Previous studies in our laboratory have demonstrated that cannabinoids administered intravenously attenuate the duration of nocifensive behavior and block the development of hyperalgesia produced by intraplantar injection of capsaicin. In the present study, we extended these observations and determined whether cannabinoids attenuate capsaicin-evoked pain and hyperalgesia through spinal and peripheral mechanisms, and whether the antihyperalgesia was receptor mediated. Separate groups of rats were pretreated 7 min before capsaicin with an intrathecal injection of vehicle or the cannabinoid receptor agonist WIN 55,212-2 at doses of 0.1, 1.0 or 10 microg in 10 microl. Although the intrathecal application of WIN 55,212-2 did not alter nocifensive behavior following capsaicin, it produced a dose-dependent decrease in hyperalgesia to heat and mechanical stimuli. Intrathecal pretreatment with the CB1 receptor antagonist SR141716A (10 microg) blocked the antihyperalgesia produced by WIN 55,212-2. The ability of intrathecal administration of WIN 55,212-2 to attenuate hyperalgesia was not due to motor deficits since the highest dose of WIN 55,212-2 did not alter performance on the rota-rod test. To investigate whether cannabinoids attenuated capsaicin-evoked hyperalgesia through peripheral mechanisms, separate groups of rats were pretreated with an intraplantar injection of WIN 55,212-2 at doses of 0.1, 1.0, 10 or 30 microg in 100 microl 5 min before capsaicin. Intraplantar pretreatment with WIN 55,212-2 produced a dose-dependent attenuation of hyperalgesia to heat, but did not attenuate mechanical hyperalgesia or the duration of nocifensive behavior. The inactive enantiomer WIN 55,212-3 did not alter the development of hyperalgesia. SR141716A (100 microg) co-injected with WIN 55,212-2 (30 microg) partially attenuated the effects of WIN 55,212-2 on hyperalgesia to heat. Intraplantar injection of the highest dose of WIN 55,212-2 did not interfere with the development of hyperalgesia following capsaicin injection into the contralateral paw. These data show that cannabinoids possess antihyperalgesic properties at doses that alone do not produce antinociception, and are capable of acting at both spinal and peripheral sites.
Cold‐freeze injury at −4 degrees C to the rat sciatic nerve produces mechanical allodynia and thermal hyperalgesia [M.A. Kleive, P.S. Jungbluth, J.A. Uhlenkamp, K.C. Kajander, Cold injury to rat sciatic nerve induces thermal hyperalgesia or analgesia, 8th World Congress on Pain, Vancouver, BC, Canada, August 1996 (Abstract).]. The NMDA receptor, an excitatory amino acid (EAA) receptor, appears to be involved in the development of allodynia and hyperalgesia following nerve injury. The role, if any, of the kainate receptor, another EAA receptor, remains unknown. In the current study, we evaluated whether (2S,4R)‐4‐methylglutamic acid (SYM‐2081), a recently developed kainate receptor antagonist, attenuates increased responsiveness following cold injury to the sciatic nerve. During baseline testing, Sprague‐Dawley rats were evaluated for frequency of withdrawal from van Frey filaments and latency of withdrawal from a radiant thermal source. Animals were then anesthetized, the left sciatic nerve was exposed, and the nerve was cooled to −4 degrees C for 15 min (n = 24). For control rats (n = 24), all procedures were identical except that the nerve was maintained at 37 degrees C. Testing resumed on the third day following surgery. On the fifth post‐operative day, SYM‐2081 (150 or 100 mg/kg), fentanyl citrate (0.04 mg/kg) or vehicle was injected intraperitoneally. Injury to the rat sciatic nerve induced a significant increase in withdrawal frequency and a significant decrease in withdrawal latency (ANOVA, p < 0.05). SYM‐2081 and fentanyl significantly reduced these responses (p < 0.05). These results suggest that kainate and opioid receptors are involved in the mechanical allodynia and thermal hyperalgesia that develop following cold injury to the sciatic nerve.
There has been a significant amount of interest in developing a more rapid and cost-effective test to identify bacterial pathogens in plaque. DNA probe technology may meet both these objectives, it is more rapid and cost-effective when compared to culture methods. The purpose of this study was to compare an automated DNA probe test with classical culture methods for identifying Bacteroides forsythus and Porphyromonas gingivalis in subgingival plaque of patients with adult periodontitis. Subgingival plaque samples were collected from sites with moderate to severe periodontitis and divided into two aliquots for analysis by either DNA probe or culture methods. When the DNA probe method was compared with the culture method (gold standard), the sensitivity and specificity for B. forsythus were 92.0% (SE = 3.4%) and 50.5% (SE = 7.8%), respectively; for P. gingivalis they were 52.2% (SE = 8.7%) and 74.7% (SE = 5.9%), respectively. Detection of B. forsythus and P. gingivalis by DNA probe correlated with probing depth (P = 0.01 for B. forsythus and P = 0.03 for P. gingivalis). It was concluded the DNA probe test was comparable to culture methods in detecting B. forsythus. In addition, when compared to the culture method, a better correlation was obtained with DNA probe detection of B. forsythus or P. gingivalis and clinical parameters.
Coronary artery bypass grafting improves 3-year survival by approximately 30% to 50% and physical functioning by approximately one New York Heart Association class in patients with moderate to severe left ventricular dysfunction and limiting angina. However, the operative mortality ranges from 5% to 30% depending on patients' ejection fractions and comorbidity. It is not clear whether patients whose predominant symptom is heart failure rather than angina benefit from bypass surgery or how much ischemia is required to justify surgical intervention. Clinical outcomes after angioplasty have not been adequately studied to determine the relative risks and benefits compared with bypass grafting.
A two‐frequency radar was operated at Homer, Alaska, to determine the wavelength dependence between 139‐ and 398‐Mhz auroral echoes. The 139‐Mhz radar echoes were, on the average, 22 db greater in amplitude than those received with the 398‐Mhz radar, resulting in a wavelength dependence of λ5. In addition, a trend for the amplitude difference to grow larger as the echoes increased in amplitude was found. Doppler measurements confirm a velocity for the electron irregularities of about 400 km/sec from east to west before magnetic midnight.
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