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N Hiatt

Publications and source records attributed to N Hiatt.

At least 19 recordsLinked to original sources
PubMed1997

The conquest of Addison's disease.

BACKGROUND: A review of the understanding and treatment of adrenal insufficiency was undertaken to emphasize common themes in the history of endocrine disorders. METHODS: Literature survey. RESULTS: The presence of the adrenal glands, initially ignored by anatomists, was first described by Eustachius and later confirmed by Casserius. Bartholin identified the glands as ductless. In 1855, Thomas Addison described the clinical syndrome of adrenal insufficiency. Medullary hormonal effects were described by Oliver and Shäfer in 1895; epinephrine was isolated by Takamini, and the secretory patterns were characterized by Cannon. Cortical function was elucidated by Biedl and Stewart and Rogoff, and the first cortical hormones were synthesized by Reichenstein. Hormonal replacement therapy paved the way for the first bilateral adrenalectomy, which was performed in 1950. CONCLUSIONS: This review underscores the historical themes in endocrine diseases: discovery of the glands, identification of their hormonal products, use of the hormones for therapy, and biosynthesis for pharmacologic applications.

Addison Disease↗
PubMed1995

Vagal modulation of the insulin secretory response to KCl loading in nephrectomized dogs.

In K-loaded intact and nephrectomized control dogs there is a four-to five-fold increase of basal serum insulin. With beta receptor blockade in K-loaded intact animals the increase of basal serum insulin is less than 1/4 to that in controls; in those with nephrectomy, the increase is similar to that in controls. Cervical vagotomy in K-loaded intact dogs does not alter (influence) the increase of serum insulin; in those with nephrectomy there is a striking increase. In K-loaded intact dogs cervical vagotomy added to beta receptor blockade has no influence i.e., the response is the same as that to blockade alone; in those with nephrectomy, the increase produced by vagotomy is suppressed. Results suggest that in controls with nephrectomy, the insulin secretory response does not involve beta receptors of pancreatic islet B cells owing to restraint by efferent impulses in the cervical vagi. Interruption of the impulse by vagotomy releases the restraint, with resulting hyperactivity; the accompanying hyperinsulinemia may be the result of suppression of the hyperactive receptors by beta receptor blockade.

Adrenergic beta-Antagonists↗
PubMed1995

The forgotten first career of Doctor Henry Van Dyke Carter.

BACKGROUND: While Henry Gray's Anatomy: Descriptive and Surgical, first published in 1858, is distinguished by superb illustrations, its original illustrator is remembered for an entirely different set of accomplishments, notably significant contributions to tropical medicine. STUDY DESIGN: Literature review. RESULTS: Dr. Henry Van Dyke Carter, Professor of Anatomy and Physiology and subsequently Dean of the Grant Medical College in Bombay, India, was a skillful researcher and keen clinician who made significant contributions to tropical medicine, including the discovery of Spirillum minus, the spirochetal organism that causes relapsing fever. For his discoveries he was honored by both the British Medical Association and the English government. Before his departure for India in 1858, however, he and Henry Gray worked at St. George's Hospital Medical School and collaborated on the first edition of the text that is still the "Bible" of anatomy to many medical students. His drawings have appeared in every subsequent edition, up to the present day. CONCLUSIONS: During his first career as a medical illustrator, Carter was responsible for the drawings that have helped generations of physicians to master the intricacies of human anatomy.

History, 19th Century↗
PubMed1992

Insulin modulation of chronotropic response to Adrenaline in diabetic dogs.

In 8 unanesthetized dogs, 10-21 days post pancreatectomy, the cardiac chronotropic response to rapid infusion of a pharmacological dosage of Adrenaline was begun. During the subsequent month, the response was recorded electrocardiographically on 19 occasions. On 8 occasions, animals were treated with continuous intravenous administration of fluids and insulin up to the time of the test; on 11, insulin was omitted for 18 hours before Adrenaline injection. Insulin treated animals responded with the typical brief initial bradycardia, followed by some 2 minutes of ventricular tachycardia, and restoration of preinjection heart rate and electrocardiograph pattern within 5 minutes. On those occasions when insulin was omitted, the tachycardia was replaced by ventricular bradycardia. The altered chronotropic response of non-insulin treated dogs indicates impairment of their cardiac beta receptors.

Animals↗
PubMed1990

Heparin mediates transmembrane potassium transfer in hyperkalemic dogs.

Unheparinized, ureter-ligated control dogs that are potassium loaded, i.e., infused with 2 mEq of KCl/kg until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear (end point), transfer 57 +/- 4% (1.7 +/- 0.1 mEq/kg) of administered potassium to intracellular fluid. Heparinized controls transfer 73 +/- 1% (3.2 +/- 0.2 mEq/kg); with simultaneous alpha-adrenoreceptor blockade, that proportion increases to 81 +/- 2% (4.80 +/- 0.7 mEq/kg) and with simultaneous beta-receptor blockade it is 58 +/- 3% (1.1 +/- 0.1 mEq/kg). In potassium loaded, ureter-ligated dogs, heparin increases transmembrane potassium transfer as effectively as does a dosage of atropine large enough to cross the blood-brain barrier and its influence on potassium transfer, like that of atropine, is suppressed by beta-adrenoreceptor blockade.

Animals↗
PubMed1990

Aminophylline activation of adrenaline mediated transmembrane K transfer in hyperkalemic dogs.

Ureter ligated control dogs that are K loaded by infusion with 2 mEq KCl/kg.h until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear, transfer somewhat more than half the K load to intracellular fluid. The proportion is not significantly changed by adrenalectomy, but increased by treatment with aminophylline; the treatment has no effect on K transfer in adrenalectomized animals. Insulin is not involved; in dogs with adrenalectomy and pancreatectomy treatment with pharmacological dosages of adrenaline (Abbot), beta agonist activity is as effective as that with aminophylline. We conclude that aminophylline improves K transfer, by investifying beta agonist activity of endogenous adrenaline; it is known that increased beta agonist activity enhances beta receptor mediated K transfer in K loaded ureter ligated, intact and adrenalectomized dogs.

Adrenalectomy↗
PubMed1988

Amyand's hernia.

Explore the source record for details and available documents.

Appendicitis↗
PubMed1988

K transfer in ureter ligated dogs loaded with KCl.

In control ureter ligated dogs infused with 2 mEq KCl/kg.h until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear, a kaluresis independent K homeostatic mechanism delays the development of hyperkalemia by transferring some 55% of administered K to intracellular fluid. In preparations with cervical trunk vagotomy the proportion increases to about 70%; but not if the adrenals are simultaneously removed or denervated. A dosage of atropine that crosses the blood-brain barrier is an exact substitute for cervical vagotomy. Our findings suggest that ureter ligated K loaded dogs, ureteral and/or renal afferent vagal fibres to the brain release a "muscarinic" neurotransmitter(s) that modulated neural traffic in rami of splanchnic nerves to the adrenal medulla.

Adrenal Glands↗
PubMed1987

Kaluresis independent K homeostasis in dogs: activity after ureter ligation and pancreatectomy.

In ureter ligated dogs intravenous administration of KCl stimulates both insulin secretion and activity of a kaluresis independent K homeostatic mechanism (K transfer capacity) that retards the development of hyperkalemia by transferring K to intracellular fluid. If the preparation is K loaded by infusion with 2 mEq KCl/kg/hr until prelethal ECG changes of hyperkalemic cardiotoxicity appear, about 50% of administered K is transferred. An increased proportion--70%--is transferred if the animal is K loaded 70 minutes after pancreatectomy--when serum immunoreactive insulin is fixed at less than 4 uU/ml. That proportion (70%) is unchanged by simultaneous adrenalectomy, but is reduced to less than 40% by propranolol blockade of B receptors. Increased post pancreatectomy K transfer capacity apparently involves K transfer mediated by B receptors that are activated by an extra-adrenomedullary B agonist(s). Findings also indicate that residual post pancreatectomy insulin biological activity mediates K transfer.

Animals↗
PubMed1986

Kaluresis independent K-homeostasis: glucagon and B receptor blockade in pancreatectomized dogs.

Seventy minutes post pancreatectomy, in dogs that are K loaded - made abruptly hyperkalemic and "life threatened" - by infusion with 2 mEgKC1/kg-/hr until prelethal ECG changes of hyperkalemic cardiotoxicity appear, a kaluresis independent K homeostatic mechanism transfers about 2/3 of administered K to intracellular fluid. Treatment of K loaded pancreatectomized dogs with glucagon or a B receptor blockading dosage of propranolol does not alter the proportion transferred, but treatment with glucagon and propranolol reduces it. It appears that in pancx dogs there is a reciprocal relation between insulin and B receptor mediated K transfer and that glucagon is involved in activity of the kaluresis independent K homeostatic mechanism.

Animals↗
PubMed1982

Insulin and beta receptor modulation of K homeostasis in nephrectomized dogs with hyperkalemia.

In nephrectomized dogs infused with 2 mEq KCl/kg/hr a homeostatic mechanism retards the development of hyperkalemia by transferring about 70% of the K load to intracellular fluid. beta Adrenergic receptor activity is importantly involved in the transfer process; halting it with propranolol reduces the proportion transferred to less than 35%. The addition of pancreatectomy increases the involvement of beta receptor activity; propranolol treatment now reduces the proportion transferred to less than 20%. Insulin treatment, on the other hand, not only improves transfer of a K load, it also alters the response to propranolol. Nephrectomized dogs treated with 2 U insulin/kg/hr deposit some 80% of the infused K in intracellular fluid. After beta receptor blockade, nearly 90% is transferred. The results suggest that in the K homeostatic mechanism of nephrectomized dogs, insulin and beta receptors may be reciprocally related. K transfer mediated by beta receptors improves after pancreatectomy, and insulin mediated K transfer improves after beta receptors are inactivated.

Aldosterone↗
PubMed1981

Transmembrane K transfer in hyperkalemic dogs.

In a dog K loaded by infusion of 2 mEq KCl/kg/hr, kaluresis plays a relatively small part in slowing the development of hyperkalemia and cardiotoxicity. These are largely retarded by a non-renal mechanism that transfer most of the infused K from extracellular to intracellular fluid. Treatment with beta receptor blocking dosages of propranolol significantly reduces K transfer capacity, but it also markedly diminishes the KCl stimulated secretory response of insulin, a powerful mediator of K transfer. In dogs in which diminution of the insulin response is prevented by administration of exogenous hormone, beta receptor blockade has no effect on K transfer capacity. Thus, it appears that decreased insulin secretion is responsible for the observed fall of K transfer capacity in dogs with beta receptor blockade. However, other evidence suggests that our results can also mean that a K load elicits the secretion of enough insulin to mediate K transfer in the presence of beta receptor blockade; if the hormone response is absent or deficient, beta receptors may be importantly involved in mediation of K transfer to intracellular fluid.

Animals↗