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Biomedical subjects

H Heath

Publications and source records attributed to H Heath.

At least 145 records · Page 8Linked to original sources
PubMed1982

Parathyroid, renal, and skeletal responses to induced hypocalcemia in the dog.

This study was designed to determine 1) whether the plasma immunoreactive parathyroid hormone (IPTH) response to acutely attained, constant (8 h) hypocalcemia is biphasic, and 2) if so, how kidney and bone respond to these changing plasma IPTH levels. We initiated constant hypocalcemia (decrement of Ca, 1.7 mg/dl) in six conscious dogs using the "calcium clamp" technique. Plasma IPTH concentrations increased maximally (fivefold) within 15 min and then decreased gradually over 1 h to a constant, but still elevated level (3.2-fold increase). Urinary excretion of phosphate and hydroxyproline increased more slowly, reaching plateaus at 1.75 h (76% increase) and 5.5 h (70% increase), respectively. The EGTA infusion rate required to maintain constant hypocalcemia was virtually constant (85 +/- 9 mumol.kg-1.h-1) after 20 min and corresponded to skeletal release of about 80 mg Ca.kg-1.day-1. The contribution of the kidney in conserving filtered calcium was relatively minor (2.0 +/- 0.5 mumol.kg-1.h-1). These data demonstrate that the parathyroid response to acute, constant hypocalcemia is biphasic and is temporally divergent from the uniphasic phosphaturic and hydroxyprolinuric responses. The ensuing increased skeletal release of calcium is very high and is maximal within minutes.

Animals↗
PubMed1982

Cimetidine treatment of azotemic secondary hyperparathyroidism.

Cimetidine, an antagonist to histamine H2-receptors, reportedly lowers serum calcium and/or serum immunoreactive parathyroid hormone (iPTH) concentrations in some patients with primary and secondary (azotemic) hyperparathyroidism. We administered the drug orally (300 mg every 6 h) to five normal volunteers and four azotemic patients with secondary hyperparathyroidism who were not undergoing chronic hemodialysis. The normal persons and one azotemic patient took the drug for 5 weeks, and the remaining azotemic patients took it for 1 week. Before treatment, all patients had elevated levels of serum iPTH (two different assay systems), with or without elevated serum calcium concentrations, and increased urinary excretion of cAMP (per 100 ml glomerular filtrate). Cimetidine treatment caused no changes in serum calcium, phosphorus, or iPTH or in urinary cAMP (expressed as nanomoles per g creatinine). Serum creatinine, however, increased significantly in patients (P less than 0.02) and control subjects (P less than 0.025), which yielded statistically significant but spurious increases of urinary cAMP when expressed per 100 ml glomerular filtrate. We conclude that short term cimetidine administration has no effect on parathyroid function in normal persons or those with azotemic hyperparathyroidism. Because of its confusing effect on serum creatinine and a possible (albeit rare) adverse effect on renal function, the drug should be used with caution in azotemic patients not yet requiring chronic dialysis.

Adult↗
PubMed1981

Biologic markers in cancer diagnosis and treatment.

We have reviewed several tumor markers that our advocates feel are now clinically useful, involve current assay technology, and are based on already available information. These include, in selected instances, estrogen receptors for breast cancer, thyrocalcitonin for medullary cancer of the thyroid, prostatic acid phosphatase for cancer of the prostate, alpha-fetoprotein for hepatocellular cancer, and carcinoembryonic antigen for monitoring colon cancer. We have considered the potential use of measurement of serum proteases and protein degradation products due to their activity as possible future areas of development, and we have explored measurement of tissue aryl hydrocarbon hydroxylase to identify populations at risk of cancer resulting from chemical carcinogenesis. It is clear that the study of tumor markers is already improving patient care in some specific areas and offers exciting potential for the future.

Acid Phosphatase↗
PubMed1981

The "calcium clamp": effect of constant hypocalcemia on parathyroid hormone secretion.

This report describes acute studies of parathyroid hormone (PTH) secretion and metabolism in conscious dogs, performed with a new technique, the "calcium clamp." Bolus injections and graded infusions of either calcium (Ca) or EGTA, respectively, increase or decrease plasma Ca to desired levels in 1-2 min; rapid determination of plasma Ca permits feedback control of the infusion rates to maintain the desired Ca concentration for prolonged periods. Using this technique, we have examined the effect in five dogs of a sustained (1 h) decrease in plasma Ca from 9.6 to 7.6 mg/dl on the secretion of PTH. Plasma immunoreactive PTH (IPTH) concentration in precaval blood increased within 1 min, peaked at 4-10 min (greater than 5 times control), but thereafter declined gradually to 57% of the maximum at 60 min, despite ongoing and constant hypocalcemia. Abrupt restoration of normocalcemia caused IPTH levels to decrease with an apparent half-time of 3.0 +/- 0.3 min (mean +/- SE). Thus, external feedback-regulated control of plasma Ca is possible in experimental animals. IPTH concentrations decline from the maximum during constant hypocalcemia, a new observation that suggests that PTH secretion and/or metabolism are altered progressively by the hypocalcemia.

Animals↗
PubMed1981

Episodic secretion of parathyroid hormone in the dog.

This study was designed to determine whether parathyroid hormone (PTH) is secreted episodically, to characterize any such rhythms, and to see whether the rhythms can be altered by stimulating PTH secretion using constant hypocalcemia. We collected blood samples at 1-min intervals for 1 h from the precava or postcava of conscious dogs during normocalcemia or induced, constant hypocalcemia. In two anesthetized normocalcemic dogs we catheterized a caudal thyroid vein and collected all the effluent blood in 1-min fractions. Immunoreactive PTH (IPTH) concentrations were determined in quadruplicate, and the results were subjected to spectral analysis. In both the precava and postcava of normocalcemic dogs, there were regular oscillations in IPTH levels with a period of 12 min (range, 10-15 min) and a +/- 14% variation about the overall mean. Although significant two- to fourfold changes in IPTH levels still occurred during constant hypocalcemia, there was no significant rhythmicity. Significant cycles in IPTH concentration (mean 8.4-min period) were observed in thyroid venous effluent plasma during normocalcemia, confirming that the phenomenon represented episodic secretion that was not affected by pentobarbital anesthesia.

Animals↗
PubMed1981

Retarded growth rate caused by glucocorticoid treatment or dietary restriction: associated changes duodenal, jejunal, and ileal calcium absorption in the chick.

Calcium (Ca) absorption is reportedly stimulated in the ileum of glucocorticoid-treated rats. Our study was designed to investigate this phenomenon in the chick; to determine to what extent any stimulation might compensate for inhibition of Ca absorption in the duodenum; and to compare any changes seen with those caused by growth retardation induced by dietary restriction alone. We assessed CA absorption from different sites in the intestine of chicks treated with betamethasone (BM; 25 micrograms/kg . day for 14 days), or diet-restricted to permit growth at the same rate as those treated with BM, using the ligated loop technique in vivo. There was a similar significant inhibition of Ca absorption in both BM-treated and diet-restricted chicks in both duodenum (to 73% and 67% of the control level, respectively) and jejunum (to 74% and 77% of the control level, respectively). Absorption of Ca from the ileum of BM-treated birds equaled that in controls, but diet-restricted chicks unexpectedly showed a 100% stimulation. We conclude that in the chick, BM treatment does not stimulate ileal calcium absorption, but diet-restriction does. The lack of effect of bM in the ileum may reduce the magnitude of the decrease in Ca absorption from the entire small intestine when compared to the duodenum and jejunum alone, but the stimulated absorption seen in the ileum of diet-restricted birds is almost sufficient to restore Ca absorption from the entire small intestine to the control level.

Aging↗
PubMed1981

Histamine and human parathyroid adenoma: effect on adenosine 3',5'-monophosphate accumulation in vitro.

We studied in vitro the presence of histamine and the effect of histamine and its antagonists on cAMP accumulation in parathyroid tissue (parathyroid adenoma or hyperplasia) from patients with primary hyperparathyroidism. Parathyroid adenomatous tissue contained 11.2 +/- 2.9 ng histamine/g wet weight (approximately 2 X 10(-5) M), as determined by a specific radioenzyme assay. Histamine caused a prominent increase in cAMP accumulation in parathyroid tissue slices in a dose-dependent manner, with half-maximal stimulation being achieved at 5 X 10(-6) M and maximal stimulation occurring at 10(-4) M histamine. The histamine H2 receptor antagonists, cimetidine and metiamide, caused profound inhibition of histamine-stimulated cAMP accumulation in the parathyroid tissue. Pyrilamine, an H1 antagonist, also inhibited histamine-stimulated cAMP accumulation. Isoproterenol, a beta-adrenergic agonist, elicited marked elevation of cAMP, and its stimulatory effect was blocked by propranolol, but the effects of histamine on cAMP levels in parathyroid tissue were not blocked by propranolol. Histamine significantly stimulated (an increase of 50%) the release of immunoreactive parathyroid hormone. The present observations demonstrate that parathyroid adenomatous tissue has a relatively high content of histamine, and the release of immunoreactive parathyroid hormone from this tissue. The effects of antagonists suggest that histamine stimulates cAMP accumulation in the parathyroid adenomatous tissue by an action on both H2 and H1 histamine receptors.

Adenoma↗
PubMed1981

The effect of dietary fructose and diabetes on the rat kidney.

To determine whether the fructose moiety of sucrose or the lack of some factor essential for the integrity of the microvascular system is responsible for the development of sucrose-induced glomerulosclerosis, a series of diets with or without such a factor and/or fructose was fed to rats over a 6-month period. Consumption of diets containing or yielding fructose caused a significant increase in kidney weight in comparison with glucose-yielding diets. Diabetic animals also exhibited an increased kidney weight. The incidence of diffuse glomerulosclerosis, tubular damage and lymphocyte infiltration was increased in the starch-diabetic, fructose- and sucrose-normal groups. Diabetic MRC 41B- and normal MRC 41B/fructose-, MRC 41B-, glucose- and starch-fed rats (with the exception of one animal in the latter group) did not develop these kidney lesions. Sucrose-, in comparison with starch-ingestion was found to produce significant increases in blood fructose and kidney fructose-1-phosphate concentration. The results are discussed in relation to blood-glucose concentration, renal-fructose metabolism and the development of glomerular and tubular damage.

Animals↗
PubMed1980

Primary hyperparathyroidism. Incidence, morbidity, and potential economic impact in a community.

We examined the incidence and clinical and economic consequences of primary hyperparathyroidism in residents of Rochester, Minn, from 1965 through 1976; 90 cases were found. From January 1, 1965, to June 31, 1974, the average annual incidence was 7.8 +/- 1.2 (mean +/- S.D.) cases per 100,000 population. However, after the introduction of routine measurement of serum calcium, the average annual incidence rose to 51.1 +/- 9.6 cases per 100,000. Even after availability of routine measurement of serum calcium, the annual incidence of primary hyperparathyroidism among persons 39 years of age or younger remained below 10 cases per 100,000. However, the annual incidence increased sharply in persons 40 or more years of age, reaching 188 cases per 100,000 among women 60 years of age and over and 92 cases per 100,000 among men 60 and over. For the last 1.5 years of the study, the average annual age-adjusted incidence of primary hyperparathyroidism was 27.7 +/- 5.8 per 100,000. The frequency of urolithiasis fell from 51 to 4 per cent (P less than 0.001), and the proportion of cases without symptoms or complications of primary hyperparathyroidism rose from 18 to 51 per cent (P less than 0.005). The median charge in 1977 for diagnosis and treatment of primary hyperparathyroidism was $1700. (N Engl J Med 302:189-193, 1980).

Adult↗