effect of agents acting on NMDA and dopamine receptors on the responses of phrenic nerve-diaphram preparations from aged rats

Alzheimer's Dementia [AD] and Parkinsonism are common in geriatric patients. The skeletal muscles are important in the proper function of aging animals and humans. This study focuses on the influence of memantine [used for moderate to severe AD] and levodopalcarbidopa [LDICD] [a corner stone in the treatment of Parkinsonism] on responses of isolated phrenic nerve-diaphragms [IPNDs] of aged male rats. From 100 aged male albino rats twenty were untreated to study in vitro effects of memantine and LD/CD on 1PNDs. Eighty rats were divided into: Group-I [Control], Group II [oral meman tine, 1 .5mg/KgId], Group-Ill, [twice daily intraperitoneal LD/CD, 25/2.5mg/kg], Group-lV [both drugs]. After three weeks of treatment, animals were sacrificed; ten rats from each group were used to harvest IPNDs to study the effect of alIamine; 10 rats were used to measure nAchR [nicotinic acetyicholine receptor] alpha subunit mRNA by PCR. Heights of indirectly elicited contractions: 63.1 +/- 4, 6. 41.5 +/- 4.5, 70.6 +/- 4.7, 53.9 +/- 3.3mm for Groups I through IV respectively, all differences were statistically significant K0.05]. Memantine treatment caused a leftward shift of sallamine log-concentration-response curve, LD/CD caused ri.htward shift. Reversal of neuromuscular block required ier neostigmine concentrations in the memantine group it smaller concentrations in the LD/CD group. In Vitro m.antine inhibited diaphragmatic responses to indirect stam1ation. Values of nAchR alpha subunit mRNA [micro g/dl]: 1 +/- f116 [control], 0.13 +/- 0.11 [memnatine], 2.3 +/- 0.94 [LD/CD], 1.18 +/- 0.71 [both drugs] [p<0.05]. Memnatine inhibits neuromuscular transmission in vitro and with in vivo treatment. LD/CD treatment rtaaces neuiomuscular transmission. Clinical implications a1 further investigation

influence of L-carnitine among other agents on the functional recovery of the isolated rat heart exposed to hypoxic cold cardioplegia

L-carnitine, is an amino acid derivative, that has previously shown a beneficial effect on skeletal and cardiac muscle function through favorable metabolic effects. This study aims to test for a possible protective effect of L-carnitine in face of cold hypoxic cardioplegia of the isolated rat heart. Sixty male albino rats were used in this study and were divided into six study groups. Isolated rat hearts from all the study groups were exposed to hyperkalemic, hypoxic cold cardioplegia for two hours with the following changes in the cardioplegic solution: Group I served as a control group with no special additions to the cardioplegic solution; for Group II, glucose in the cardioplegic solution was increased to a concentration of 22millimole [mM] for Group III methylprednisolone sodium succinate [MPSS] was added to a concentration of 100mg per liter; Group IV received verapamil in the cardioplegic solution at a concentration of 1.1 micromol/L; Group V had L-carnitine at a concentration of 1mM and for Group VI, L-carnitine was added to the cardioplegic solution a t a concentration of 4Mm. The heart rate [HR], Dp/dt, the left ventricular developed pressure [LVDP], and rate pressure product [RPP] were recorded at baseline, and at 15 and 60 minutes after the start of re-warming. Epinephrine was given to the working hearts at doses of 0.5, 1.0 and 2.0 micromol before cardioplegia and after re-warming and the changes in cardiac function parameters in response to epinephrine were recorded. Creatine phosphokinase [CPK] was measured in samples from the coronary effluent taken before cardioplegia and 15 minutes after re-warming. The control group showed a significant reduction in all cardiac function parameters after cardioplegia and re-warming [dp/dt[max], LVDP and RPP reached 40.2%, 18.8% and 8.4% of their baseline values respectively]. Significant cardiac protection was noted in the groups exposed to glucose and carnitine. Functional recovery with glucose reached 66.2% of the baseline value for the dp/dt[max], 55.2% for the LVDP and 17.5% for the RPP [p<0.01 as compared to control]. Functional recovery with carnitine 4mM reached 98.7% of the baseline value of dp/dt[max], 89.9% for the LVDP, 48.1% for the RPP [p<0.05 as compared to all the other groups]. For carnitine at the 4mM concentration the dp/dt[max] values at the end of the experiment showed no significant difference from the baseline values. Also the percentage increase in dp/dt[max] and LVDP in response to post-cardioplegic epinephrine showed no significant difference from that recorded before cardioplegia [p>0.05]. MPSS provided only transient cardiac improvement compared to the control group, while verapamil showed no protective action on cardiac function parameters. CPK results showed significantly lower post re-warming CPK with all the tested drugs

Effects of sleep deprivation on cellular immunity and interleukin-6 level in rats: increased dietary fat modulate sleep deprivation-induced immune change

Impairment of host defenses is chief among sleep deprivation outcomes, as evidenced by strikingly poor control over endogenous microorganisms. Interleukin [IL]-6 is a multifunctional cytokine. It is an inflammatory cytokine, which causes sickness manifestations. This cytokine might play a significant role in mediating the sleepiness and fatigue in the day after sleep deprivation. Leukocytosis has been a consistent finding in sleep deprivation inspite of the impaired immunity. Blood leukocyte differentials were performed to determine the cell types responsible for this finding of increased circulating white blood cell counts. Fatty acid composition of rodent diets can affect immune function as measured in vitro and in vivo and can modulates the immune response to different types of stress. This study was designed to investigate the effect of 4 days of sleep deprivation on the serum level of IL-6 and the differential count of white blood cells. Also to examine the effect of diet enriched with fat on the changes induced by sleep deprivation. Forty adult male albino rats were included in this study and were divided into 4 groups: Group I: [Control group] included 10 rats received standard rat chow and water and have normal sleep pattern, at -12 hours dark-light cycles. Group II: [Fat fed group] included 10 rats received standard rat chow enriched with corn oil and water, and have normal sleep pattern, at -12 hours dark-light cycles. Group III: [Sleep deprivation group] included 10 rats received standard rat chow and water, and was exposed to sleep deprivation. Group IV: [Fat fed and sleep deprived group] included 10 rats received standard rat chow enriched with corn oil and water, and was exposed to sleep deprivation in the same pattern as group III. Sleep deprivation was carried out by audio-visual mechanism. The results indicated decreased body weight, leukocytosis with neutrophilia and shift to the left, monocytosis and lymphopenia in sleep-deprived rats. The serum revealed an evolving pro-inflammatory state, as evidenced by high incidence of interleukin-6. Feeding the rats diet enriched with fat ameliorated the inflammatory state as evidenced by significant lower levels of IL-6 and partially corrected the change induced by sleep deprivation on the total and the differential blood count of WBCs. We can conclude that sleep deprivation has a considerable impact on the immune response. Nearly all of the immune-related events that emerged as responses to sleep deprivation have been implicated as a pro-inflammatory states that represents a risk factor for many diseases. Feeding sleep deprived rats a diet enriched in fatty acids ameliorated the effect of sleep deprivation on IL-6 secretion and partially attenuated the stimulation of inflammatory responses induced by sleep deprivation as indicated by partial correction of the body weight and WBCs count and composition

effect of peroxisome proliferator - activated gamma agonist on resistin in obese rats with type 2 diabetes

Adipocytes are highly differentiated cells and numerous genes are expressed significantly in fat cells, resistin is an adipocytokine highly expressed in murine adipose tissue. Peroxisome proliferator-activated gamma agonists [PPAR] down-regulate resistin gene expression in adipose tissue. The aim of the present work is to clarify the effect of peroxisome proliferator-activated gamma agonist [rosiglitazone] on resistin in obese rats and obese rats with type 2 diabetes. Forty eight white albino male rats of 150-250gm average weight were randomly divided into group 1: Control group [n=8], group 2: [n=8] rats received rosiglitazone, group 3s [n=32] obese rats, this group subdivided into group 3a: Obese rats recieved the drug [n=8]. Group 3b: Obese rats after induction of type 2 diabetes, Group 3c: Obese rats with diabetes and rosiglitazone [n=8]. At the time of scarification blood was collected and samples from central fat and peripheral fat was taken. The following parameters were assessed, serum glucose, triglycerides, cholesterol, insulin, serum resistin and resistin in fats. The results of the present work showed that serum glucose, insulin, triglycerides and cholesterol were significantly higher in [group 3, group 3b] compared to the control while their levels decreased after administration of the drug [Group 3c]. As regard resistin level in serum, central fat and peripheral fat were significantly higher in [group 3 and group 3b] compared to the control however its level significantly decrease after rosiglitazone administration. Also significant correlation were found between serum resistin and serum glucose, serum triglycerides and body mass index in all studied groups. Conclusion resistin seems to play an important role in development of type 2 diabetes particularly on top of obesity and its response to [PPAR] agonist may be used to relive insulin resistance in type 2 diabetes