HSDR

AcronymDefinition
HSDRHigh Speed Data Recorder
HSDRHurricane and Storm Damage Reduction (USACE)
HSDRHigh Speed Diesel Race (combustion technology)
HSDRHumane Society of Durham Region (Ontario, Canada)
HSDRHealth Systems Development and Regulation (South Dakota)
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References in periodicals archive ?
Figure 1 showed the effects of heat exposure (43[degrees]C for 60 minutes) on both [T.sub.co] and MAP in (NTDR + V) rats, (HSDR + V) rats, and (HSDR + H) rats.
Figure 2 showed that the hypothalamic levels of P[O.sub.2] and cerebral blood flow in the (HSDR + V) rats were significantly lower at 60 minutes after the start of heat exposure than in the (NTDR + V) group (~100 BPU versus ~400 BPU for CBF; ~5 mmHg versus ~20 mmHg for P[O.sub.2]; P < 0.05).
Figure 3 showed that the hypothalamic levels of 2,3-DHBA and N[O.sub.x.sup.-] in the (HSDR + V) rats were significantly higher at 60 minutes after the start of heat exposure than in the (NTDR + V) rats (~180% versus ~100 mmHg for DHBA; ~9.6 [micro]M versus ~2.6 [micro]M for N[O.sub.x.sup.-]; P < 0.05).
Figure 4 showed that the hypothalamic values of TUNEL-positive cells in the (HSDR + V) were significantly higher at 60 minutes after the start of heat stress than that in the (NTDR + V) rats (~148 cells versus ~5 cells; P < 0.01).
Figure 5 showed that the serum values of IL-1[beta], IL-6, TNF-[alpha], E-selectin, ICAM-1, lactate dehydrogenase, and MPO for (HSDR + V) were significantly higher at 60 minutes after the start of heat stress than that in the (NTDR + V) rats.
Table 3 showed that the plasma levels of both ACTH and corticosterone in the (HSDR + V) rats were significantly higher at 60 minutes after the start of heat stress than that in the (NTDR + V) rats.
Table 4 showed that the serum level of BUN, creatinine ALT, AST, and AP in the (HSDR + V) rats were significantly higher at 60 min after the start of heat stress than that in the (NTDR + V) rats.
As shown in the present study, hypothalamic ischemia, hypoxia, and neuronal apoptosis were associated with HPA impairment (evidenced by insufficient release of both ACTH and corticosterone) in HSDR which could be significantly reversed by honokiol.
In summary, we demonstrated that honokiol protected against hyperthermia, hypotension, and multiorgan injury in HSDR. The beneficial effects of honokiol might be on the reduction of (a) systemic inflammatory response syndrome molecules like TNF-[alpha], IL-1[beta]/IL-6, ICAM-1, MPO, and E-selectin in the plasma, (b) the toxic oxidizing radicals like N[O.sub.x.sup.-] and 2,3-DHBA, in the plasma, (c) the organ injury indicators like LDH, creatinine, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase in the plasma, and (d) an indicator for leukocytes accumulation like MPO in the serum, and thus leading to maintenance of HPA axis function and increased survival in rats with heatstroke-associated multiple organ dysfunction.