[Analgesic effect of buccal acupuncture on acute arthritis in rabbits and underlying mechanisms].

OBJECTIVE: To observe the analgesic effect of acupuncture and to explore its central analgesic mechanism in rheumatoid arthritis rabbits.
 Methods: A total of 60 flap-eared white rabbits were randomly assigned into a normal control group (n=6), a model group (n=6), a body-acupuncture group (n=24), and a buccal acupuncture group (n=24). The later 2 groups were further randomly assigned into 0, 0.5, 1, and 2 h subgroups, with 6 cases in each group. The rheumatoid arthritis model was established by induction of egg-albumin. In the body acupuncture group, bilateral "Xiyan" and "Zusanli" were punctured for 15 s while in the buccal acupuncture group, acupuncture was applied to "Xi" for 15 s, with the needle retaining for 30 min. The pain threshold was detected with PL-200, taking struggle movements of rabbits as a measurement index, response latency from irradiation to struggling movements as the rabbit's pain threshold. The contents of ß-endorplhin (ß-EP) and cholecystokinin-8 (CCK-8) in cerebrospinal fluid were examined by radioimmunoassay.
 Results: Compared with the control group, pain threshold and CCK-8 levels decreased significantly (P<0.01) and the concentration of ß-EP significantly increased (P<0.05) in the model group. The pain threshold in the body-acupuncture group and the buccal acupuncture group at 0 and 1 h (P<0.05 or P<0.01) increased significantly, while the ß-EP and CCK-8 contents in the body-acupuncture group and the buccal acupuncture group were significantly higher than those in the model group (P<0.01 or P<0.05). Both ß-EP and CCK-8 contents in the buccal acupuncture group at 0 h were significantly higher than those in the body-acupuncture group (P<0.05).
 Conclusion: The analgesic effect of buccal acupuncture is superior to that of body-acupuncture. Both buccal acupuncture and body-acupuncture can effectively raise the pain threshold in acute arthritis rabbits, which is closely associated with their effects in the up-regulation of ß-EP and CCK-8 contents in cerebrospinal fluid.

Decreased cholecystokinin levels in cerebrospinal fluid of patients with adult chronic hydrocephalus syndrome.

Cholecystokinin (CCK) levels were measured in cerebrospinal fluid (CSF) of patients with adult chronic hydrocephalus syndrome (ACHS) (n = 16) and compared with levels from a control group (n = 11). The CSF concentration of CCK in the ACHS group (0.79 +/- 0.53 fmol/mL) was significantly reduced (p = .002) with respect to the controls (1.55 +/- 0.54 fmol/mL). As CCK-8, the most prevalent from of CCK in the central nervous system, has been demonstrated to play a significant role in several physiological and behavioral actions, the reduced octapeptide values found in ACHS could be involved in the disturbances associated with this disorder. Continuous monitoring of intracranial pressure (ICP) demonstrated different ICP profiles in ACHS. We found that all patients with abnormal ICP records except one showed CCK values under the detection limit. Three of the 4 patients with normal ICP had CCK levels within the normal range. These preliminary studies could evidence that ICP alterations are responsible for part of the loss of brain neuropeptide levels in ACHS.

CSF cholecystokinin octapeptide in patients with bulimia nervosa and in normal comparison subjects.

Cholecystokinin octapeptide (CCK-8) appears to modulate appetitive behavior, and in rodents, anxiety-related behavior. The authors studied CCK-8 in patients with bulimia nervosa. CSF concentrations of CCK-8 were measured in 11 drug-free female patients with DSM-III-R-defined bulimia nervosa and in 16 normal subjects. The bulimic patients had significantly lower levels of CCK-8 than the comparison subjects. CCK-8 concentrations were inversely correlated with scores on the anger-hostility, anxiety, and interpersonal sensitivity subscales of the SCL-90-R. They were not significantly correlated with age, percentage of standardized average body weight, or mean weekly frequency of binge eating or vomiting. The results indicate that central CCK-8 abnormalities may play a role in the pathophysiology of bulimia nervosa.

Cholecystokinin peptides in cerebrospinal fluid: a study in healthy male subjects.

The clinical reliability of measuring cholecystokinin (CCK) peptides in the cerebrospinal fluid (CSF) has not been fully elucidated. Therefore, we have assayed CCK-8S and CCK-4 in CSF obtained from 14 healthy male subjects, lumbar-punctured at the L4-5 level following a strictly standardised procedure. CSF concentrations of free CCK-8S and free CCK-4 were used as dependent variables while age, height, body weight, atmospheric pressure and some other factors served as independent variables. It was shown that the CCK-8S ratio between the second (7-12 ml) and first (0-6 ml) CSF fractions, correlated significantly with the atmosphere pressure at the time of puncture. Neither CCK-8S nor CCK-4 displayed concentration gradients in CSF. The CCK-4 levels, expressed as pmol l-1 in the total amount of CSF were found to be positively correlated with the neuraxis distance in the lying position and negatively with the neuraxis distance in the sitting position. Furthermore, CCK-4, expressed as pmol l-1 per min of tapping-time (pmol l-1 min-1), showed a negative correlation with storage time, presumably mirroring a proteolytic process. CCK-8S and CCK-4 intercorrelated positively independently of whether expressed as pmol l-1 or pmol l-1 min-1. In conclusion, the results of this exploratory study indicate that the neuraxis distance (in the sitting and lying positions) and storage-time have to be accounted for when interpreting data on CSF levels of CCK-4. Attention has to be paid to the potential influence of atmospheric pressure on the concentration ratio of CCK-8S.

Increased cerebrospinal fluid concentrations of C- but not N-terminal cholecystokinin fragments in multiple sclerosis.

The sulfated N-terminus and the carboxyamidated C-terminus of cholecystokinin octapeptide (CCK-8) were radioimmunoassayed in cerebrospinal fluid from 19 patients with multiple sclerosis (MS) and 17 control subjects. While the N-terminal immunoreactivity was normal in all phases of MS, the concentration of C-terminal CCK immunoreactivity was significantly increased from 3.7 +/- 0.3 to 7.9 +/- 1.0 pmol/l (mean +/- S.E.M.) in both progressive and stable phases. The results indicate that C-terminal forms of CCK are released at an increased rate or that increased amounts of CCK-8 are released together with enhanced aminopeptidase activity in MS.

Cerebrospinal fluid levels of monoamine compounds and cholecystokinin peptides after exposure to standardized barometric pressure.

BACKGROUND: Connections between mood changes and weather have been described throughout the ages, and in more recent years, there have been reports on a relationship between atmospheric pressure and neurotransmitter levels in cerebrospinal fluid. METHODS: To further investigate this issue under strictly standardized conditions, we have lumbar-punctured 8 healthy males under low (963 hPa) and high (1064 hPa) barometric pressure, using a pressure chamber. RESULTS: Under high pressure, the tyrosine concentrations in the cerebrospinal fluid (CSF) were lower, while the cholecystokinin tetrapeptide (CCK-4) levels were higher. No differences between low and high pressure were found for tryptophan, 5-hydroxyindolacetic acid (5-HIAA), dopamine (DA), and sulphated cholecystokinin octapeptide (CCK-8S). The serum level of CCK-8S was higher under high pressure. On comparing concentration ratios between the second and the first CSF fraction, we found significantly increased ratios for homovanillic acid (HVA) and 4-hydroxy-3-methoxyphenylglycol (HMPG), but a decreased ratio for tyrosine under high pressure. The difference in the concentration ratios of HVA between low and high pressure correlated negatively with age. Intraspinal pressure correlated negatively with tapping time at low pressure. CONCLUSION: Our results are in line with the hypothesis that atmospheric pressure influences CSF levels of monoamine compounds and cholecystokinin peptides.

Cholecystokinin peptides in cerebrospinal fluid: a study in healthy male subjects lumbar-punctured without preceding strict bed-rest.

In a recent study we analysed the concentrations of two forms of cholecystokinin (CCK), CCK-8S (sulphated) and CCK-4 in cerebrospinal fluid (CSF) obtained from 14 healthy male volunteers lumbar-punctured after a minimum of eight hours of strict bed-rest. We have now lumbar-punctured another group of 14 healthy males, using the same procedure except for the requirement of strict bed-rest prior to puncture. In contrast to our previous study, the concentration of CCK-4 (but not CCK-8S) was significantly higher in the second CSF fraction (7-12 ml) than in the first one (0-6 ml). On using the concentration ratio between the second and first fraction, CCK-8S (but not CCK-4) correlated positively with the atmospheric pressure, which is in contrast to our previous study in which a significant negative correlation was found. When the lumbar CSF concentrations were expressed as the concentration per minute of tapping-time (an estimate of the mass flow), atmospheric pressure, age and the neuraxis distance in the lying position made significant contributions to the variance in CCK-8S. A significant positive correlation with atmospheric pressure was found for CCK-4. In conclusion, the results indicate that the question of strict bed-rest or not prior to lumbar puncture may have to be considered when interpreting data on lumbar CSF concentrations of CCK. A controlled study is warranted.

Blood-CSF barrier to CCK and effect of centrally administered bombesin on release of brain CCK.

The purpose of this study, in part, was to determine the ability of cholecystokinin (CCK-33/39 and CCK-8) to penetrate the blood cerebrospinal fluid (CSF) barrier in dogs by measuring these forms of CCK in plasma and in CSF. In addition, the effectiveness of centrally administered bombesin in releasing brain CCK-33/39 and CCK-8 was evaluated. Six groups of five dogs each were studied. Each group received one of the following: (1) intravenous infusion of CCK-33/39 (1.3 micrograms/kg/hr); (2) intravenous infusion of CCK-8 (0.4 micrograms/kg/hr); (3) intrathecal infusion of CCK-33/39 (1.3 micrograms/kg/hr); (4) intrathecal infusion of CCK-8 (0.5 micrograms/kg/hr); (5) intravenous infusion of bombesin (1 micrograms/kg/hr); and (6) intrathecal infusion of bombesin (1 microgram/kg/hr). Plasma concentrations of CCK-33/39 significantly increased during intravenous infusion of CCK-33/39 (from basal of 84 +/- 8 to 142 +/- 2 pg/ml) or bombesin (from basal of 78 +/- 13 to 325 +/- 87 pg/ml); however, CSF perfusate concentrations of CCK-33/39 did not increase. CCK-33/39 levels of the CSF perfusate increased significantly (P less than .05) from 211 +/- 84 to 9,873 +/- 3,368 pg/ml during intrathecal infusion of CCK-33/39, but failed to rise simultaneously in the systemic circulation. Similarly, intravenous infusion of CCK-8 caused a fivefold elevation in plasma CCK-8 levels and no change in CSF perfusate levels of CCK-8; moreover, intrathecal infusion of CCK-8 failed to elevate peripheral CCK-8 levels, despite CSF perfusate CCK-8 levels of 92,300 +/- 18,598 pg/ml. Intrathecal concentrations of neither CCK-33 nor CCK-8 were affected by intravenous or intrathecal administration of bombesin. We conclude that CCK-33/39 and CCK-8 do not penetrate the blood-cerebrospinal fluid barrier in dogs, and centrally administered bombesin is ineffective in causing release of cholecystokinin from brain tissue into the CSF.