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T E Jackson

Publications and source records attributed to T E Jackson.

12 recordsLinked to original sources
PubMed1986

Vacuum-assisted perfusion of the dog hindlimb.

A method for rapidly changing perfusion pressure to the relatively intact dog hindlimb using vacuum assistance is proposed and demonstrated. The hindlimb of an anesthetized dog is inserted into a rigid sealed enclosure for application of a partial vacuum. The circulation of the hindlimb remains entirely intact except for a single large noncollapsible catheter placed in the femoral vein and connected to a servo-pump. The servo-pump maintains the venous pressure equal to the enclosure pressure even when this pressure is in the partial vacuum state. The automatically adjusted pumping rate of this pump also provides a continuous measure of the blood flow in the limb as it returns the blood via a jugular catheter. In nine dogs the systemic arterial pressure was maintained constant, and the enclosure pressure and venous pressure were set to subatmospheric levels, thus changing the perfusion pressure to any desired value up to 220 mmHg. The procedure had minimal impact on the central circulation, suggesting that the technique may be useful in studying hemodynamics of the hindlimb or other organs at high perfusion pressure, which has always been difficult to achieve experimentally. In the nine dogs, blood flow responses were observed at both elevated and reduced perfusion pressure. The changes in measured blood flow induced by the changes in perfusion pressure were variable but were generally directly proportional to perfusion pressure in the steady state.

Animals↗
PubMed1984

Multiplicative interaction between angiotensin II and K concentration in stimulation of aldosterone.

The interaction of angiotensin II and plasma K concentration in stimulating aldosterone secretion was studied in a group of six dogs by determining the aldosterone response to three levels of angiotensin II while the dogs were maintained on three levels of K intake. The levels of angiotensin were 1) the endogenous level, 2) the concentration resulting from infusion of 5 ng X kg-1 X min-1, and 3) the concentration resulting from infusion of 10 ng X kg-1 X min-1. Each level was maintained for 5 days. The three rates of K intake were 10, 100, and 200 meq/day, each maintained for 3 wk. Data were analyzed from days 1, 2, and 5 of the angiotensin infusion periods. The regressions obtained from plotting plasma K (PK) versus aldosterone concentration on day 5 of each level of infusion were 1) for no infusion (endogenous PRA = 0.4 to 0.5 ng ANG I X ml-1 X h-1), aldosterone = 5.04 X PK - 16.56; 2) for 5 ng X kg-1 X min-1 infusion, aldosterone = 12.20 X PK - 39.09; and 3) for 10 ng X kg-1 X min-1 infusion, aldosterone = 35.50 X Pk - 119.31. Each regression was significantly different (P less than 0.001) from the other two. The plasma K axis intercepts, which are the points at which aldosterone secretion is zero, were 3.29, 3.20, and 3.36 for the regression from the 0, 5, and 10 ng X kg-1 X min-1 infusion rates, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1984

Comparison of a class of regression equations.

The method described in this paper offers a means of comparing linear regression equations with many parameters by utilizing joint parameter confidence regions. It is useful when comparing sets of data in which each set is represented by a similar regression equation. The method consists of establishing a full-rank linear model with the data sets to be considered and then testing hypotheses concerning parameters of the model. It is conveniently expressed in matrix algebra form and is amenable to computer analysis.

Regression Analysis↗
PubMed1984

Effects of sodium intake on steady-state potassium excretion.

The effects of changes in sodium intake on the steady-state relationship between plasma potassium concentration and potassium excretion were studied in 15 chronically adrenalectomized dogs. Throughout the experiments the dogs received aldosterone at a rate of 50 micrograms/day and methylprednisolone at 1 mg/day. The relationship between plasma potassium and steady-state potassium excretion was obtained by changing potassium intake from 10 to 30 to 100 meq/day, each level being maintained for 7-10 days. At the conclusion of each period at a given level of potassium intake, plasma potassium and excretion were measured and plotted, plasma potassium being the independent variable. Such a relationship was obtained while the dogs were on three different levels of sodium intake: 10, 100, and 200 meq/day. The curves from the data obtained at 100 and 200 meq/day sodium intake both were shifted to the left of the curve obtained at 10 meq/day (P less than 0.05), although the 100 and 200 meq/day curves were not different from each other. On the basis of these data one could predict that, at a plasma potassium concentration of 4.0 meq/liter, the animals would excrete potassium at a rate of 17 meq/day on a 10 meq/day sodium intake, 37 meq/day on a 100 meq/day sodium intake, and 47 meq/day on a 200 meq/day sodium intake. Urine flow and electrolyte concentration data are consistent with the hypothesis that the sodium intake effect on potassium excretion was mediated through increases in distal nephron flow rate and decreases in distal nephron potassium concentration.

Aldosterone↗
PubMed1982

Relationship between anti-diarrheal activity and binding to calmodulin.

Several neuroleptics known to bind to calmodulin were tested for anti-diarrheal activity and were compared with the opiate anti-diarrheals loperamide and diphenoxylate. All inhibited the intestinal fluid secretion induced by 16,16-dimethyl prostaglandin E2 and castor oil-induced diarrhea in rats as a function of dose, the order of potency being loperamide approximately equal to diphenoxylate greater than chlorpromazine greater than promethazine greater than amitriptyline. The opiates loperamide and diphenoxylate were found to compete with [3H]trifluoperazine binding to calmodulin in the presence of calcium. These opiates were approximately 3 times more potent inhibitors of [3H]trifluoperazine binding than chlorpromazine. A positive correlation between calmodulin binding and anti-diarrheal activity was demonstrated.

16,16-Dimethylprostaglandin E2↗
PubMed1982

Effects of aldosterone on potassium distribution.

To assess the effects of long-term changes in aldosterone on potassium distribution within the body, two groups of experiments were conducted. In the first, seven normal dogs received continuous infusion of aldosterone at a high physiological rate, 250 micrograms/day. Total exchangeable potassium (Ke) and plasma potassium concentration (KP) were measured before and 4 and 6 days after aldosterone infusion. KP fell by 20% while Ke decreased by 8% after 6 days of infusion; the ratio between extracellular and total body potassium had been altered by the aldosterone infusion. In the second study, 10 adrenalectomized dogs received aldosterone infusion first at 50 micrograms/day, then at 250 micrograms/day. While on each level of aldosterone infusion, three levels of potassium intake were given by iv infusion. When the animals were in electrolyte balance at each level of aldosterone and potassium (after at least 7 days on each level of infusion), Ke (expressed as meq/kg) and KP were measured. The two variables were plotted against each other, Ke being the independent variable. Data taken while the dogs received 50 micrograms/day aldosterone were described by the equation, KP = 0.100Ke + 0.055, while those obtained at 250 micrograms/day were fitted by the equation, KP = 0.057Ke + 1.30. The correlation coefficients for the two were 0.778 and 0.760, respectively. The regressions were significantly different at a level of P less than 0.02. Data from the two groups of experiments are consistent with the hypothesis that aldosterone alters the distribution of potassium between the intra- and extracellular spaces, a greater portion of total potassium being intracellular at higher levels of aldosterone.

Aldosterone↗
PubMed1981

Blood pressure regulation: basic concepts.

In this paper we have attempted to explain the difference between proportional pressure control systems and the renal-blood volume-pressure control mechanism, which is an infinite gain pressure control system. Because of this infinite gain of the kidney mechanism, this mechanism has the capability of returning arterial pressure all the way back to the control leve. Furthermore, this mechanism can override the other pressure control mechanisms because of its extreme control capability. On the other hand, the renal-blood volume mechanism for pressure control itself be controlled by many other factors. These other factors are said to change the pressure "set-point" level of the renal system, and then the renal system automatically brings the pressure to the set-point level. It is especially noteworthy, however, that some of the factors that play extreme roles in short-term pressure control-such as heart strength, vascular capacity, and total peripheral resistance-will not alter the long-term arterial pressure level (unless they in some way concurrently alter the set-point of the kidney mechanism).

Aldosterone↗
PubMed1977

Transient response of glomerular filtration rate and renal blood flow to step changes in arterial pressure.

Measurement of rapid renal hemodynamic changes were made for 90 s in pentobarbital-anesthetized dogs following step increases and decreases in renal arterial pressure between 80 and 120 mm Hg. Transient analysis was used to observe time characteristics of the autoregulatory relationships which are obscured in steadystate measurements. Temporal decoupling of blood flow and glomerular filtration rate (GFR) occurred with both step increases and decreases of arterial pressure. Steady-state autoregulation of blood flow was attained in about 30 s, whereas steady-state autoregulation of GFR was not demonstrably attained even 90 s after the arterial pressure maneuver. The temporal decoupling of renal blood flow and GRR supports the concept of transient involvement of proximal tubular dynamics and efferent resistance changes during acute autoregulation of GFR following step changes in arterial pressure.

Animals↗