The reproducibility and accuracy of plasma volume estimation in the sheep with both 131I gamma globulin and Evan's blue.
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Animals↗
Biomedical subjects
G W Boyd
Publications and source records attributed to G W Boyd.
Stress and disease: the missing link. A vasospastic theory. I. Acute myocardial infarction - a potentially reversible event?
A review of the evidence in acute myocardial infarction indicates that it might well be initiated by coronary artery spasm, and that coronary thrombosis, although important in tipping the balance between severe damage and death of heart muscle, may merely be secondary to the spasm-induced reduction in coronary blood flow.
Angina Pectoris↗
Stress and disease: the missing link. A vasospastic theory. II. The nature of degenerative arterial disease.
An analysis of the evidence indicates that the initiation and progress of atherosclerosis might well be explained by repeated bouts of arterial constriction in relation to life stresses, through increased blood flow velocity and turbulence at points of constriction, and consequent endothelial damage, plasma insudation into the wall, and intimal smooth muscle cell - connective tissue proliferation.
Aneurysm↗
Stress and disease: the missing link. A vasospastic theory. III. Stress, vasospasm and general disease.
The potential importance of vasospasm, with or without consequent thrombosis, as a mechanism in general disease is discussed and the evidence examined in one organ, namely the brain. It is concluded that vasospasm might be important in a number of neurological disorders, including migraine, epilepsy, and even some of the schizophrenia-like illnesses. Repeated ischaemic cell damage from vasospasm is also discussed as a possible factor initiating autoimmune disease and cancer. The similarities between viral transformation and neoplasia have led to the proposition that much cancer might be explained if as a species we have evolved by the gradual build-up of viruses.
Arteries↗
The patho-physiology of chronic arterial hypertension: a hypothesis.
An important unresolved problem in hypertension is how an elevated blood pressure from any cause may eventually become self-sustaining and apparently independent of the initiating event. Folkow has suggested that this results from arteriolar narrowing due to a physiological response or " structural adaptation" to the higher pressure, but it is suggested here that the histological appearances within arterioles in chronic hypertension are much more in keeping with a pathological process, and not vastly different from those observed after intimal damage to larger arteries in experimental atherosclerosis. From this, it is proposed that the arteriolar narrowing is secondary to the endothelial damage which arises when a maintained cardiac output is forced through a constricted arteriolar bed, so increasing substantially the shearing stress on their walls.
Arterioles↗
On the relationship between cardiac output and peripheral arterial resistance.
The concept of 'whole body auto-regulation' is a somewhat unsatisfactory explanation of the increased peripheral arterial resistance which follows a rise in cardiac output in 'volume' forms of hypertension. This analysis suggests that the resistance change may be due to the sodium retention and increased cardiac output having a direct effect to alter haemodynamics of flow through the arterioles in such a way as to damage their walls, and so lead to the gradual development of structural arteriolar narrowing. Studies are presented in the DOCA/salt hypertensive rat consistent with this proposal.
Animals↗
Onset and offset of structural arteriolar changes in DOCA/salt hypertension in the rat.
1. Structural changes in resistance vessels were studied sequentially (a) by hindquarter perfusion and (b) by planimetry of renal arterioles less than or equal to 20 micrometers radius, for 10 weeks during development of DOCA (deoxycorticosterone acetate)/salt hypertension in uninephrectomized rats and 5 weeks after cessation of DOCA treatment. 2. Blood pressure and haemodynamically significant structural change increased progressively during DOCA treatment and both had partially reversed 5 weeks after cessation of DOCA. 3. Arteriolar structural changes contribute progressively to the hypertension during 10 weeks DOCA treatment. Partial reversal of structural changes contributes to the fall in blood pressure after cessation of DOCA. The persisting postDOCA hypertension can be attributed to relatively irreversible structural changes.
Animals↗
The distribution of arteriolosclerosis along the arterioles in DOCA hypertensive rats.
The development of structural changes along the length of small arterioles (mean internal diameter 20-30 microns) was studied in uninephrectomized DOCA/salt hypertensive rats over a period of 10 weeks, by casting the arteriolar branchings in the ileum with Microfil (coloured silicone rubber). Along with a reduction in mean arteriolar diameter, irregular structural changes, manifested as focal narrowings along the arteriolar lengths, developed in the hypertensive animals, becoming most marked after 8-10 weeks. The severity of the changes appeared to be related to both the level and duration of the hypertension. The irregular nature of the changes is difficult to account for on the basis of any direct local pressure effect.
Animals↗
Prevention of structural arteriolar changes in DOCA hypertension with hydrallazine.
Structural changes in resistance vessels were studied by (a) hindquarter perfusion; and (b) planimetry of cross-sections of renal arterioles in uninephrectomized rats treated for 10 weeks with saline and either DOCA (deoxycorticosterone acetate), DOCA plus hydrallazine, vehicle plus hydrallazine or vehicle only. DOCA-treated rats developed hypertension and structural change. Addition of hydrallazine prevented both hypertension and the development of structural change. Structural arteriolar change in DOCA/salt hypertension is related to the high blood pressure or a closely associated factor rather than some other effect of DOCA.
Animals↗