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Biomedical subjects

J W Shaw

Publications and source records attributed to J W Shaw.

At least 37 records · Page 2Linked to original sources
PubMed1977

Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia.

Urinary cyclic AMP (UcAMP) appropriate for the serum calcium concentration was determined in normal subjects during the base-line state and during alteration in their serum calcium concentrations by saline and calcium infusions. This was compared to the UcAMP in 76 patients with hypercalcemia and 5 patients with hypocalcemia. In 54 of 56 patients with primary hyperparathyroidism, the UcAMP was inappropriately high for their serum calcium concentration, the 2 exceptions having renal failure. In four patients with vitamin D intoxication, sarcoidosis, milkalkali syndrome, and thiazide-induced hypercalcemia and in five patients with hypocalcemia due to hypoparathyroidism, the UcAMP was appropriately low for their serum calcium concentration. In 16 patients with nonparathyroid neoplasms, 10 had UcAMP levels that were inappropriately high suggesting ectopic parathyroid hormone (PTH)-mediated hypercalcemia and 6 had UcAMP levels that were appropriately low suggesting that their hypercalcemia was due to osteolytic factors other than PTH. Correlations between UcAMP, serum calcium concentration, and carboxyl-terminal immunoreactive PTH suggest that random UcAMP is a sensitive accurate reflection of circulating biologically active PTH. If there is adequate renal function (serum creatinine concentration less than 2.0 mg/dl), a random UcAMP expressed as mumol/g creatinine and analyzed as a function of the serum calcium concentration completely separates patients with PTH and non-PTH-mediated hypercalcemia.

Adult↗
PubMed1975

Epinephrine-induced alterations in urinary cyclic AMP in hyper- and hypothyroidism.

Although ratios of urinary cyclic AMP (cAMP) to creatinine were found in this study to be elevated in hyperthyroidism, as previously reported, this elevation appears to result primarily from a decrease in the rate of urinary creatinine excretion associated with the hyperthyroid state and not to be due to an increase in the urinary cAMP production rate. Indeed, there was no significant alteration observed in the urinary cAMP excretion found in 15 hyper-, 12 eu-, and 5 hypothyroid subjects. However, a slight, but significant increase in the 24-hour urinary cAMP excretion was noted in ambulating hyperthyroid subjects (8.5 +/- 2.4 muMol/day; normal 5.2 +/- 1.6 muMol/day; P less than .05). In contrast, the effect of the infusion of 0.05 mug/kg/min of epinephrine over a 2-hour period, resulted in a significantly greater rise in urinary cAMP excretion in hyperthyroid patients (0.83 +/- 0.07 muMol/h) compared to euthyroid subjects (0.53 +/- 0.4 muMol/h; P less than .005). Furthermore, hypothyroid subjects had no significant rise in urinary cAMP excretion after epinephrine infusion (P less than .001). Cardiovascular end-organ response to the epinephrine infusion was also greater in the hyperthyroid subjects and virtually absent in the hypothyroid group. These results suggest that there may be a significant alteration in the cAMP generating systems in states of thyroid hormone excess or insufficiency, and that provocative stimuli, such as epinephrine, may have its end-organ response modified by thyroid hormone effects on adenylate cyclase-cyclic AMP generating systems.

Adult↗
PubMed1973

The action of carbon dioxide on constricted airways.

1. In artificially ventilated open-chest cats and dogs ventilation with 5-15% CO(2) reversed the bronchoconstriction caused by drugs or by pulmonary artery occlusion. Total lung resistance, ;static' lung compliance, and intratracheal or intrabronchial pressure at constant pump stroke were measured.2. CO(2) reduced resistance and increased compliance of the lung during infusions of 5-hydroxytryptamine (5-HT), histamine and acetylcholine in cats. In dogs CO(2) reduced resistance during 5-HT infusions; it caused small reductions in intratracheal pressure but no significant change in resistance during infusions of histamine and acetylcholine. Even in cats CO(2) had a larger effect during 5-HT than during histamine and acetylcholine infusions.3. Occlusion of a pulmonary artery caused increases in resistance and decreases in compliance in the affected lobes of both cats and dogs. These changes were partly reversed by ventilation with high CO(2) mixtures.4. The bronchodilator action of CO(2) took place over a wide range of P(a, CO2) values (20-100 torr).

Acetylcholine↗
PubMed1971

Pulmonary vasodilator and vasoconstrictor actions of carbon dioxide.

1. Three preparations were used to study the actions of CO(2) on the pulmonary vasculature: isolated rat and cat lungs perfused at a constant flow rate with homologous blood and a lobe of cat lung perfused at a constant flow rate in vivo. In all three changes in pulmonary artery pressure (P(Pa)) reflected changes in pulmonary vascular resistance.2. In the isolated rat lung CO(2) caused vasodilatation when vascular tone was high. The lung was first ventilated with N(2) causing a rise in P(Pa). CO(2) caused vasodilatation during hypoxia whether the initial blood CO(2) level was low or normal and in spite of a fall in blood pH which usually augments the constrictor action of N(2).3. In the rat lung ventilation with CO(2) from the control state usually caused weak vasoconstriction. Reducing blood pH with acids also caused weak vasoconstriction while alkali caused vasodilatation.4. The over-all effect of CO(2) on the pulmonary vasculature depends on a balance between a vasoconstrictor action probably caused by carbonic acid and vasodilatation caused by some other property of the molecule. The dilator action is powerful in the isolated rat lung.5. By contrast, in both cat lung preparations, no direct evidence for a vasodilator action of CO(2) was obtained. Ventilation with CO(2) when vascular tone was raised by hypoxia, drugs or acids caused further vasoconstriction. From the control state CO(2) caused strong vasoconstriction.6. Indirect evidence from other work suggests that a pulmonary vasodilator action of CO(2) exists in the cat but is usually masked by the strong vasoconstrictor action of carbonic acid. In life the dilator mechanism may be important when pH changes caused by CO(2) are minimized by renal compensation.

Acetates↗
PubMed1970

Stimulus-response curves for the pulmonary vascular bed to hypoxia and hypercapnia.

1. In anaesthetized open-chest cats and dogs, blood flow and gas tensions were measured in a circuit inserted into a pulmonary vein while ventilating the lobe which it drained with low O(2) and high CO(2) mixtures.2. Both hypoxic and hypercapnic mixtures caused a reduction in blood flow from the lobe.3. Stimulus-response curves relating blood flow to pulmonary venous P(O2) and P(CO2) were obtained. Those for hypoxia were usually asymptotic in shape; the curves became steep below 100 torr and flow sometimes fell to zero. The mean reduction in blood flow for every 20 torr fall in P(O2) was 15.7% in cats and 11.8% in dogs. Those for hypercapnia were steep at first but levelled out at high P(CO2) values; the maximum reduction in flow was 40-60% as vasoconstriction was only observed over a limited P(CO2) range.4. Hypoventilation of the lobe led to a reduction in blood flow. This was mainly attributable to hypoxia though other factors such as hypercapnia may sometimes have contributed.5. Total occlusion of the bronchus of an O(2)-filled lobe caused blood flow to fall in two phases. The first phase could be attributed to a rise in P(CO2) and the second to a fall in P(O2).6. The results confirm the hypothesis that hypoxia is an important factor regulating local blood flow in relation to local ventilation.

Animals↗