Publications by authors named "M Zaar"

Exercise facilitates cerebral lactate uptake, likely by increasing arterial lactate concentration and hence the diffusion gradient across the blood-brain barrier. However, nonspecific β-adrenergic blockade by propranolol has previously reduced the arterio-jugular venous lactate difference (AV) during exercise, suggesting β-adrenergic control of cerebral lactate uptake. Alternatively, we hypothesized that propranolol reduces cerebral lactate uptake by decreasing arterial lactate concentration.

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Background: To study central hypovolemia in humans, lower body negative pressure (LBNP) is a recognized alternative to blood removal (HEM). While LBNP mimics the cardiovascular responses of HEM in baboons, similarities in hemostatic responses to LBNP and HEM remain unknown in this species.

Methods: Thirteen anesthetized baboons were exposed to progressive hypovolemia by HEM and, four weeks later, by LBNP.

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Article Synopsis
  • This study investigated how adrenaline affects blood clotting using thrombelastography (TEG) and Multiplate analyses in both splenectomized individuals and healthy controls.
  • Healthy subjects showed significant improvements in clot formation and platelet activity after adrenaline infusion, while splenectomized subjects only experienced a reduction in time to initial fibrin formation.
  • In liver transplant patients, adrenaline also enhanced clot formation during a critical surgical phase, reinforcing the idea that the spleen plays a major role in adrenaline's boost to hemostatic competence.
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Heat stress followed by an accompanying hemorrhagic challenge may influence hemostasis. We tested the hypothesis that hemostatic responses would be increased by passive heat stress, as well as exercise-induced heat stress, each with accompanying central hypovolemia to simulate a hemorrhagic insult. In aim 1, subjects were exposed to passive heating or normothermic time control, each followed by progressive lower-body negative pressure (LBNP) to presyncope.

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This study examined to what extent the human cerebral and femoral circulation contribute to free radical formation during basal and exercise-induced responses to hypoxia. Healthy participants (5♂, 5♀) were randomly assigned single-blinded to normoxic (21% O) and hypoxic (10% O) trials with measurements taken at rest and 30 min after cycling at 70% of maximal power output in hypoxia and equivalent relative and absolute intensities in normoxia. Blood was sampled from the brachial artery (a), internal jugular and femoral veins (v) for non-enzymatic antioxidants (HPLC), ascorbate radical (A, electron paramagnetic resonance spectroscopy), lipid hydroperoxides (LOOH) and low density lipoprotein (LDL) oxidation (spectrophotometry).

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