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IV Sils

Publications and source records attributed to IV Sils.

3 recordsLinked to original sources

Effect of nitric oxide synthase inhibition on regional blood flow during hyperthermia.

The loss of compensatory splanchnic vasoconstriction during hyperthermia was assessed in rats after administration of either 0, 10, 30, or 100mg/kg N(w)-nitro-L-arginine methyl ester,L-NAME. Rectal temperature (T(re)), heart rate (HR), mean arterial blood pressure (MAP), breathing frequency (BF), and renal, mesenteric and caudal blood flows (Q(R), Q(M) and Q(C)) were measured until irreversible cardiovascular collapse occurred. HR, MAP and BF increased as T(re) rose to 42 degrees C, then fell as circulatory collapse occurred. As dose increased T(re) at collapse decreased. Q(M) decreased until a T(re) of 41.5-42 degrees C and then increased. Q(R) and Q(C) were unaffected by either hyperthermia orL-NAME. Inhibition of NO synthase did not prevent the circulatory collapse of heatstroke; the higher doses ofL-NAME may have exacerbated the onset of circulatory failure.

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Hyperthermia-induced changes in the vascular permeability of rats: a model system to examine therapeutic interventions.

Extravasation in the heart, liver, lung, kidney, spleen, gastrocnemius, and duodenum was quantified in normothermic and hyperthermic (core temperature (T(c))=41.5, 42, or 42.6 degrees C) rats. Following attainment of the target T(c), Evans blue (Eb) was administered via jugular cannula; the animals were anesthetized, exsanguinated, tissues removed and washed in saline, and Eb extracted with formamide. There was significantly (p<0.05) more Eb (µg/g of dry wt of tissue, mean+/-SD) in the tissues of severely hyperthermic (T(c)=42.6 degrees C) rats vs that of control rats: liver - 198+/-39 vs 125+/-28, kidney - 376+/-68 vs 176+/-60, and small intestine - 170+/-49 vs 106+/-20. This model may be useful in evaluating the efficacy of treatment modalities designed to sustain vascular integrity in the face of environmental insult.

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Hyperthermic effects on reticuloendothelial system particulate uptake.

Reticuloendothelial system (RES) particulate uptake (PU) of vascular debris influences survival from extreme hyperthermia. Little is known of the effect of extreme hyperthermia, unrelated to fever, on RES PU shortly after reaching a maximum core temperature (T(c)). Relative to normothermic rats (T(c)=38.0 degrees C), rats at T(c)=42.6 degrees C had significantly higher, while T(c)=42.0 degrees C rats had significantly lower total RES tissue (lung, liver, spleen) PU of fluorescent microspheres (1 µ), when compared to rats at T(c)=42.6 or 38.0 degrees C. These findings suggest at T(c)=42.6 degrees C, rats were not actively thermoregulating. As such, more blood remained in the core than in the periphery, which resulted in greater core RES tissue PU. In contrast, to reduce or control core heat, rats at T(c)=42.0 degrees or 38.0 degrees C directed more blood to the periphery, which reduced core RES tissue PU. Blood flow patterns as directed by the state or degree of active thermoregulation is likely an influence of hyperthermia on RES PU.

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