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Biomedical subjects

N Hiatt

Publications and source records attributed to N Hiatt.

At least 37 records · Page 2Linked to original sources
PubMed1979

Influence of epinephrine and propranolol on transmembrane K transfer in anuric dogs with hyperkalemia.

In anuric dogs K loaded by infusion of 2 mEq of KCl per kg per hr the quantity of K transferred to intracellular fluid in ureter-ligated animals is considerably less than in nephrectomized ones; the combination of ureter ligation and hyperkalemia seems to suppress transmembrane K transfer. In the present investigation we found that treatment of K loaded ureter-ligated dogs with epinephrine markedly increased the animals' ability to transfer K to intracellular fluid, and that administration of propranolol (with and without epinephrine) reduced K transfer capacity below the control level. Further, we found that propranolol treatment of K-loaded nephrectomized dogs produced a striking diminution of K transfer ability. The data suggest that beta adrenergic receptors are importantly involved in the transmembrane K transfer of K-loaded anuric dogs, and that ureter ligation and hyperkalemia suppress K transfer capacity by blocking beta receptors.

Animals↗
PubMed1978

Epinephrine enhancement of potassium-stimulated immunoreactive insulin secretion. Role of beta-adrenergic receptors.

Although epinephrine stimulates insulin release by activation of beta-adrenergic receptors, its dominant effect (mediated by stimulation of alpha-adrenergic receptors) is an inhibition of insulin secretion that is powerful enough to suppress the secretory activity of insulin's most potent stimulants. The insulin-secretory response to potassium chloride (KCl) infusion, however, is not suppressed; in fact, in ureter-ligated dogs simultaneously infused with 360 microgram. epinephrine per hour and 2 mEq. KCl per kilogram per hour, insulin release is actually increased about threefold (over controls). Propranolol blockade of beta-adrenergic receptors essentially abolishes the insulin response to KCl infusion, with and without epinephrine. It is unlikely that KCl, like epinephrine, provokes insulin release by direct stimulation of the beta-adrenergic receptors of the beta cells of the pancreatic islets. However, potassium in some way enhances the beta adrenergic (secretory) activity of epinephrine and blunts its usually dominant alpha-adrenergic (inhibitory) effect.

Animals↗
PubMed1977

Enhancement of K transfer to intracellular fluid by cerebral artery K-loading.

Intact, UL, and pancreatectomized UL dogs were loaded with K by administration of 2 mEq KCl/kg/hr through a cerebral (vertebral) artery. K transfer to ICF was calculated and compared with that computed in control animals K-loaded through a PV. At the same rate of K administration, the change of route from PV to VA markedly increased transmembrane K transfer, even in the absence of insulin; the increase seems a specific response to K. KCl administration via a VA, with a resulting abrupt rise in the serum K concentration of cerebral blood, activates a K transfer mechanism (possibly by stimulation of a K-sensitive CNS receptor) that is strikingly unlike the insulin-mediated one stimulated by intravenous KCl. Hyperkalemic dogs may have more than one mechanism for maintaining K homeostasis, depending on the rate at which K enters the circulation.

Animals↗
PubMed1976

Inhibition of transmembrane K transfer in ureter-ligated dogs infused with KCl.

In anuric dogs loaded with K by infusion with 2 meq KCl/kg per h until prelethal hyperkalemic cardiotoxicity appears, the extent of transmembrane K transfer depends on the origin of the anuria. Animals with bilateral ureter ligation transfer a mean of 1.2 meq/kg to intracellular fluid, while those with bilateral nephrectomy transfer more than 2.5 times as much (3.1 meq/kg). Further, if dogs with functioning kidneys are ureter ligated or nephrectomized after approximately 45 min of K loading, K transfer ultimately falls as infusion continues. The fall is precipitate and over 90% in ligated animals; but it is gradual, and only 10% in those that are nephrectomized. Finally, K transfer, because of the absence of insulin, is negligible in K-loaded pancreatectomized dogs with bilateral ureter ligation, but fairly substantial in pancreatectomized animals with bilateral nephrectomy. The data suggest that ureter ligation and hyperkalemia activate a renal mechanism that interferes with the transfer of infused K to intracellular fluid. The mechanism may involve the renin-angiotensin II-aldosterone system to a limited degree.

Animals↗
PubMed1975

Kaluresis and diuresis after administration of antidiuretic hormone to hyperkalemic dogs.

Dogs infused with 2 meq KCl/kg per h exhibit electrocardiographic evidence of prelethal cardiotoxicity in about 3 h when serum potassium reaches a level between 10.2-10.5 meq/liter. During this time, their urine output of 30 ml/h is equal to the volume of KCl infused. Studies of the potassium distribution in these animals indicate that 20 percent of the infused ion is added to the extracellular fluid and red blood cell mass, 20 percent is excreted in the urine, while the remaining 60 percent is unaccounted for and presumably transferred to intracellular fluid. Dogs treated with moderately large doses of antidiuretic hormone intramuscularly before and during KCl infusion delay development of prelethal cardiotoxicity for about 5 h, with serum potassium levels comparable to those of untreated dogs. In addition, treated animals display a considerable diuresis and kaluresis with urine volumes nearly 4 times that of the volume infused. The potassium ion distribution in animals given antidiuretic hormone is much different from that of untreated dogs, with 55 percent of the infused ion found in the urine, about 15 percent in extracellular fluid and red blood cell mass, and only 30 percent presumably transferred to intracellular fluid. Transfer of potassium to intracellular fluid was calculated to be 3.1 plus or minus 0.7 meq/kg in antidiuretic-hormone-treated animals and 3.8 plus or minus 0.7 meq/kg in untreated (control) animals. Since these values are, within experimental error, quite comparable, it is possible that antidiuretic-hormone-induced kaluresis and diuresis are involved in protecting some animals from the effects of hyperkalemia by delaying the attainment of cardiotoxic blood levels.

Animals↗
PubMed1975

Kaluresis and cardiac sensitivity to hyperkalaemia in intact and adrenalectomized rabbits.

Rabbits K loaded by infusion of 2 meq KCl/kg/hr excrete over 55% of the administered K in the urine and do not develop prelethal ECG changes until mean serum K attains to 14.9 meq/liter, i.e., 11.8 meq/liter above the average preinfusion level. Four hours after bilateral adrenalectomy there is a profound diminution of urinary K loss in K loaded rabbits--less than 7% of the infused K is excreted. There is, however, no significant change in cardiac sensitivity to hyperkalemia. K loaded dogs lose only about 20% of infused K in the urine and develop prelethal ECG changes at similar to 10.2 meq/liter, i.e., 5.6meq/liter above the mean of the preinfusion levels. After adrenalectomy, urinary K loss is only moderately diminished (12% of infused K is still found in the urine), but cardiac sensitivity to K is markedly increased: prelethal ECG changes appear at a serum K level of similar to 7.6 meq/liter--about 2.9 meg/liter above the preinfusion value.

Adrenal Glands↗
PubMed1975

Cardiac sensitivity to hyperkalemia in adrenalectomized dogs.

In dogs with bilateral adrenalectomy loaded with K by infusion of 2 mEq KCI/kg/hr there is a marked increase of cardiac sensitivity to hyperkalemia. Typical ECG changes begin at lower serum K levels (5-6 mEq/l) and the prelethal arrhythmias that signal the imminent onset of fatal when mean serum K is 7.6 mEq/l, 2.9 mEq/l above the average pre-infusion level. In control dogs, ECG changes start above 8 mEq K/liter, and prelethal arrhythmias appear between 9.5 and 10.2 mEq/l, a mean increase of 5.6 mEq/l above the average preinfusion level.

Adrenal Glands↗