Nitric oxide and thromboxane A2-mediated pulmonary microvascular dysfunction

OBJECTIVES: To examine whether the lung releases nitric oxide (NO) in response to thromboxane A2 and to examine the local release of NO as a protective compensatory mechanism by which the lung responds to the proinflammatory and vasoactive effects of thromboxane A2. DESIGN: The lungs of anesthetized Sprague-Dawley rats were perfused in vitro with Krebs-Henseleit buffer that contained an inhibitor of NO synthase (nitroglycerinenitro-L-arginine methyl ester [L-NAME]) (10(-4) mol/L), an NO donor (sodium nitroprusside) (10(-8) mol/L), or perfusate alone. Following equilibration, the thromboxane A2 receptor agonist 9,11-dideoxy-11alpha, 9alpha-epoxymethanoprostaglandin F2alpha(U-46619) (7.1 X 10(-8) mol/L) was added to the perfusate. Fifteen minutes later, the capillary filtration coefficient, pulmonary arterial pressure, and vascular resistance were measured. Pulmonary NO release was assessed by quantitating the release of cyclic guanosine monophosphate into the perfusate. RESULTS: The capillary filtration coefficient of lungs exposed to U-46619 was 3.5 times greater than that of lungs perfused with buffer alone (P<.05). The addition of sodium nitroprusside reduced the increase in capillary filtration coefficient associated with U-46619 by 50% (P<.05) whereas L-NAME had no effect. The addition of U-46619 to the perfused lung caused a 3.0+/-0.4 mm Hg increase in pulmonary artery pressure (P<.01) with a corresponding rise in total vascular resistance (P<.05). This effect was exacerbated by L-NAME (P<.05) and inhibited by sodium nitroprusside (P<.05). Exposure of the isolated lungs to U-46619 caused a 4-fold increase in cyclic guanosine monophosphate levels within the perfusate. CONCLUSION: These data are consistent with the hypothesis that NO release may be an important protective mechanism by which the lung responds to thromboxane A2.     

The cerebellum is necessary for rabbit classical eyeblink conditioning with a non-somatosensory (photic) unconditioned stimulus

The present research investigated the acquisition of classically conditioned eyeblinks in rabbits using a light flash unconditioned stimulus (US), as well as the contribution of deep cerebellar nuclei to such an association. Two independent groups of animals experienced three phases of training: (1) pre-lesion delay conditioning using either a light- (Group 1) or an air puff-US (Group 2), (2) post-lesion testing of response performance, and (3) post-lesion acquisition to the opposite US. During the initial acquisition (720 trials), the groups did not differ with regard to their rate of learning or their overall level of responding. To assess the contribution of the cerebellum to the maintenance of responding, the interpositus nucleus was electrolytically lesioned and animals were given 8 days of additional training. Both groups exhibited a profound reduction in conditioned responding (CR) and showed no signs of recovery over the remainder of this phase (480 trials). Animals were then shifted to the opposite US (same eye) and given 12 days of training to assess the effect of interpositus lesions on the acquisition of CRs to a novel US. No learning was observed during this phase, regardless of whether animals experienced the light- or air puff-US. These results demonstrate: (1) the ability of a non-somatosensory stimulus to serve as a US during classical eyeblink conditioning; and (2) a common reliance on deep cerebellar nuclei for both somatosensory- and non-somatosensory-based reflexive motor learning. The findings are discussed in reference to the processing of conditioning stimuli within the brainstem-cerebellar circuitry that underlies eyeblink conditioning.     

The trough line: a radiographic sign of posterior shoulder dislocation.

Over 50% of posterior dislocations of the shoulder are not recognized initially because of failure to appreciate the subtle clues available on the standard frontal projection. In 15 of 20 cases of posterior dislocation, two parallel lines of cortical bone were identified on the medial aspect of the humeral head. One line represents the medial cortex of the humeral head. The other was found to represent the margin of a troughlike impaction fracture. This is designated the "trough line". This line proved to be an important clue in the recognition of posterior dislocations of the shoulder.