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Thyrotropin-releasing hormone (TRH) injected into the retrotrapezoid nucleus (RTN) of anesthetized rats produces a large, prolonged stimulation of ventilatory output (C. L. Cream, A. Li, and E. E. Nattie. J. Appl. Physiol. 83: 792-799, 1997). Here we inject or dialyze TRH into the RTN of conscious rats. In 6 of 17 injections (200 nl, 3.1 +/- 1.7 mM), ventilation (VE) increased 31% by 10 min, with recovery by 60 min. With dialysis, each animal of one group (n = 5) received, in random order, 10 mM TRH, 10 mM TRHOH (a metabolite of TRH), and artificial cerebrospinal fluid (aCSF); each animal of a second group (n = 5) received aCSF and 1 mM TRH. TRHOH and aCSF had no sustained effects. TRH (1 mM) increased VE (32%, P < 0.02, by 10 min, with recovery by 60 min), O(2) consumption (VO(2); 19%, P < 0. 03), and body (rectal) temperature (T(re); 0.5 degrees C, P < 0.09). TRH (10 mM) increased VE (78%, P < 0.01, by 10 min, with no recovery at 60 min), VO(2) (48%, P < 0.01), and T(re) (1.0 degrees C, P < 0. 01). TRH also induced arousal. The tissue volume affected in dialysis, estimated by spread of dialyzed fluorescein (332.3 mol wt, mol wt of TRH = 362.4), was 1,580 +/- 256 nl for 10 mM (n = 5) and 590 +/- 128 nl for 1 mM (n = 5). We conclude that 1) the RTN is involved in the integration of VE, VO(2), T(re), and arousal and 2) TRH may establish the responsiveness of RTN neurons.

We injected thyrotropin-releasing hormone (TRH; 10 nl; 0.25, 0.5, 1.0, or 10 mM), its inactive free acid form (TRHOH; 1 mM), or a metabolite with low TRH-receptor binding affinity, histidine-proline diketopiperazine (cHP; 1 mM), into the retrotrapezoid nucleus of anesthetized rats. Injection location was verified by anatomic analysis. Lower doses (0.25-0.5 mM) significantly increased both the product of integrated phrenic amplitude and frequency (Phr . f) and f for 20-30 min compared with artificial cerebrospinal fluid control injections. Higher doses (1. 0-10 mM) produced greater and long-lasting stimulation of Phr . f, Phr, and f and of blood pressure. This stimulation reached values 150% of baseline and durations of 270 min after a single injection. TRHOH (1 mM ) or cHP (1 mM) had no effect on Phr but increased f, as did 1 mM TRH. We conclude that TRH has a very powerful stimulatory effect in the retrotrapezoid nucleus region on Phr . f, with the Phr response seemingly specific for TRH receptors. Similar responses of f to TRHOH and cHP suggest it may be nonspecific.

Background Pasteurella multocida is a gram-negative pathogen commonly associated with soft tissue infections caused by bites or scratches from household animals. However, P. multocida infections have been reported without prior zoonotic exposure or associated soft tissue or skin infection in immunocompromised individuals. Case A 73-year-old patient with history significant for multiple malignancies including lung cancer presented to the emergency department with a fever, chills, and rigor. Patient denied any zoonotic exposure and did not have any soft tissue or skin structure infection. Laboratory testing and imaging revealed sepsis secondary to pneumonia and further lower respiratory cultures grew Pasteurella . Subsequent laboratory cultures indicated P. multocida bacteremia. Conclusion This case aims to advance awareness of the possibility of P. multocida infection in patients who do not have any known zoonotic exposure or identifiable skin or soft tissue infection. Nasopharyngeal colonization in immunocompromised individuals could be a source for invasive infection. Patients who have a pre-existing lung disease are susceptible for developing Pasteurella pneumonia, which can serve as the source of bacteremia.

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