Sheng li xue bao : [Acta physiologica Sinica]
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A sepsis model induced by cecal ligation and puncture was used to study the role of endogenous carbon monoxide in hypotension pathogenesis of rats during septic shock. After administration of zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO),blood pressure (BP),HO activity and carbon monoxide (CO) release from vascular muscle tissue were measured. ⋯ These findings suggest that HO activity and CO release within vascular musculature are increased during septic shock; inhibition of HO may elevate BP of rats during septic shock through a decrease of endogenous CO production. It is concluded that endogenous CO derived from vascular muscle cells plays an important role in regulating vascular tone, and the up-regulation of HO activity followed by subsequent CO production contributes to hypotension pathogenesis during septic shock.
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Experiments were carried out on male SD rats anesthetized with urethane (700 mg/kg) and chloralose (35 mg/kg). The results were as follows: (1) The pressor response could be elicited by electrical stimulation of dorsol part of midbrain periaqueductal gray (dPAG) for 5 s every 5 min. ⋯ This pressor response could be decreased by electrolytic cauterization of paraventricular (PVN) area, but unaffected by electrolytic lesion of fornix, anterior hypothalamic area, nucleus dorsomedialis hypothalami and nucleus ventromedicalis hypothalami. (2) Microinjection of an AVP-V1 receptor antagonist (CH2)5 [Tyr(Me)2AVP] (each side 0.1 nmol/0.1 microliter) into the bilateral rostral ventrolateral medulla (rVLM) partially inhibited the pressor response induced by PVN stimulation or by microinjection of D,L-homocysteric acid (DLH) (0.1 mol/0.2 microliter) into the PVN, but the mean artrtial pressure (MBP) and heart rate (HR) did not show any change when an AVP-V1 receptor antagonist or DLH was only used. (3) Microinjection of an AVP-V1 receptor antagonist into the bilateral rVLM partially inhibited the pressor response induced by dPAG stimulation. Therefore it is suggested that the effect of vasopression (AVP) released from PVN on the pressor response induced by dPAG stimulation is partly mediated by activation of AVP-V1 receptor in the rVLM.
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Experiments were performed on male SD rats anaesthetized with urethane (700 mg/kg) and chloralose (35 mg/kg). The results showed that mean arterial pressure (MBP) increased signifigantly and heart rate (HR) had no signifigant change by bilateral microinjection AVP(10 pmol/0.1 microliter/site) into the rostral ventrolateral medulla (rVLM), while both MBP and HR were not changed by application of an AVP-V1 receptor antagnoist. ⋯ The above results suggest that AVP in the rVLM can elevate MBP and midbrain defence area stimulation can cause pressor response. Both these effects are related to activation of AVP-V1 receptors in the rVLM.
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Oxygen is an active stimulus of cerebral blood vessels. Hyperoxia can induce decrease in cerebral blood flow and intracranial pressure, but hypoxia increases cerebral blood flow and intracranial pressure. Both hyperoxia and hypoxia play an opposite role in cerebral circulation and intracranial pressure. Recent studies of cerebral circulation and intracranial pressure under hyperoxia and hypoxia were reviewed in the present paper with special reference to the correlation between cerebral circulation and intracranial pressure.
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Experiments were performed on 32 rabbits anaesthetized with alpha-chloralose and urethane, paralyzed with flaxidil and artificially ventilated. The pressor response was elicited by stimulation of dorsal part of midbrain periaqueductal gray (dPAG). Intravenous injection of diazepam (2 mg/kg) or intracerebroventricular application of flurazepam (2 mg/50 microliters) resulted in attenuation of the pressor response induced by the stimulation of midbrain. ⋯ Microinjection of flurazepam of the same dosage into caudal ventrolateral medulla (cVLM), however, had no depressant effect. Pretreatment with bicuculline in rVLM prevented the inhibitory effect of flurazepam on the pressor response. These results mentioned above suggest that diazepam or flurazepam inhibits the pressor response evoked by midbrain stimulation, and the effect may be mediated by the activation of the GABAA receptor in rVLM.