Comparison of the effects of three different combinations of general anesthetics on the electroretinogram of dogs

The objective of this study is to compare the effects of three different anesthetic combinations on the electroretinogram in the same animals under similar laboratory conditions. Thiopental–isoflurane (TI), medetomidine–ketamine (MK), and xylazine–ketamine (XK) were used on each of 12 healthy miniature schnauzer dogs (MS) with a period of at least 3 weeks in between subsequent anesthesia protocols, using the Dog Standard Protocol. The scotopic ERGs consisted of scotopic low stimulus strength (S) responses designated S1, S2, S3, S4, and S5, at 1, 5, 10, 15, and 20 min after dark adaptation, respectively, and scotopic standard stimulus strength (S-ST) responses. The photopic ERGs consisted of a photopic single flash (P) response and 31 Hz flicker (P-FL) responses. For S-ST (2.5 cd s/m²), the amplitude of the a-wave using TI was significantly lower than that using MK (adjusted P = 0.05) and XK (adjusted P = 0.03), and the implicit time of the a-wave was significantly shorter than that using MK (adjusted P = 0.04). For P (2.5 cd s/m²), the amplitude of the b-wave using XK was significantly higher than that using MK (adjusted P = 0.01). The implicit times of the b-wave using TI was significantly longer and shorter than that of MK for S1, S2 and P-FL and for S4 and S-ST, respectively, and than that of XK for S2 and P-FL and for S5 and S-ST, respectively. The results of the present study showed that TI affected both the amplitude and the implicit time of the a-wave for S-ST and the implicit time of the b-wave relatively more so than was the case when using XK or MK. Therefore, it appears that either XK or MK could be advantageous to use rather than TI for clinical studies.     

Reversal of vascular 18F-FDG uptake with plasma high-density lipoprotein elevation by atherogenic risk reduction

Vascular 18F-FDG uptake marker represents inflammation in atherosclerotic lesions, but whether inflammation can be reversed by risk-modifying interventions has not, to our knowledge, been demonstrated. In this study, we evaluated the change of vascular 18F-FDG uptake in response to lifestyle intervention on serial PET/CT scans and further assessed how the findings relate to atherogenic risk reduction. METHODS: A total of 60 healthy adults underwent 18F-FDG PET/CT scans and atherogenic risk-factor assessment at baseline and again after 17.1 +/- 8.3 mo of practicing lifestyle modification. The PET/CT images were evaluated for the presence of vascular 18F-FDG lesions, and vessel-to-blood-pool 18F-FDG ratios were measured. Indices from summed ratios of positive lesions were compared and correlated to atherogenic risk factors. RESULTS: At follow-up, significant reductions in diastolic blood pressure (P < 0.05), total cholesterol (P < 0.05), and low-density lipoprotein level (P < 0.05) and an increase in high-density lipoprotein (HDL) level (P < 0.0001) were demonstrated. On the initial PET/CT scan, 50 of 60 subjects showed 1 or more 18F-FDG-positive lesions (5.9 +/- 5.0/subject), leading to a total of 352 vascular sites. On follow-up, 18F-FDG-positive lesions were significantly reduced to 2.1 +/- 2.2 sites per subject (P < 0.0001) and a total of 124 sites (64.8% reduction). Follow-up 18F-FDG-positive rates were significantly reduced for the aorta and iliac arteries. In addition, significant reductions in the whole-body 18F-FDG index from 1.39 +/- 1.23 to 0.53 +/- 0.59 (P < 0.0001) and carotid 18F-FDG index from 0.08 +/- 0.16 to 0.03 +/- 0.06 (P = 0.01) were shown. The whole-body 18F-FDG index correlated with total cholesterol (P < 0.05) and HDL level (P < 0.05), and the magnitude of reduction in the 18F-FDG index closely correlated to the amount of increase in plasma HDL level (P = 0.005). CONCLUSION: Our study demonstrated that vascular 18F-FDG uptake is reversed in response to atherogenic risk reduction by lifestyle intervention and that the magnitude of improvement correlates to increases in plasma HDL levels. Thus, serial 18F-FDG PET/CT may be useful for monitoring improvements in the inflammatory component of atherosclerotic lesions in response to risk modification.     

Anatomical considerations of selective pudendal neurectomy

The pudendal nerve was examined in 100 cadavers of both sexes. Because of the variable number of trunks of the pudendal nerve, 5 types were distinguished: one-trunked; two-trunked, rectopudendal; two-trunked, pudendo-penile (or-clitoridal); three-trunked, recto-perineo-penile (or-clitoridal); four-trunked, recto-perineo-perineopenile (or-clitoridal). The authors' suggestions make it possible to perform selective pudendectomy, consisting in denervation of the sphincter urethrae muscle by neurectomy of the perineal branches of the pudendal nerve.     

Effects of prolonged administration of neurotensin, arginine-vasopressin, NPY, and bombesin on blood TSH, T3 and T4 levels in the rat

Adult female rats were i.p. infused (Alzet osmotic minipumps) with neurotensin (NT, 2 micrograms/rat/day for 7 days), arginine-vasopressin (AVP, 2 micrograms/rat/day for 8 days), bombesin (BM, 0.75 microgram/rat/day for 7 days) or injected with neuropeptide Y (NPY, 0.5 microgram/rat twice a day for 4 days). NT infusion increased absolute and relative thyroid gland weight and decreased serum T4 level, while serum TSH and T3 levels remained unchanged. AVP treatment increased thyroid gland weight and serum TSH and T4 levels and a similar effect was induced by prolonged BM infusion. On the other hand, NPY administration had no effect either on thyroid gland weight or on serum TSH, T4 and T3 levels. Results of the present study thus clearly demonstrate a potent stimulatory action of AVP and BM on thyroid gland function and suggest that this effect is mediated by the pituitary gland. On the contrary, prolonged NT infusion decrease serum T4 level while NPY had no effect on thyroid gland function.     

Inhibition of Expression of Hypoxia-inducible Factor-1α mRNA by Nitric Oxide in Hypoxic Pulmonary Hypertension Rats

Hypoxiaisadirectfactorcausinghypoxicpul monaryhypertension (HPH) .hypoxiainduciblefac tor 1α (HIF 1α)isfoundtobethemostcrucialfactorsofarwhichmediatesthecellularresponsetohypoxi a[1] .OurpreviousstudyrevealedthatoverexpressionofHIF 1andendothelin 1(ET 1…