Publications by authors named "P Reinstrup"

The cerebral blood flow, CBF, is an important clinical parameter in neuro-intensive care. The possibility to continuously monitor CBF, computed from referential ICP, rICP (calculated from measured intracranial pressure, ICP, and central venous pressure, CVP) and venous outflow resistance, Rv, could importantly improve patient care. For the CBF(1) method the pulsative part of CBF (with rICP increase due to vascular volume increase) gives the venous outflow resistance, Rv.

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The intracranial pressure (ICP) curve with its different peaks has been comprehensively studied, but the exact physiological mechanisms behind its morphology has not been revealed. If the pathophysiology behind deviations from the normal ICP curve form could be identified, it could be vital information to diagnose and treat each single patient. A mathematical model of the hydrodynamics in the intracranial cavity over single heart cycles was developed.

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The physiology underlying the intracranial pressure (ICP) curve morphology is not fully understood. Recent research has suggested that the morphology could be dependent on arterial cerebral inflow and the physiological and pathophysiological properties of the intracranial cavity. If understood, the ICP curve could provide information about the patient's cerebrovascular state important in individualizing treatment in neuro intensive care patients.

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Background: The underlying physiology of the intracranial pressure (ICP) curve morphology is still poorly understood. If this physiology is explained it could be possible to extract clinically relevant information from the ICP curve. The venous outflow from the cranial cavity is pulsatile, and in theory the pulsatile component of venous outflow from the cranial cavity should be attenuated with increasing ICP.

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Neutrophils are crucial mediators of host defense that are recruited to the central nervous system (CNS) in large numbers during acute bacterial meningitis caused by Streptococcus pneumoniae. Neutrophils release neutrophil extracellular traps (NETs) during infections to trap and kill bacteria. Intact NETs are fibrous structures composed of decondensed DNA and neutrophil-derived antimicrobial proteins.

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