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In the present study we sought evidence for the hypothesis that norepinephrine (NE) can cause constriction of lymph vessels in the canine forelimb perfused at constant flow. Mechanical venous compression (small-vein pressure approximately equal to 45 mmHg), intra-arterial infusion of histamine (16
Regional left ventricular myocardial blood flow was studied in an experimental model of pulmonary edema and microembolization (PEM) ventilated with positive end-expiratory pressure (PEEP). The analysis was based on a 3-dimensional extension of the autocorrelation function used to assess the spatial
The effects of intraventricular application of norepinephrine (NE) on the development of vasogenic edema was studied in mongrel dogs randomly divided into a control and an experimental group (NE group). Vasogenic edema was produced by infusion of a 2.0 M NaCl solution (hypertonic saline)
Unilateral cerebral contusion is associated with an early (30 min) increase in norepinephrine (NE) turnover followed by a later (6-24 h) depression of turnover which is bilateral and widespread throughout the brain. Blockade of NE function during the first few hours after traumatic brain injury
Pulmonary edema and hemorrhage (PEH) was induced in rats by cerebral compression and intraveneous norepinephrine. We used scintiphotographic method to demonstrate the blood volume change in the lung subsequent to the hemodynamic events that cause PEH. A specific isotope, Indium-113m, was chosen for
The role of norepinephrine and excitatory amino acids in edema of the spinal cord after an acute experimental compression injury was studied in rats. Control rats received the compression injury only. Intraspinal norepinephrine was depleted in one rat group by injection of 6-hydroxydopamine (6-OHDA)
Arterial concentrations of given norepinephrine (NE) were measured after bolus administration in dogs with normal lungs and in those with oleic acid-induced lung edema. In both groups, the peak NE concentration was given by blood samples taken 30 sec after injection and the concentration showed a
OBJECTIVE
Reduction of cerebral perfusion during the early phase after traumatic brain injury is followed by a later phase of normal to increased perfusion. Thus, pharmacologically elevating mean arterial blood pressure with the aim of improving cerebral perfusion may exert different time-dependent
N-Methylthiobenzamide (NMTB) is a pneumotoxin which causes pulmonary edema and hydrothorax in rodents. Reserpine has been shown to attenuate the pneumotoxicity induced by NMTB. Some of that evidence suggests that the protection afforded by reserpine occurs independently of its capacity to reduce
Biomarkers are essential to unravel the locked pathophysiology of any disease. This study investigated the role of biomarkers and their interactions with each other and with the clinical parameters to study the physiology of high-altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) against
Following traumatic brain injury, catecholamines given to ameliorate cerebral perfusion may induce brain damage via cerebral arteriolar constriction and increased neuronal excitation. In the present study the acute effects of norepinephrine and dopamine on pericontusional cortical perfusion (rCBF),
Stimulation with norepinephrine (NE) leads to pulmonary edema and pleural effusion in rats. These pulmonary fluid shifts may result from pulmonary congestion due to the hemodynamic effects of NE and/or inflammation with an increase in vascular permeability. The contribution of these two factors were
We investigated the effects of acute hypoxia (10% O2) on plasma level of atrial natriuretic peptide (ANP) and pulmonary hemodynamics in five subjects with a history of high-altitude pulmonary edema (HAPE). Plasma renin activity and plasma levels of aldosterone, epinephrine and norepinephrine were