High-grain diet feeding altered the composition and functions of the rumen bacterial community and caused the damage to the laminar tissues of goats.

In the current intensive production system, ruminants are often fed high-grain (HG) diets. However, this feeding pattern often causes rumen metabolic disorders and may further trigger laminitis, the exact mechanism is not clear. This study investigated the effect of HG diet feeding on fermentative and microbial changes in the rumen and on the expression of pro-inflammatory cytokines and matrix metalloproteinases (MMPs) in the lamellar tissue. In all, 12 male goats were fed a hay diet (0% grain; n=6) or an HG diet (56.5% grain; n=6). On day 50 of treatment, samples of blood, rumen content, and lamellar tissue of hooves of goats were collected. The data showed that compared with the hay group, HG-fed goats had lower (P<0.05) rumen pH but higher (P<0.05) total volatile fatty acids and lactate in the rumen and higher (P<0.05) lipopolysaccharide (LPS) levels in the rumen and blood. HG diet feeding altered the composition of rumen bacterial community, and correspondingly, the results suggested that their functions in the HG group were also altered. HG diet feeding increased (P<0.05) the expression of interleukin-1ß, interleukin-6, tumour necrosis factor-α and MMP-2 mRNA in the lamellar tissues compared with the hay group. Correlation analysis indicated that the expression of pro-inflammatory cytokines were positively correlated with MMP-2 expression in lamellar tissues. Overall, these results revealed that HG feeding altered the patterns of rumen fermentation and the composition and functions of rumen bacterial community, and lead to higher levels of LPS in the peripheral blood, and further activated the inflammatory response in lamellar tissues, which may progress to the level of laminar damage.

[Effect of sanwu hypotensive decoction on blood pressure and lymphokine activated killer cell in patient of primary hypertension and spontaneously hypotensive rats].

OBJECTIVE: To investigate the effect of Sanwu hypotensive decoction (SWHD) on blood pressure (BP) and lymphokine activated killer cell (LAK) and possible mechanism. METHODS: Thirty mild hypertension patients were treated with SWHD for 8 weeks, the levels of BP, proliferative ability and activity of LAK cell, SOD-like substance expressed by LAK cell and its radical scavenger ability before and after treatment were observed using randomized, single blinded, self-control, paralled assay, and compared with other 30 patients treated with captopril for control. In an experimental study, the vasodilatory response of thoracic aortic ring to acetylcholine and nitroglycerine, and effect of LAK cell, standard reagent of SOD, SWHD on the response were observed and compared in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKR). RESULTS: After SWHD treatment, along with lowering of BP, the proliferative ability, activity SOD-like substance expressed by LAK cell and its radical scavenger ability increased significantly. CONCLUSION: SWHD is not only an effective hypotensive agent, but also an immunoregulator.

[Clinical and experimental study of improving left ventricular diastolic function by total saponins of panax notoginseng].

OBJECTIVE: To investigate the effect of total saponins of Panax Notoginseng (TSPNS) on left ventricular diastolic function in patients with essential hypertension (EH) and possible mechanism. METHODS: Left ventricular diastolic function (peak E, peak A, E/A, A area fraction, E area fraction), left ventricular muscle mass index (LV-MI), intraerythrocytic calcium and calcium pump activity on erythrocytes membrance of 30 patients with EH before and after the combined treatment of captopril and TSPNS were measured. Captopril was used singly on 30 patients above mentioned that were also studied as self-control. Observation of TSPNS and normal saline was used on a matched control in treating SHR rats. WKY rats of similar age were also studied as normal control. RESULTS: Left ventricular diastolic function were improved markedly by TSPNS. The activity of calcium pump on membrance of sarcoplasmic reticulum were increased and the myocardial intracellular calcium were decreased and the left ventricular muscle mass were reduced after treatment of TSPNS. The calcium and calcium pump of erythrocyte showed marked simple correlation with myocardial cell. CONCLUSIONS: The TSPNS could improve myocardial relaxation function due to enhancing calcium pump activity and inhibiting intracellular calcium overload and lightening left ventricular muscle mass.

Are physiological effects of sleep deprivation in the rat mediated by bacterial invasion?

Recent reports have indicated that rats subjected to total sleep deprivation (TSD) by the disk-over-water method and sacrificed when death appeared imminent showed aerobic bacteria in their blood. Yoked control rats did not. Extrapolating from these results, it has been suggested that the late body temperature declines and eventual deaths of TSD rats are caused by septicemia, and that other, earlier-appearing effects of TSD-including weight loss, increased energy expenditure, and regulation of temperature at a higher level-might be mediated by impaired host defenses against bacterial invasion. Three measures of aerobic bacterial invasion were used to evaluate these hypotheses: bacteremia, bacterial colonization in major organs of filtration (liver, kidney, and mesenteric lymph nodes), and adherence of bacteria to the cecal wall. Experiment 1 showed nonsignificant trends toward more bacterial invasion in 4-day TSD rats compared to yoked control rats and no relationship between the bacterial indicators and the early TSD effects. Experiment 2 showed that the elimination of aerobic bacterial infection by antibiotic treatment did not prevent the early TSD effects in 4-day TSD rats. Experiment 3 showed that the elimination of aerobic bacterial invasion in TSD rats did not eliminate the late temperature decline or the progression towards death. The results showed no significant evidence of aerobic bacterial invasion early in TSD and no indication that the major effects of TSD were dependent upon aerobic bacterial invasion.

Sleep deprivation in rats with preoptic/anterior hypothalamic lesions.

Chronic total sleep deprivation (TSD) of rats by the disk-over-water method reliably produces initial increases and subsequent decreases in waking intraperitoneal (Tip) and hypothalamic (Thy) temperatures, progressive increases in energy expenditure, skin lesions on the tail and plantar surfaces, debilitated appearance, and eventual death. We investigated the possible role of the preoptic/anterior hypothalamus (POAH) in the mediation of the TSD effects by comparing these effects in POAH-lesioned and unlesioned rats. Bilateral POAH lesions sufficient in size to impair homeothermic responses to changes in ambient temperature did not produce TSD-like temperature changes under baseline ambient temperatures of 28-29 degrees C, implying that the thermoregulatory changes produced by TSD do not result from impairment of the lesioned area. However, the possibility remains that the TSD effects are mediated by damage to POAH areas that were not lesioned. During TSD, lesioned and unlesioned rats showed similar progressive increases in energy expenditure, but the lesioned rats showed earlier, steeper, and eventually greater declines in Tip and Thy. This result suggests that in unlesioned rats the POAH may counter-regulate against, and thereby attenuate, the reduction in heat retention caused by TSD. This failure of regulation in lesioned rats is consistent with their impaired response to ambient temperature change and implies that, in unlesioned rats, some POAH thermoregulatory mechanisms continue to function normally during TSD. Lesioned rats did not show the characteristic TSD-induced early increases in Tip and Thy. This result could imply either that heat retention was so compromised that body temperatures did not rise in spite of a TSD-induced increases in thermoregulatory setpoint, or that the setpoint increase in unlesioned rats is POAH-mediated. Notwithstanding the greater Tip and Thy declines in lesioned rats, they survived the TSD procedure longer than the unlesioned rats, thus supporting previous indications that death did not result from hypothermia.

Sleep deprivation in the rat: XX. Differences in wake and sleep temperatures during recovery.

We examined the relationship between wake and sleep peritoneal temperature (T(ip)) during recovery from short-term (five rats, 5 days of deprivation) and long-term (nine rats, 14-21 days) total sleep deprivation (TSD). Mammalian body temperature normally declines in the passage from wakefulness to sleep. Recovery from TSD featured reductions of the typical wake-sleep T(ip) differences. Previous studies from our laboratory have shown that chronic TSD in the rat produces a progressive rise in energy production and an initial rise in wake T(ip), followed by a later fall in T(ip) to below baseline that becomes more acute as death becomes imminent. During recovery from both short-term TSD (wherein pre-recovery wake T(ip) was still above baseline) and long-term TSD (wherein pre-recovery wake T(ip) had fallen to below baseline), wake T(ip) and energy production quickly returned towards baseline. On the first recovery day, both short- and long-term TSD rats showed mean non-rapid eye movement (NREM) and paradoxical sleep (PS) T(ip) values that were slightly, although not significantly, above mean wake T(ip). In short-term TSD rats, wake-NREM and wake-PS T(ip) differences were reduced from baseline significantly (p < 0.0025) on the first recovery day and nonsignificantly on the remaining three recovery days. In long-term TSD rats, wake-NREM and wake-PS T(ip) differences were significantly (p < 0.001) reduced from baseline on the first four recovery day block. On the last four recovery day block, wake-sleep T(ip) differences tended to return toward baseline. Hypothalamic wake-sleep temperature differences in long-term TSD rats showed similar reductions during recovery. The reduction of wake-sleep temperature differences in recovery does not support either energy reduction or cooling functions for sleep.

[Effect of shenmai injection on sIL-2R NK and LAK cells in patients with advanced carcinoma].

Serum interleukin-2 receptor (sIL-2R) level activities of natural killer cell (NK) and lymphokine activated killer cell (LAK) cells were determined in 60 patients with advanced carcinoma (AC) before and after treatment with Shenmai injection (SMI), 40 healthy persons were taken as non-carcinoma control (NC). The results showed that: Serum sIL-2R level in AC were much higher than those in NC (P < 0.05) and activities of NK and LAK cells in AC were much lower than those in NC (P < 0.05) before treatment. There was no significant difference among gastric cancer, colonic carcinoma and lung cancer (P < 0.05). After treatment with SMI we also found that the level of sIL-2R in all patients were obviously lower (P < 0.05) while the activity of NK and LAK cells were significantly higher than that prior treatment (P < 0.05). Linear correlation was not found between sIL-2R and NK, LAK cells. These data suggested that the immune function was compromised in AC. The mechanism of the inhibitory effect of SMI on carcinoma might be related to the activity of biological response modifier.