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H D Green

Publications and source records attributed to H D Green.

At least 19 recordsLinked to original sources
PubMed1984

Pulse wave velocity and morphological changes associated with early atherosclerosis progression in the aortas of cynomolgus monkeys.

To determine the time course of changes in arterial stiffness and corresponding morphology during atherosclerosis progression, we determined pulse wave velocity (PWV) in cynomolgus monkeys fed atherogenic (test) and control diets over an 18-month period. At 6-month intervals, thoracic and abdominal aortic PWVs were determined with a pressure transducer retracted down the aorta in 5 cm increments. Iliac artery PWV was determined from the abdominal aortic pressure to a noninvasive femoral pulse. Groups of individual cardiac cycles, triggered by the ECGs, were sampled on a computer and the velocities (PWV) of the pulse wave fronts were calculated. There was no significant difference between groups until 18 months when test animal PWVs in the thoracic (7.44 +/- 0.83 m X s-1) and abdominal (8.52 +/- 0.67 m X s-1) aorta were significantly greater than those of controls (5.02 +/- 0.51 and 6.24 +/- 0.53 m X s-1, respectively), indicating increased arterial stiffness. There was no change in iliac PWV, 10.96 +/- 0.74 m X s-1 for 18-month test compared with 9.44 +/- 0.89 m X s-1 for controls. Constant infusion of nitroprusside and noradrenaline lowered and raised blood pressure and PWV in all groups, and PWV changes due to drug-induced pressure changes were greater in atherosclerotic than in control arteries. Systolic pressure of 18-month test and pulse pressure of 12- and 18-month test groups were significantly greater than controls under all drug conditions, also indicating increased vessel stiffness. Morphometric evaluation of histological aortic cross sections revealed early, noncomplicated atherosclerosis showing gradual increases in the ratio of intimal to medial cross-sectional area in the thoracic (1.24 +/- 0.30 after 18 months) and abdominal (1.70 +/- 0.42 after 18 months) aortas, compared with control ratios of essentially zero. The fraction of the internal elastic lamina covered with atherosclerotic lesions, and maximal intimal thickness also showed significant increases during the test diet period. These data show that early atherosclerosis resulted in aortic but not iliac stiffening which was detected by increased PWV before development of significant stenotic lesions.

Animals↗
PubMed1979

Noninvasively and invasively measured pulsatile haemodynamics with graded arterial stenosis.

Pulsatile haemodynamics associated with graded degrees of experimentally produced stenosis were studied in the canine femoral artery. Invasively determined pulsatile blood flow and noninvasively determined blood velocity with Doppler ultrasound were measured an average of 1.3 and 2.3 cm proximal to the stenosis, respectively. Pulsatile blood pressure was measured 0.6 cm proximal and 3.7 cm distal to the stenosis. With increasing severity of stenosis there were progressive increases in the femoral artery hydraulic input impedance moduli and in the ratio of the impedance moduli to the zero harmonic impedance (or total resistance). This resulted in: a) a progressive reduction in the Fourier harmonic moduli and pulsewave amplitudes of flow, velocity, and distal pressure; b) a progressive increase in the fifth-seventh proximal pressure harmonic moduli; but c) little change in mean proximal pressure or its first 4 harmonic moduli. The data confirm the well known phenomena of a 'critical stenosis' in that there is little decrease in resting mean blood flow until there is a 70 to 80 stenosis (area reduction). Also the oscillatory portions of the femoral artery data were more sensitive to the changes in stenosis than were the nonoscillatory parameters, which confirms previously reported findings from the thoracic aorta. However, the femoral artery haemodynamics exhibited a greater amount of frequency dependent behaviour than the thoracic aorta which is probably the result of a more complex interaction of reflections from the stenosis and from the periphery in the femoral artery than in the thoracic aorta. The sensitive changes in oscillatory haemodynamics may provide a useful basis for noninvasive and invasive physiological assessment of human peripheral atherosclerotic stenosis and of experimental stenosis in animals.

Animals↗
PubMed1978

Aortic pulse wave velocity, elasticity, and composition in a nonhuman primate model of atherosclerosis.

Aortic pulse wave velocity was determined in Macaca fascicularis monkeys fed either atherogenic or control diets for 36 months. The foot-to-foot velocity and apparent phase velocities of the second through seventh Fourier harmonics at a given diastolic pressure in the atherosclerotic monkeys were 1.5 to 2.0 times the values for the control animals. More than 80% of the aortic intimal surface of the atherosclerotic monkeys was covered with fibrous or fatty plaque, which approximately doubled wall thickness and wall thickness to radius ratio. Angiochemical evaluations showed no difference in collagen or elastin concentration (as a fraction of lipid and mineral-free dried aorta), but the atherosclerotic aortas were 1.5 to 2.0 times that of control in collagen and elastin content (defined as the absolute quantity beneath a square centimeter of intimal surface). Total cholesterol and calcium concentrations in the atherosclerotic aortas were more than 10 times the values for the control aortas. The static circumferential distensibility of the excised atherosclerotic aortas was significantly less than control, but there was no difference in incremental (Young's) modulus of elasticity. The in vitro pressure-strain elastic modulus of the atherosclerotic aortas was more than twice that of control, which was predicted from the enhanced wave velocity. The significantly increased stiffness of the atherosclerotic arteries appeared to be due mainly to the increased wall thickness caused by the atherosclerotic plaques rather than to material changes described by Young's modulus. Extensive medial damage, however, also was present and could have had a major influence on stiffness. Atherosclerosis therefore can result in increased aortic stiffening, detectable by pulse wave velocity, even if there is no change in the overall Young's modulus of elasticity.

Animals↗
PubMed1978

The role of coronary adrenergic receptors in the response to nitroglycerine and the regulation of large and small vessel resistance.

The role of coronary adrenergic receptors in response to nitroglycerine and in the regulation of large and small coronary vascular resistance was evaluated in two separate studies involving fifteen anesthetized mongrel dog preparations, before and after alpha- and beta-adrenergic blockade, respectively. Coronary blood flow (CBF) was measured through the left anterior descending (LAD) coronary artery by a non-cannulating electromagnetic flow probe. Pressure catheters were inserted into the arch of the aorta and into a distal apical branch of the LAD coronary artery to measure, respectively, aortic pressure (coronary perfusion pressure (PA), peripheral coronary pressure )PC), and coronary artery pressure gradient (PG = PA -PC). End-diastolic resistances to flow were computed as: (a) large coronary end-diastolic resistance (RL = PG/CBF), and (B) small coronary end-diastolic resistance (RS = PC/CBF). Nitroglycerine (NG) alone increased RL to approximately 180--220% of control and reduced RS to about 60% of control, respectively. Following pharmacologic blockade with propranolol (PRO), NG increased RL to about 180% of control and reduced RS to about 60% of control. Following alpha blockade with phenoxybenzamine (PBZ), NG decreased RL to about 78% of control and decreased RS to about 56% of control. It is concluded that while the overall effect of NG on the coronary vascular resistance is one of vasodilation, RL appears to be increased transiently and RS transiently decreased. Alpha adrenergic blockade appears to abolish this response. The increase in RL in response to NG appears to be associated with the systemic hypotensive effect in response to NG. It is proposed that the observed increase in RL is produced by the increase in cardiac sympathetic nerve activity which is initiated by the systemic hypotensive effect of NG.

Animals↗
PubMed1975

Microvascular control in intestinal mucosa of normal and hemorrhaged rats.

The mucosal microcirculation in innervated and denervated small intestine was studied using anesthetized rats. Denervation did not cause significant (P greater than 0.05) diameter changes in the precapillary vasculature; however, venules did constrict significantly. These results indicate minimum neural control in the precapillary vasculature during the resting state. The innervated precapillary vasculature constricted during both the carotid occlusion reflex and hemorrhagic hypotension. The diameter of the denervated precapillary vasculature was unchanged during the carotid occlusion reflex and dilated during hemorrhage. The responses of innervated and denervated precapillary vasculatures were attributed to increased neural activity and autoregulatory mechanisms, respectively. Neither innervated nor denervated venules responded during the carotid occlusion reflex. During hemorrhage, however, innervated venules constricted and denervated vessels dilated. The vasoconstriction of the innervated vasculature during hemorrhage contributed to a stoppage of blood and epithelial detachment; these responses did not occur in the dilated, denervated vasculature. Therefore, neural vasoconstriction, qualitatively similar to that in normal animals during the baroreceptor reflex, is a contributing cause to the vascular and tissue impairment in the intestinal mucosa during hemorrhage.

Animals↗