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Biomedical subjects

W M Manger

Publications and source records attributed to W M Manger.

41 records · Page 3Linked to original sources
PubMedDate not supplied

Norepinephrine infusion in normal subjects and patients with essential or renal hypertension: effect on blood pressure, heart rate, and plasma catecholamine concentrations.

Infusion of NE in seven normal subjects and 13 patients with essential or renal hypertension caused a pronounced initial rise of systolic pressure in only seven hypertensives and one normotensive. This hyperresponsiveness was not a constant finding in essential or renal hypertensives but usually occurred in patients with highest preinfusion pressures. In some of the latter, following the pronounced rise in pressure when NE infusion was started (0.05 mug/kg/min), pressure did not increase further (probably due to reflexly reduced cardiac output) despite progressively increasing the infusion rate to 0.1 and 0.2 mug/kg/min. Hyperresponsiveness could not be attributed to increased NE concentrations at receptor sites since it was not significantly correlated with elevations of NE plasma concentrations; in some essential hypertensives, mild pressure increases occurred despite marked elevations of arterial plasma NE. Since hyperresponsiveness occurred in some patients with essential and some with renal hypertension, it could not be used to differentiate these two groups of hypertensives. The mechanism for hyperresponsiveness remains unclear but may be better explained by vascular structure alterations than by hyperreactive vascular smooth muscle per se; however, a combination of these factors could participate. During NE infusion, reflex bradycardia was associated with elevated pressure and was slightly more pronounced in normotensives; this was probably related to diminished baroreflex sensitivity in essential hypertensives and due to "resetting" of their baroreceptors. During high rates of NE infusion (0.2 mu/kg/min), higher arterial plasma NE concentrations in essential hypertensives than in normotensives could result from reduction in blood flow to organs important in inactivating circulating NE; however, a defective inactivating mechanism for NE in some essential hypertensives cannot be totally excluded.

Adult↗
PubMedDate not supplied

Pheochromocytoma: current diagnosis and management.

BACKGROUND: Pheochromocytoma is a catecholamine-secreting tumor of chromaffin cells that causes hypertension. OBJECTIVE: To review the clinical presentation, diagnosis, and treatment of this disease. SUMMARY: Pheochromocytoma can mimic a number of other diseases, making recognition difficult. Hypertension may be paroxysmal or sustained. The signs and symptoms of pheochromocytoma are mostly due to hypercatecholaminemia, hypertension, complications, or coexisting diseases; however, measurements of catecholamines and their metabolites in the plasma and urine may be normal between "attacks", and other conditions can elevate these values. The clonidine suppression test confers specificity to the clinical and laboratory findings, and magnetic resonance imaging is the most reliable method of locating a tumor. Surgical resection is successful in 90% of patients; however, the disease is fatal if it is not detected and treated. CONCLUSIONS: Pheochromocytoma should be suspected in patients with paroxysmal or sustained hypertension, particularly if symptoms are present.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Effect of pheochromocytoma and hypophysectomy on blood pressure and catecholamines in NEDH rats.

The New England Deaconess Hospital (NEDH) rat provides a valuable model with which to study pheochromocytoma (P); 59% of male rats 700 to 900 days old and 81% of those 900 days or older developed spontaneous P. One transplantable P (P259), when implanted into other NEDH rats, markedly increased plasma norepinephrine and dopamine as well as blood pressure, and usually caused death within 4 weeks. Even without P, about 83% of NEDH rats became hypertensive by 131/2 weeks of age and remained moderately hypertensive until 2 years of age when some animals developed spontaneous P and hypertension became severe. Whether a common mechanism is responsible for early appearance of hypertension and later development of P remains to be determined. Hypophysectomized NEDH rats remained normotensive or slightly hypotensive despite marked elevations of plasma norepinephrine and dopamine caused by P259 implantation; furthermore, survival was prolonged to 3 months. Catecholamine concentrations in plasma and RBC were usually quite similar, indicating that red blood cells play a significant role in inactivating circulating catecholamines. Unlike the normal adrenal, P259 in NEDH rats contains mainly norepinephrine and dopamine with little epinephrine; it appears that P259 is deficient in the enzyme phenylethanolamine-N-methyltransferase (PNMT), which converts norepinephrine to epinephrine. Why hypophysectomy prevents hypertension and prolongs life in rats with P259 implants is unclear; adrenal cortical and thyroid deficiency may play a role. Preliminary observations indicate that hypophysectomy can prevent spontaneous development of P in NEDH rats.

Adrenal Gland Neoplasms↗