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Home > Research > Some of Dr. David H. Streeten's Abstracts Regarding Orthostatic Intolerance (OI):

Some of Dr. David H. Streeten's Abstracts Regarding Orthostatic Intolerance (OI)

These are some examples of Orthostatic Intolerance (OI) being corrected with an inflatable pressure suit (MAST - military anti-shock trousers) providing lower body (abdomen and legs) compression of 45-50 mm Hg pressure.

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Delayed orthostatic intolerance.

Streeten DH, Anderson GH Jr.

Department of Medicine, State University of New York Health Science Center, Syracuse 13210.

Arch Intern Med 1992 May;152(5):1066-72

Comment in: Arch Intern Med 1992 May;152(5):919

In seven patients who presented with lightheadedness, fatigue, "weakness," and sometimes syncope, blood pressure was found not to fall after standing for 3 to 4 minutes but to fall severely, frequently with syncope or presyncopal symptoms, after 13 to 30 minutes when measured every minute with an automatic device. This delayed orthostatic hypotension could be corrected with inflation of a pressure suit to 45 mm Hg. Its mechanism was further investigated with measurements of plasma catecholamines, plasma cortisol and aldosterone responses to corticotropin, and the effects of norepinephrine infusions on blood pressure and venous contractility. There was normal or excessive orthostatic norepinephrine release in all patients, evidence of impaired venous innervation in the legs in some, and various disorders in the other patients. Since therapeutic improvement in the orthostatic hypotension greatly reduced the symptoms, we concluded that orthostatic hypotension occurring after more than 10 minutes of standing is a potentially debilitating and often correctable disorder.

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Orthostatic hypertension. Pathogenetic studies.

Streeten DH, Auchincloss JH Jr, Anderson GH Jr, Richardson RL, Thomas FD, Miller JW.

Hypertension 1985 Mar-Apr;7(2):196-203

Among 1800 referred hypertensive patients, 181 had recumbent diastolic blood pressures (DBP) below 90 mm Hg and standing DBP above 90 mm Hg. Orthostatic increments in DBP were greater in these orthostatic hypertensive patients than in 181 persistently hypertensive patients and 134 normotensive subjects. In 12 patients with orthostatic hypertension, the orthostatic fall in cardiac output (27.3 +/- 2.9%, measured by a respiratory method) was double that in 8 normotensive subjects (13.3 +/- 3.7%, p less than 0.01). An inflated pressure suit over the pelvis and lower limbs prevented the excessive fall in cardiac output and significantly reduced (p less than 0.02) the excessive rise in standing DBP in orthostatic hypertensive patients. Gravitational pooling of blood in the legs and reduction of blood in the head was measured by external gamma counting of autologous erythrocytes labeled with sodium pertechnetate Tc 99m through ports in fixed positions over the leg and the temple. Orthostatic intravascular pooling was significantly greater (p less than 0.01) in orthostatic hypertensive subjects than in normotensive subjects, and the magnitudes of orthostatic pooling and orthostatic increases in DBP were closely correlated (r = +0.85). Plasma norepinephrine concentrations were similar in recumbency and after sustained handgrip exercise, but significantly greater (p less than 0.01) after 5 to 60 mins of standing in orthostatic hypertensive subjects than in normotensive subjects. Our results indicate that orthostatic hypertension is common and that its mechanism in representative patients involves excessive orthostatic blood pooling, which results in decreased venous return, decreased cardiac output, increased sympathetic stimulation (presumably through low-pressure cardiopulmonary receptors), and excessive arteriolar, but not venular, constriction.

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Abnormal orthostatic changes in blood pressure and heart rate in subjects with intact sympathetic nervous function: evidence for excessive venous pooling.

Streeten DH, Anderson GH Jr, Richardson R, Thomas FD

Department of Medicine, SUNY Health Science Center, Syracuse 13210.

J Lab Clin Med 1988 Mar;111(3):326-35

The normal ranges of orthostatic changes in blood pressure and heart rate have been defined in 92 individuals aged 18 to 64 years. In 34 individuals whose symptoms (especially orthostatic light-headedness) suggested cerebral ischemia, but in whom none of the known causes of orthostatic hypotension could be identified, we have found one or more of five theoretically possible orthostatic circulatory derangements: systolic hypotension, diastolic hypotension, diastolic hypertension, excessive narrowing of the pulse pressure, and tachycardia after standing for at least 3 minutes. The orthostatic disorders of blood pressure and heart rate identified in the 34 patients were significantly reduced, almost always into the normal range, by external pressure of 45 to 50 mm Hg applied through an inflatable pressure suit. After labeling with sodium pertechnetate Tc 99m and reinjecting the erythrocytes contained in 3 to 6 ml blood, external gamma counting over a fixed site in the calf, both in the recumbent and in the standing posture, showed excessive gravitational pooling of blood in the legs of five patients with orthostatic diastolic hypertension, of four with orthostatic narrowing of the pulse pressure, and of 10 with orthostatic tachycardia alone. Plasma norepinephrine concentrations were usually normal in recumbency and elevated above normal limits during standing for 15 to 30 minutes in the 18 patients so observed. Red cell mass, plasma volume, and circulating blood volume were subnormal in more than half the seven patients in whom these measurements were made. We conclude that most of the patients with idiopathic sympathicotonic abnormalities of orthostatic blood pressure control have a venous pooling syndrome often aggravated by hypovolemia, the cause(s) of which remains to be determined.

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Vascular responsiveness to norepinephrine in sympathicotonic orthostatic intolerance.

Miller JW, Streeten DH.

Department of Medicine, State University of New York Health Science Center, Syracuse 13210.

J Lab Clin Med 1990 May;115(5):549-58

Sympathicotonic orthostatic intolerance (hypotension, tachycardia, or both) is associated with normal or excessive orthostatic increases in plasma norepinephrine concentration and is reversible by the inflation of a military anti-shock trouser suit enveloping the lower limbs and abdomen. These facts suggest that one possible mechanism of the disorder might be a defect in alpha-adrenergic receptor or postreceptor responsiveness of the veins or arterioles. We have investigated in 11 patients and 15 healthy controls the blood pressure and heart rate responses to increasing rates of intravenous norepinephrine infusion (1 to 16 micrograms/min), the dorsal hand vein contractile responses to increasing rates of norepinephrine infusion (1 to 256 ng/min) with a linear variable differential transformer, and the platelet alpha 2-adrenergic receptor densities and dissociation constants. No statistically significant difference in any of these parameters was found between the normal subjects and nine of the 11 patients with orthostatic intolerance. The venous contractile response to norepinephrine was excessive in one patient and was virtually absent in another. Because supersensitivity of the hand veins to norepinephrine suggests up-regulation of alpha 2-receptors resulting from postganglionic autonomic insufficiency, this finding in one patient with sympathicotonic orthostatic hypotension might have been caused by venous denervation. The venous unresponsiveness to norepinephrine in the other patient presumably resulted from a defect in the venous receptors or smooth muscle function. It is evident that norepinephrine responsiveness and the innervation of the arterioles and hand veins was normal in the other nine patients, in whom the defect must have been mediated by some other mechanism.

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Pathogenesis of hyperadrenergic orthostatic hypotension. Evidence of disordered venous innervation exclusively in the lower limbs.

Streeten DH.

Department of Medicine, State University of New York Health Science Center, Syracuse 13210.

J Clin Invest 1990 Nov;86(5):1582-8

The pathogenesis of hyperadrenergic orthostatic hypotension was studied in eight patients. Correction of the abnormal orthostatic changes by an inflated pressure suit (MAST) confirmed previous evidence of excessive gravitational pooling of blood in the leg veins. Intravenous L-norepinephrine infusion raised diastolic blood pressure in the same relationship to the infusion-induced increments in plasma norepinephrine concentrations as in normal subjects, indicating normal arteriolar responses. Contractile responses of the veins to infused L-norepinephrine were measured with a linear variable differential transformer (LVDT). The venous responses of hand veins in the patients fell within the 95% confidence limits of the responses of normal hand veins, as did the responses of foot veins in the seven normal subjects. However, foot veins of the patients with hyperadrenergic orthostatic hypotension, and both hand and foot veins of patients with "diffuse" autonomic failure, were supersensitive to norepinephrine, as reflected by a steeper slope of the regression of log (norepinephrine infusion rate) on percentage reduction in venous distensibility, and a significantly lower ED50 (i.e., norepinephrine infusion rate that induced 50% reduction in venous distensibility). The findings suggest anatomical or functional postganglionic denervation of lower limb veins causing excessive gravitational blood pooling with consequent orthostatic hypotension in these patients.

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Mechanisms of orthostatic hypotension and tachycardia in patients with pheochromocytoma.

Streeten DH, Anderson GH Jr.

Department of Medicine, State University of New York Health Science Center, Syracuse 13210, USA.

Am J Hypertens 1996 Aug;9(8):760-9

We have explored the pathophysiological mechanisms of orthostatic hypotension and orthostatic tachycardia, found to be present in 83% and 61% respectively of 18 patients with subsequently proven pheochromocytoma. Orthostatic increases in plasma norepinephrine (NE) concentrations were significantly greater in the patients than in normal control subjects. Intravenous infusions of NE at 1, 2, 4, 8, and 16 micrograms/min induced similar increases in plasma NE levels but smaller increments in systolic and diastolic BP in the pheochromocytoma patients than in normal control subjects. This was reflected by a significantly greater increment in plasma NE concentration required to raise systolic BP by 15 mm Hg and diastolic BP by 7 mm Hg in the pheochromocytoma patients than in the normal subjects (P < .05 and P < .01, respectively). Measurements of venous contractile responses to locally infused NE by the dorsal hand vein (LVDT) technique revealed significantly reduced slopes of the regressions of log NE infusion rate on change in venous diameter in the pheochromocytoma patients compared with normal subjects. The results indicate reduced responsiveness of the vasculature to NE in patients with pheochromocytoma, probably due to down-regulation of alpha-adrenergic receptors resulting from persistent elevation of the physiological agonist NE. This was shown by other authors to be present in circulating platelets. The pathophysiological importance of the subnormal venous responses to the orthostatic hypotension and tachycardia in the patients were supported by the finding that the orthostatic changes were corrected by lower body compression to 45 mm Hg with a MAST pressure suit.

Copyright © 1985, 1988, 1990, 1992, 1996 by Dr. David H. Streeten

Note: These are PubMed abstracts. Bold has been added for emphasis on use of inflatable pressure suit (MAST).

Note: Dr. David H. Streeten died September of 2000. His research and understanding of Orthostatic Intolerance (OI) will always be greatly appreciated.

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