Association of sudden infant death syndrome with grossly deranged iron metabolism and nitric oxide overload

Reid, G.M.

doi:10.1054/mehy.1998.0833

Cited by 10 publications

(7 citation statements)

References 24 publications

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“…Organ‐specific cell death with increased apoptotic rates and thymic stress changes are common pathologic findings during sepsis [46,47]. It has been suggested that NO is responsible for some of the organ damage described in autopsy reports of infants who died of SIDS [15]. We have previously reported that the most prominent and frequent treatment‐related lesions occurred in RAIV‐infected animals 6 h after administration of endotoxin.…”

Section: Discussionmentioning

confidence: 99%

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Alteration in regulation of inflammatory response to influenza a virus and endotoxin in suckling rat pups: a potential relationship to sudden infant death syndrome

Blood‐Siegfried¹

2004

FEMS Immunology and Medical Microbiology

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Data increasingly implicate a possible role of immune and inflammatory responses to infection in sudden infant death syndrome (SIDS). We have previously described a dual challenge model that results in pathology, organ damage, vascular collapse and unexplained death similar to that seen in SIDS. In this study, we examined changes in inflammatory cytokine mRNA in the lung and liver and regulation of pathways associated with nitric oxide production. Our data suggest that priming of the immune system by mild viral infection disturbs normal inflammatory response to endotoxin. This results in an increased nitric oxide synthase production, most likely the cause of liver pathology and clotting abnormalities.

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Section: Discussionmentioning

confidence: 99%

“…Nitric oxide is an important part of the immune response to bacterial and viral infections, and NO stimulated inflammation is an important cause of mortality in influenza A infections [14]. It has also been suggested that NO is responsible for some of the organ damage described in autopsy reports of infants dying of SIDS [15].…”

Section: Introductionmentioning

confidence: 99%

Alteration in regulation of inflammatory response to influenza a virus and endotoxin in suckling rat pups: a potential relationship to sudden infant death syndrome

Blood‐Siegfried¹

2004

FEMS Immunology and Medical Microbiology

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“…Elevated NO expression has been found to be associated with organ damage described in autopsy reports of infants who died of SIDS. NOS mRNA up-regulation has been observed after endotoxin administration in animal models for the study of SIDS (13,14).In vitro and in vivo studies indicated that NO has inhibitory properties at the carotid body and that eNOS is primarily responsible for this effect (15,16). Administration of NO donors to the carotid body reduces its chemosensory response to a decrease in oxygen concentration (16).…”

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confidence: 99%

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confidence: 99%

Ventilatory Response to Hypoxia during Endotoxemia in Young Rats: Role of Nitric Oxide

2007

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Administration of Escherichia coli endotoxin attenuates the ventilatory response to hypoxia (VRH) in newborn piglets, but the mechanisms responsible for this depression are not clearly understood. Nitric oxide (NO) production increases during sepsis and elevated NO levels can inhibit carotid body function. The role of endothelial NO on the VRH during endotoxemia was evaluated in 26 young rats. Minute ventilation (V E ) and oxygen consumption (VO 2 ) were measured in room air (RA) and during 30 min of hypoxia (10% O 2 ) before and after E. coli endotoxin administration. During endotoxemia, animals received placebo (PL, n ϭ 8); a nonselective nitric oxide synthase (NOS) inhibitor (N G -nitro-L-arginine methyl ester, L-NAME, n ϭ 9), or a neuronal NOS (nNOS) inhibitor (7-nitroindazole, 7-NI, n ϭ 9). During endotoxemia, a larger increase in V E was observed only during the first min of hypoxia in the L-NAME group when compared with PL or 7-NI (p Ͻ 0.001). VRH was similar in the PL and 7-NI groups. A larger decrease in VO 2 at 30 min of hypoxia was observed in L-NAME and 7-NI groups when compared with PL (p Ͻ 0.03). These data demonstrate that the attenuation of the early VRH during endotoxemia is in part mediated by an inhibitory effect of endothelial NO on the respiratory control mechanisms. (Pediatr Res 62: 134-138, 2007) C hanges in breathing pattern and apnea episodes are frequently observed in newborns and infants with sepsis (1). In adult humans, endotoxin administration results in changes in the basal respiratory pattern and dyspnea (2). We previously demonstrated that endotoxin infusion in newborn piglets produced attenuation of the VRH (3). In a pilot study, we also observed similar respiratory behavior in 4-to 6-wkold rats. The interaction of hypoxia, infection, and cytokine abnormalities has been suggested as a possible mechanism of sudden infant death syndrome (SIDS) (4).The mechanisms that explain the changes in breathing pattern during sepsis are not clearly understood. Respiratory muscle fatigue or alterations in lung mechanics and metabolic rate have been associated with the respiratory changes observed during Gram-positive and negative septicemia in piglets (3,5,6). Particularly, the attenuation in the VRH observed after endotoxin administration to unanesthetized newborn piglets was associated with a significant decrease in VO 2 (3). Sepsis can induce the release of inflammatory mediators such as cytokines; prostaglandins, and NO (7,8), which may be responsible for the alterations of the breathing pattern observed during endotoxemia and also may be an important component of many deaths attributed to SIDS (4).It is known that NO is an active participant in the pathophysiology of endotoxemia (9). NO is synthesized from Larginine by three different isoenzymes of NOS: neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS) (10). Increased eNOS activation and endothelial NO release have been observed shortly after endotoxin administration (11,12). Elevated NO expression has been fou...

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“…Compromised cerebral autoregulation might contribute to the pathophysiology of sudden unexplained death in epilepsy patients (SUDEP), a poorly understood but significant cause of mortality in seizure disorders [2,36]. In sudden infant death syndrome (SIDS), impaired cerebral autoregulation may contribute to cerebral hypoperfusion and other factors leading to death [29]. Similarly, dysfunction of cerebral blood flow modulation and of cerebral autoregulation might increase the risk of SUDEP [2,36].…”

Section: Discussionmentioning

confidence: 99%

Cerebral autoregulation improves in epilepsy patients after temporal lobe surgery

et al. 2004

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Patients with temporal lobe epilepsy (TLE) often show increased cardiovascular sympathetic modulation during the interictal period, that decreases after epilepsy surgery. In this study, we evaluated whether temporal lobectomy changes autonomic modulation of cerebral blood flow velocity (CBFV) and cerebral autoregulation. We studied 16 TLE patients 3-4 months before and after surgery. We monitored heart rate (HR), blood pressure (BP), respiration, transcutaneous oxygen saturation (sat-O(2)), end-expiratory carbon dioxide partial pressure (pCO(2)) and middle cerebral artery CBFV. Spectral analysis was used to determine sympathetic and parasympathetic modulation of HR, BP and CBFV as powers of signal oscillations in the low frequency (LF) ranges from 0.04-0.15Hz (LF-power) and in the high frequency ranges from (HF) 0.15-0.5Hz (HF-power). LF-transfer function gain and phase shift between BP and CBFV were calculated as parameters of cerebral autoregulation. After surgery, HR, BP(mean), CBFV(mean), respiration, sat-O(2), pCO(2) and HF powers remained unchanged. LF-powers of HR, BP, CBFV and LF-transfer function gain had decreased while the phase angle had increased (p<0.05). The reduction of LF powers and LF-gain and the higher phase angle showed reduced sympathetic modulation and improved cerebral autoregulation. The enhanced cerebrovascular stability after surgery may improve autonomic balance in epilepsy patients.

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Association of sudden infant death syndrome with grossly deranged iron metabolism and nitric oxide overload

Cited by 10 publications

References 24 publications

Alteration in regulation of inflammatory response to influenza a virus and endotoxin in suckling rat pups: a potential relationship to sudden infant death syndrome

Alteration in regulation of inflammatory response to influenza a virus and endotoxin in suckling rat pups: a potential relationship to sudden infant death syndrome

Ventilatory Response to Hypoxia during Endotoxemia in Young Rats: Role of Nitric Oxide

Cerebral autoregulation improves in epilepsy patients after temporal lobe surgery

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