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Biomedical subjects

E E Muirhead

Publications and source records attributed to E E Muirhead.

At least 73 records · Page 4Linked to original sources
PubMed1976

Malignant hypertension in blacks. Malignant intrarenal arterial disease as observed by light and electron microscopy.

Volhard and Fahr recognized that hypertensive intrarenal vascular disease could be divided into two groups corresponding to the clinical states of benign and malignant hypertension. Since that time, numerous papers on malignant hypertension, primarily dealing with European derived populations, have emphasized fibrinoid necrosis of small arteries and arterioles as the lesion of malignant hypertension, although some have also recognized a myxoid intimal lesion as characteristic. Today in the United States, however, a significant proportion of malignant hypertension occurs in blacks. In the present study, patients have lacked fibrinoid necrosis of arterioles and only rarely have had some atypical necrosis of small arteries. The prominent, but not pathognomonic, lesion in this series is a myxoid intimal thickening of small arteries consisting of smooth muscle cells, acid mucopolysaccharides, basement membrane-like materal, collagen, and other amorphous and unidentified material, probably plasma derived.

Adult↗
PubMed1976

Anti-hypertensive lipid tissue from culture of renomedullary interstitial cells of the rat.

1. Allogenic transplants of cultured renomedullary interstitial cells exert a powerful anti-hypertensive action. The blood pressure of hypertensive animals usually drops slowly over 8-12 h whereas the pulse is unchanged or reduced. 2. Lipids derived from the cultured cells exert a similar anti-hypertensive action. 3. The anti-hypertensive action of transplanted cultured cells almost certainly results from the secretion of a substance(s) that acts in the manner of a hormone. The tissue culture lipid is a prime candidate hormone. 4. The relationship of the kidney to the hypertensive state is considered to entail pro- and anti-hypertensive actions. The pro-hypertensive actions include (a) activation of the renal pressor system (mainly renin-angiotensin), (b) failure to prevent sodium and fluid overloading because of either an injured or absent kidney or the excessive action of mineralocorticoids (mainly aldosterone). The antihypertensive actions of the kidney include (a) the relief of sodium and fluid overloading through diuresis-natriuresis and (b) the action of the reno-medullary interstitial cell hormone (the antihypertensive renomedullary hormone).

Animals↗
PubMed1976

Functional-morphological correlates of renomedullary interstitial cells.

1. Indomethacin treatment of renomedullary interstitial cells (RIC) causes a marked increase in number and size of their lipid droplets. The anti-hypertensive function is retained. 2. After multiple passages in tissue culture, RIC lose their ability to produce an anti-hypertensive effect in hypertensive animals. Along with this functional loss, lipid droplets and a prominent cisternal system become attenuated or disappear. 3. We conclude that preservation of the lipid granule-cisternal organelle relationship is important in preservation of the anti-hypertensive endocrine function of RIC.

Antihypertensive Agents↗
PubMed1976

Indomethacin and blood pressure control.

Blood pressure of indomethacin-treated and control rabbits was measured directly every hour in an automated device for 7 to 10 days. Indomethacin treatment was without effect, and the mean aortic pressure of all rabbits varied generally between 65 and 80 mm. Hg. Since the indomethacin treatment was adequate to block the prostaglandin synthetase system, it is concluded that either circulating prostaglandin is not involved in blood pressure control or other regulatory mechanisms can readily compensate for absence of prostaglandin.

Animals↗
PubMed1975

Treatment of patients with severe hypertension by inhibition of angiotensin-converting enzyme.

1. The results of the administration of the nona-peptide inhibitor (SQ 20,881) of the enzymatic conversion of angiotensin I into angiotensin II in twelve severe hypertensive patients are presented. 2. Administration of the compound was associated with a fall in blood pressure in ten of twelve patients. 3. Four patients had a normal plasma renin activity (PRA) with a range of 1.6-3.7 ng h-1 ml-1 and eight patients had a high PRA with a range of 5.0-74 ng h-1 ml-1. Two of the patients with normal PRA had no fall in blood pressure despite receiving 2 mg/kg of the compound. Two patients with normal PRA, however, did respond, thus indicating that a high PRA is not necessary for a response to the inhibitor compound. 4. It was found that haemodialysis or diuresis with frusemide enhanced the blood pressure response to the compound. 5. The presence of a measured low total blood volume was found to be associated with an exaggerated fall in blood pressure to a small dose of compound (0.125 mg/kg) in one patient.

Blood Pressure↗
PubMed1975

Malignant hypertension due to musculo-mucoid intimal hyperplasia of intrarenal arteries. Absence of renal fibrinoid necrosis.

Severe essential hypertension in a subset of American black subjects is associated with marked stenosis of interlobular arteries and arterioles of the kidneys, observed by renal biopsy and binephrectomy specimens. The interlobular arterial stenosis is caused by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material, and acid mucopolysaccharide. Because of this makeup, we propose the term "musculo-mucoid intimal hyperplasia" for this lesion. The media of these arteries appears maximally dilated, and by electron microscope displays degenerative changes of the smooth muscle cells. The arterioles are thickened, due mainly to hyalinization, but also due to the musculo-mucoid change (onionskin effect). The smooth muscle cells are degenerated and atrophic. These patients do not exhibit fibrinoid necrosis of the arteries, arterioles, and glomeruli, presumably because of the rapidity of the development of the arterial stenotic lesion. Accordingly, the glomeruli are destroyed by ischemia, and there is no evidence of glomerulitis (no "Kombinations" form of Fahr). A unifying hypothesis concerning renal hypertensive arterial disease is suggested by these studies. This hypothesis places the main emphasis for all the morphological expressions of the intrinsic visceral vasculature on changes involving the main functional unit of the vessel wall, the medical smooth muscle.

Acute Kidney Injury↗