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Dive into the research topics where R. D. Bastron is active.

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Featured researches published by R. D. Bastron.


Circulation Research | 1974

Impaired Autoregulation of Blood Flow and Glomerular Filtration Rate in the Isolated Dog Kidney Depleted of Renin

George J. Kaloyanides; R. D. Bastron; Gerald F. DiBona

The effect of renin depletion on autoregulation of renal blood flow and glomerular filtration rate was examined in an isolated perfused kidney preparation. Group 1 dogs received a normal-sodium diet, group 2 dogs received deoxycorticosterone acetate (DOCA) and a high-sodium diet, group 3 dogs received DOCA and a sodium-deficient diet, group 4 dogs received a high-sodium diet without DOCA, and dogs in groups 5 and 6 were treated just like dogs in groups 1 and 2, respectively. Renin release was stimulated by decreasing renal arterial pressure to 50 mm Hg. An increase in renal arterial pressure from 100 to 160 mm Hg was associated with an impaired autoregulatory response in kidneys from group 2 dogs and in two kidneys from group 4 dogs; these kidneys exhibited suppressed or absent renin release in response to a decrease in renal arterial pressure. A separate group of experiments demonstrated that DOCA plus a high-sodium diet completely depleted the kidney of renin stores, indicating that decreased renin secretion reflected depletion of renal renin content. Infusing angiotensin II (0.22 ± 0.06 μg/min) into the renal artery of group 2 kidneys did not normalize the autoregulatory response. A decrease in renal arterial pressure from 150 to 50 mm Hg was associated with impaired autoregulation of glomerular filtration rate and renal blood flow in kidneys from group 6 dogs; renin secretion was undetectable in these kidneys. All kidneys from groups 1, 3, and 5 and the remaining six kidneys from group 4 exhibited a normal autoregulatory response and normal renin release. In groups 1–3, zonal blood flow was measured using the radiolabeled microsphere technique. Only in group 2 did a significant redistribution of fractional blood flow from the inner to the outer cortex occur. These experiments demonstrate that renin depletion impairs the capacity of the kidney to autoregulate blood flow and glomerular filtration rate; thus the data are consistent with the hypothesis that the renin-angiotensin system participates in the autoregulatory response.


Experimental Biology and Medicine | 1973

Effect of Increased Perfusion Pressure on Proximal Tubular Reabsorption in the Isolated Kidney

Gerald F. DiBona; George J. Kaloyanides; R. D. Bastron

Summary The present experiments demonstrate that raising renal perfusion pressure in the isolated kidney caused a significant increase in sodium excretion in the absence of detectable changes in proximal tubule sodium transport suggesting that the natriuresis resulted primarily from a decrease in sodium transport along more distal nephron segments. The constancy of SNGFR/Cin argues against a role for redistribution of glomerular filtrate in the natriuresis.


Experimental Biology and Medicine | 1974

Response of the Isolated Kidney to Acute Volume Expansion with Equilibrated Blood

George J. Kaloyanides; Gerald F. DiBona; R. D. Bastron

Summary The effect of acute volume expansion of a dog with equilibrated blood on sodium excretion in an isolated kidney perfused with blood from the volume expanded animal was examined. A significant increase in absolute and fractional sodium excretion was observed in the isolated kidney that could not be explained on the basis of changes in renal hemodynamics or physical factors and thus suggests that a humoral mechanism may have mediated the natriuretic response. The magnitude of the natriuresis was less than that previously reported when the isolated kidney was perfused with blood from a chronically DOCA and NaCl loaded animal. It is suggested that a humoral natriuretic mechanism may participate in the renal regulation of sodium balance and that the activity of this mechanism may undergo an adaptive increase in response to chronic extracellular volume expansion


Acta Anaesthesiologica Scandinavica | 1982

Effect of Supramaximal Vagal Stimulation in Combination with Hypoxia, Respiratory Acidosis and Deep Halothane Anaesthesia on Cardiovascular Function in Dogs

K. Korttila; R. D. Bastron

Vagal reflexes are generally recognized as a possible cause of cardiac arrest during anaesthesia. Studies were performed to determine whether hypoxia, respiratory acidosis or deep halothane anaesthesia modify the cardiovascular effect of vagal stimulation (VS) in dogs. The animals were anaesthetized with intravenous urethane and chloralose, and paralysed with metocurine. Normal temperature and arterial blood gas variables were maintained and supramaximal VS was applied to the distal end of both vagus nerves for 5 min. No differences were found in any of the variables measured among the time periods when VS was repeated five times in six control dogs receiving urethane‐chloralose basal narcosis only to determine the effects of time. VS resulted in 15 ± 3 s (mean ± s.e. mean) of asystole. Heart rate, cardiac output (CO) and mean arterial pressure (MAP) were still significantly decreased (p < 0.001) and central venous pressure, right atrial pressure. pulmonary capillary wedge pressure (PCW), systemic (SVR) and pulmonary vascular resistance significantly increased (p < 0.01 ‐ P < 0.001) at the end of stimulation when compared to values before VS in all 24 dogs. Neither hypoxia [Pao2 5.3 kPa (40 mmHg)] nor respiratory acidosis [pH 7.00, Paco2 10.6 kPa (80 mm Hg)] modified these effects of VS. VS during halothane anaesthesia (1.6% end‐tidal concentration) resulted in further significant decreases (P < 0.05 ‐ P < 0.001) in CO, MAP, mean pulmonary arterial pressure. PCW and SVR when compared to VS under basal narcosis. VS under halothane anaesthesia combined with hypoxia or respiratory acidosis did not decrease the cardiovascular parameters as much as VS under halothane Anaesthesia alone. VS alone, or in combination with hypoxia or respiratory acidosis, failed to cause persistent asystole.


Anesthesiology | 1977

Anesthesia and the Kidney

R. D. Bastron; S. Deutsch; Richard I. Mazze

In this age of modern era, the use of internet must be maximized. Yeah, internet will help us very much not only for important thing but also for daily activities. Many people now, from any level can use internet. The sources of internet connection can also be enjoyed in many places. As one of the benefits is to get the on-line anesthesia and the kidney book, as the world window, as many people suggest.


Experimental Biology and Medicine | 1975

Effect of blood volume expansion on tubule sodium transport in the isolated dog kidney.

George J. Kaloyanides; Gerald F. DiBona; R. D. Bastron

Summary Nonrecollection end-proximal tubule micropuncture technique and the microsphere method for estimating fractional distribution of renal cortical blood flow were applied to further define the mechanism of the natriuresis in the isolated dog kidney in response to volume expansion with equilibrated blood. Following volume expansion sodium excretion increased +79 ± 24 μEq/min (P < 0.01) in the face of significant decreases in inulin clearance (CIN) and renal blood flow (RBF) and in the absence of changes in renal perfusion pressure, plasma protein concentration or packed cell volume. (TF/P)IN of end-proximal tubular fluid decreased from 1.65 ± 0.03 to 1.53 ± 0.04, P < 0.025, and proximal tubule absolute reabsorption decreased from 36 ± 3 to 29 ± 2 nl/min, P < 0.05. The decrease in absolute reabsorption, however, was balanced by a decrease in single nephron GFR (SNGFR) so that no increase in distal delivery of fluid (VTF) out of the proximal tubule was detected. SNGFR/CIN remained constant. No change in fractional distribution of RBF was detected. The data indicate that volume expansion with equilibrated blood depresses proximal tubule fractional and absolute reabsorptive rates in the isolated kidney but since VTF did not increase, they imply that the natriuresis derives from a decrease in sodium transport along more distal nephron segments.


Neurology | 1962

Unusual chromophobe adenoma of the pituitary. Report of a case.

R. D. Bastron

The patient, A. R., a 52-year-old white widower, apparently was in good health until the evening before he died. That night he was heard to cry out shortly after going to bed. He was found in a generalized convulsion, which lasted several minutes, and was immediately sent to a local hospital. He was unconscious but blood pressure and pulse were normal when he arrived at the hospital at 10:30 P.M. He had a second convulsion ten minutes later. The next morning he complained of difficulty seeing, but he was incoherent and could not elaborate on his visual trouble. He had 3 more convulsions that morning and was transferred to the State University of Iowa hospitals. Respiratory distress developed, however, and he died around 12:30 P.M. while en route. He had complained of pain over the cervical vertebrae of one weeks duration but never of headaches, visual trouble, or symptoms relative to a hypopituitary state before the morning of his death.


Experimental Biology and Medicine | 1972

Response of the Isolated Kidney to Saline Infusion

Gerald F. DiBona; George J. Kaloyanides; R. D. Bastron

Summary The isolated perfused dog kidney responds to saline infusion with a decrease in fractional and absolute sodium re-absorption in the proximal tubule. These results appear to be best explained by a reduction in plasma protein concentration.


Acta Anaesthesiologica Scandinavica | 1972

“H” Reflex During Ketamine Anesthesia

R. D. Bastron; S. D. Gergis; J. L. Hoyt; Martin D. Sokoll

Ketamine, 2 mg/kg intravenously, was given to 12 male volunteers. “H” reflex amplitude was increased in every subject with a mean rise of 145 % occurring 5 min after the start of injection. There was a high incidence of hallucinations (100 %) and airway obstruction (50 %).


American Journal of Physiology | 1973

Effect of ureteral clamping and increased renal arterial pressure on renin release.

George J. Kaloyanides; R. D. Bastron; Gerald F. DiBona

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K. Korttila

Helsinki University Central Hospital

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