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Biomedical subjects

P M Trivedi

Publications and source records attributed to P M Trivedi.

9 recordsLinked to original sources

Preoperative cardiac drug administration in general surgical patients: A completed audit.

The aim of this study was to audit the preoperative administration of regular cardiac medication in general surgical patients and to determine if this can be improved with simple ward-based education. The notes and drug charts of 102 general surgical adult inpatients undergoing elective operations were analysed prospectively. It was noted whether the patient was on regular morning cardiac medication, whether this was given and, if not, whether a reason was recorded on the drug chart. An information sheet and brief verbal reinforcement was given to nursing staff and junior doctors and the review repeated in 111 patients. There was no significant difference in the number of patients on regular cardiac medication between the two review groups; 42% patients had one or more drugs omitted in the initial review. After education this reduced significantly to 20% (p = 0.023). When omissions on medical instruction were excluded, this became highly significant (p = 0.0029). There was also a significant decrease in the number of times 'nil by mouth' was stated as the reason for omission. As a general principle, all regular cardiac medication should be given preoperatively even when nil by mouth as there is evidence that abrupt withdrawal can have serious consequences. This audit demonstrates that with simple education, the proportion of regular cardiac drugs administered preoperatively can be significantly increased.

Cardiovascular Agents↗

Brain-derived neurotrophic factor modulates nociceptive sensory inputs and NMDA-evoked responses in the rat spinal cord.

Central sensitization, the hyperexcitability of spinal processing that often accompanies peripheral injury, is a major component of many persistent pain states. Here we report that the neurotrophin, brain-derived neurotrophic factor (BDNF), is a modulator of excitability within the spinal cord and contributes to the mechanism of central sensitization. BDNF, localized in primary sensory neuron cell bodies and central terminals, potentiates nociceptive spinal reflex responses in an in vitro spinal cord preparation and induces c-fos expression in dorsal horn neurons. NMDA receptor-mediated responses, known as a major contributor to central sensitization, were significantly enhanced by exogenous BDNF. Systemic NGF treatment, a procedure that mimics peripheral inflammatory states, raises BDNF levels in sensory neurons and increases nociceptive spinal reflex excitability. This increased central excitability is reduced by trkB-IgG, a BDNF "antagonist." We also show directly that inflammatory pain-related behavior depends on BDNF release in vivo. Thus behavioral nociceptive responses induced by intraplantar formalin and by intraplantar carageenan are significantly attenuated by trkB-IgG. Hence BDNF is appropriately localized and regulated in inflammatory states and is sufficient and necessary for the expression of central sensitization in the spinal cord. We propose that BDNF may function as a modulator of central sensitization in pathological states, and our results suggest that pharmacological antagonism of BDNF may prove an effective and novel analgesic strategy for the treatment of persistent inflammatory pain states.

Animals↗

Hookworm anaemia.

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Anemia, Hypochromic↗