delayed fall in renal blood flow and attendant anuria which occurred under decamethonium represent the central effects of increasing concentrations of carbon dioxide in the absence of thiopental. Submitted on November 5, 1958

1958 ◽  
Vol 194 (1) ◽  
pp. 115-119 ◽  
Author(s):  
Joseph E. Stone ◽  
J. Wells ◽  
W. B. Draper ◽  
Richard W. Whitehead

Mongrel dogs lightly anesthetized with thiopental sodium were used as experimental animals. After suitable controls were taken the changes in renal blood flow, urine volume, venous blood pH, blood pressure and heart rate, respiratory rate and volume and relative blood cell volume were measured at intervals during inhalation of 30% carbon dioxide in oxygen for 30 minutes. No anesthetic was administered during the period when CO2 was inhaled. No constant change in pH, hematocrit or heart rate was observed to result from the CO2 inhalation. Respiratory rate increased throughout the experiments. The inhalation of 30% carbon dioxide in oxygen produced a marked reduction in renal blood flow, concomitant with a marked oliguria. The renal ischemia under these conditions was prevented by pharmacological block of the left renal nerves (by injection of 5 ml of .5% tetracaine into the peripelvic area of the kidney). The pharmacologically denervated kidney continued to secrete urine in somewhat diminished quantities while the undenervated kidney developed severe oliguria or anuria. It is postulated that the renal ischemia observed in these experiments is a component of a generalized centrally induced vasoconstrictor response to the inhalation of a high concentration of carbon dioxide.


1975 ◽  
Vol 229 (1) ◽  
pp. 178-184 ◽  
Author(s):  
Hardaker WT ◽  
TC Graham ◽  
AS Wechsler

Hemorrhagic hypotensin in anesthetized dogs produced a redistribution of renal blood flow from the outer to the inner cortex. The role of adrenergic mechanisms in this redistribution was studied in anesthetized dogs using a radioactive microspheres to determine intrarenal blood flow. Neither renal denervation, nor pretreatment with reserpine altered the characteristic redistribution of renal cortical flow during hemorrhage. These observations suggest that neither intact renal nerves nor circulating catecholamines are necessary for the redistribution of renal intracortical blood flow during hemorrhagic hypotension, and the role of myogenic autoregulation is emphasized.


Author(s):  
Reetu R. Singh ◽  
Zoe McArdle ◽  
Lindsea C. Booth ◽  
Clive N. May ◽  
Geoff A. Head ◽  
...  

Majority of patients with hypertension and chronic kidney disease (CKD) undergoing renal denervation (RDN) are maintained on antihypertensive medication. However, RDN may impair compensatory responses to hypotension induced by blood loss. Therefore, continuation of antihypertensive medications in denervated patients may exacerbate hypotensive episodes. This study examined whether antihypertensive medication compromised hemodynamic responses to blood loss in normotensive (control) sheep and in sheep with hypertensive CKD at 30 months after RDN (control-RDN, CKD-RDN) or sham (control-intact, CKD-intact) procedure. CKD-RDN sheep had lower basal blood pressure (BP; ≈9 mm Hg) and higher basal renal blood flow (≈38%) than CKD-intact. Candesartan lowered BP and increased renal blood flow in all groups. 10% loss of blood volume alone caused a modest fall in BP (≈6–8 mm Hg) in all groups but did not affect the recovery of BP. 10% loss of blood volume in the presence of candesartan prolonged the time at trough BP by 9 minutes and attenuated the fall in renal blood flow in the CKD-RDN group compared with CKD-intact. Candesartan in combination with RDN prolonged trough BP and attenuated renal hemodynamic responses to blood loss. To minimize the risk of hypotension-mediated organ damage, patients with RDN maintained on antihypertensive medications may require closer monitoring when undergoing surgery or experiencing traumatic blood loss.


1960 ◽  
Vol 199 (3) ◽  
pp. 495-498 ◽  
Author(s):  
Jimmy B. Langston ◽  
Arthur C. Guyton ◽  
William J. Gillespie

Experiments of this study indicate that the kidney does not normally autoregulate its blood flow; in these experiments a change in perfusion pressure always resulted in a corresponding change in renal blood flow when the kidney was not subjected to surgical trauma. On the other hand, when renal ischemia was induced or when the perirenal tissues were intentionally damaged, autoregulation of renal blood flow occurred in every instance. Two possible theories are discussed for this autoregulation: a) blockage of the renal lymphatic drainage and b) disruption of the blood supply to the walls of the renal and intrarenal arteries.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Maryam Maleki ◽  
Mehdi Nematbakhsh

Background. Renal ischemia/reperfusion (I/R) is one of the major causes of kidney failure, and it may interact with renin angiotensin system while angiotensin II (Ang II) type 2 receptor (AT2R) expression is gender dependent. We examined the role of AT2R blockade on vascular response to Ang II after I/R in rats.Methods.Male and female rats were subjected to 30 min renal ischemia followed by reperfusion. Two groups of rats received either vehicle or AT2R antagonist, PD123319. Mean arterial pressure (MAP), and renal blood flow (RBF) responses were assessed during graded Ang II (100, 300, and 1000 ng/kg/min, i.v.) infusion at controlled renal perfusion pressure (RPP).Results.Vehicle or antagonist did not alter MAP, RPP, and RBF levels significantly; however, 30 min after reperfusion, RBF decreased insignificantly in female treated with PD123319 (P=0.07). Ang II reduced RBF and increased renal vascular resistance (RVR) in a dose-related fashion (Pdose<0.0001), and PD123319 intensified the reduction of RBF response in female (Pgroup<0.005), but not in male rats.Conclusion.The impact of the AT2R on vascular responses to Ang II in renal I/R injury appears to be sexually dimorphic. PD123319 infusion promotes these hemodynamic responses in female more than in male rats.


2014 ◽  
Vol 64 (11) ◽  
pp. B125
Author(s):  
Waleed Kadro ◽  
Maya Turkmani ◽  
Hussam Rahim ◽  
Cathy John ◽  
Zaid Zaki ◽  
...  

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