Whole blood viscosity parameters and cerebral blood flow.

Grotta, James C.; Ackerman, Robert H.; Correia, John A.; Fallick, G; Chang, Joshua

doi:10.1161/01.str.13.3.296

Cited by 210 publications

(92 citation statements)

References 36 publications

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“…These differences in hemodynamic responses may be attributed to the difference in pharmacological action between calcium channel blockers and L-arginine. Blood viscosity is a parameter that defines the blood velocity (45)(46)(47). Therefore, effects on blood viscosity may provide a possible explanation of the difference in pharmacological action between calcium channel blockers and L-arginine.…”

Section: Discussionmentioning

confidence: 99%

Low-dose l -arginine administration increases microperfusion of hindlimb muscle without affecting blood pressure in rats

Ohta

Takagi

Sato

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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The objective of this work was to evaluate the influence of exogenous L-arginine on the capillary blood flow of peripheral tissues of normotensive subjects. Rats were anesthetized with sodium pentobarbital, and the blood flow of femoral, dorsal, and ventral skin and gastrocnemius and soleus muscle was measured by laser Doppler flow and microsphere methods to compare the blood flow before and after the L-arginine infusion. L-Arginine lowered the mean blood pressure in a dose-dependent manner, but a statistically significant reduction in mean blood pressure was detected only at a high dose of 500 mg/kg of body weight. The significant blood flow increment was detected after the L-arginine infusion at doses of 50 and 150 mg/kg without causing hypotension. Nicardipine, a calcium channel blocker, also increased the skin blood flow, but the blood flow increment and blood pressure fall were comparable. A significant increment in microperfusion was detected in gastrocnemius, soleus muscle, and ventral skin compared with control group by the microsphere method. No adverse effects were observed during L-arginine and microsphere infusion. The present work indicates that L-arginine infusion increases muscle capillary blood flow in rats that are not performing exercise. Supplementation with L-arginine might provide additional blood flow at rest and during exercise and result in the improvement of muscle performance and exercise capacity.exercise ͉ nitric oxide N itric oxide (NO) is a widespread signaling molecule that is involved in mammalian physiological processes including the relaxation of blood vessels (1-3), immune function (4), inhibition of platelet aggregation (5, 6), and neurotransmission (7). The amino acid L-arginine is the natural precursor for the formation of NO (8), and exogenous L-arginine administration causes the relaxation of blood vessels through the action of NO (9, 10). Although NO synthase, the enzyme that produces NO from L-arginine, is theoretically saturated with its natural substrate, exogenous L-arginine administration leads to increased NO production, and this phenomenon is known as the arginine paradox (9, 10). Therefore, many investigators have been interested in the effects of supplementation with L-arginine to produce increased beneficial effects of NO, including prevention of the progression of atherosclerosis (11, 12), prevention of pulmonary artery endothelial dysfunction (13, 14), enhancement of cellular immune response of T lymphocytes (4), and amelioration of hypertension (15,16). Other studies indicate that oral supplementation of L-arginine also corrects endothelial dysfunction of chronic heart failure (17), and it increases exercise capacity in patients with precapillary pulmonary hypertension by increasing peak oxygen consumption and decreasing pulmonary arterial pressure and pulmonary vascular resistance thorough the action of NO (18).Because oxygen and carbon dioxide exchange takes place only in the capillary bed, the peripheral blood flow correlates with the rate of oxygen uptake...

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Section: Discussionmentioning

confidence: 99%

Low-dose l -arginine administration increases microperfusion of hindlimb muscle without affecting blood pressure in rats

Ohta

Takagi

Sato

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…One study found an inverse relation between Hct and cerebral blood flow. 10 Another described a higher baseline Hct value to be independently associated with infarct growth and a lesser chance of successful reperfusion after acute ischemic stroke. 11 Several studies demonstrated a U-shaped relation between outcome parameters and Hct levels, 9,12-14 suggesting an optimal midrange Hct level between 42% and 45%.…”

mentioning

confidence: 99%

Cerebral Oxygen Transport Failure?: Decreasing Hemoglobin and Hematocrit Levels After Ischemic Stroke Predict Poor Outcome and Mortality

Kellert

Martín²,

Sýkora³

et al. 2011

Stroke

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Background and Purpose-Although conceivably relevant for penumbra oxygenation, the optimal levels of hemoglobin (Hb) and hematocrit (Hct) in patients with acute ischemic stroke are unknown. Methods-We identified patients from our prospective local stroke database who received intravenous thrombolysis based on multimodal magnet resonance imaging during the years 1998 to 2009. A favorable outcome at 3 months was defined as a modified Rankin Scale score Յ2 and a poor outcome as a modified Rankin Scale score Ն3.

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“…We interpret this finding in the following way: when studied early, acute-phase responses in stroke patients may be primarily related to events other than the stroke, (e.g., prior infection); beyond 48 hours, acute-phase responses from the stroke itself predominate, resulting in comparable fibrinogen levels for patients with and without infection. Increased fibrinogen levels may contribute to the pathogenesis of cerebral infarction by multiple mechanisms; there is an inverse relation between fibrinogen levels and cerebral blood flow, 32 middle cerebral artery blood velocity in the elderly, 33 cerebral vascular reactivity, 34 and, perhaps, fibrinolytic activity. 35 In addition, fibrinogen serves as the major intercellular link for platelet aggregation via the glycoprotein Ilb-IIIa complex.…”

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confidence: 99%

Immunohematologic characteristics of infection-associated cerebral infarction.

Ameriso

Wong

Quismorio

et al. 1991

Stroke

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We evaluated 50 consecutive patients with acute ischemic stroke to assess the prevalence of systemic infection preceding the neurological event We analyzed the immunohematologic characteristics of patients with and without signs and/or symptoms of a preceding infectious process. Patients were examined <,7 days after cerebral infarction and evaluated for fibrinogen, anticardiolipin antibodies, fibrin D-dimer (a fragment of cross-linked fibrin), plasminogen activator inhibitor-1, and protein S. Of the 50 patients, 17 had symptoms of infection beginning <,l month before the stroke (11 had upper respiratory tract infections, three urinary tract infections, two subacute bacterial endocarditis, and one pneumonia). Compared with patients without infection, patients with infection had significant increases in fibrin D-dimer concentration (53±1.1 versus 4.7±0.9 log-transformed ng/ml,/?<0.05) and cardiolipin immunoreactivity, IgG isotype (1.8±1J versus l.l ±0.9 log-transformed phospholipid units,p<0.04), and, when studied r s 2 days after the stroke, increased fibrinogen levels (459±126 versus 360±94 mg/dl, p<0.Q5). In conclusion, infection-associated cerebral infarction is common and is associated with substantial immunohematologic abnormalities. (Stroke 1991^22:1004-1009)

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Whole blood viscosity parameters and cerebral blood flow.

Cited by 210 publications

References 36 publications

Low-dose l -arginine administration increases microperfusion of hindlimb muscle without affecting blood pressure in rats

Low-dose l -arginine administration increases microperfusion of hindlimb muscle without affecting blood pressure in rats

Cerebral Oxygen Transport Failure?: Decreasing Hemoglobin and Hematocrit Levels After Ischemic Stroke Predict Poor Outcome and Mortality

Immunohematologic characteristics of infection-associated cerebral infarction.

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