Energy Metabolism of the Heart and the Liver in Brain-Dead Dogs as Assessed by 31P NMR Spectroscopy

Kitai, Toshiyuki; Terasaki, Mitsuhiro; Okamoto, Ryuichi; Ozawa, Kazue; Morikawa, Shigehiro; Inubushi, Toshiro

doi:10.1006/jsre.1993.1191

Cited by 10 publications

(3 citation statements)

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“…However, despite an initial drop in HEP during the autonomic storm, studies have found that HEP concentrations remain conserved thereafter. [21][22][23] This result is consistent throughout species and analytical methods. Two studies found that the right ventricle (RV) post-BSD, was susceptible to a drop in HEP; however, these results failed to reach…”

Section: The Heart Donorsupporting

confidence: 68%

“…25 The catecholamine storm reportedly lasts between 3-30 mins, after which levels return to baseline. 19,[26][27][28] This creates 2 haemodynamic phases post-BSD, the hyperdynamic phase [19][20][21] (hypertension, tachycardia, [22][23][24] vasoconstriction) and the hypoactive phase (hypotension, bradycardia, loss of vasomotor tone). 29 Total sympathectomy or adrenergic antagonism has been shown to ameliorate these effects, confirming the deleterious role of catecholamines.…”

Section: Catecholamine Stormmentioning

confidence: 99%

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Peritransplant Cardiometabolic and Mitochondrial Function: The Missing Piece in Donor Heart Dysfunction and Graft Failure

et al. 2021

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Primary graft dysfunction (PGD) is an important cause of morbidity and mortality after cardiac transplantation. Donor brain stem death (BSD) is a significant contributor to donor heart dysfunction (DHD) and PGD. There remain substantial gaps in the mechanistic understanding of peritransplant cardiac dysfunction. One of these gaps is cardiac metabolism and metabolic function. The healthy heart is an 'omnivore', capable of utilising multiple sources of nutrients to fuel its enormous energetic demand. When this fails, metabolic inflexibility leads to myocardial dysfunction. Data have hinted at metabolic disturbance in the BSD donor and subsequent HTx, however, there is limited evidence demonstrating specific metabolic or mitochondrial dysfunction. This review will examine the literature surrounding cardiometabolic and mitochondrial function in the BSD donor, organ preservation, and subsequent cardiac transplantation. A more comprehensive understanding of this subject may then help to identify important cardioprotective strategies to improve the number and quality of donor hearts.

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Section: The Heart Donorsupporting

confidence: 68%

Section: Catecholamine Stormmentioning

confidence: 99%

Peritransplant Cardiometabolic and Mitochondrial Function: The Missing Piece in Donor Heart Dysfunction and Graft Failure

et al. 2021

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“…The electron-microscopic examination findings, which indicated the integrity of hepatic mitochondria to be well preserved, may support this view. Kitai et al [27] also reported the energy metabolism of the liver as being satisfactorily maintained in brain-dead dogs.…”

Section: Discussionmentioning

confidence: 98%

Protective Effects of Urinary Trypsin Inhibitor (UTI) on Hepatic Microvasculature in Hypotensive Brain-Dead Rats

Itabashi

Yoshiya²,

Takahashi³

et al. 2002

Eur Surg Res

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Background/Aims: We examined the protective effects of a protease inhibitor, urinary trypsin inhibitor (UTI), on livers of brain dead rats associated with systemic hemodynamic instability. Methods: Brain death was induced by inflating a balloon catheter placed in the epidural space in rats followed by intravenous administration of UTI for 6 h. The hemodynamic, functional and morphological changes in the liver were examined. Results: The induction of brain death resulted in a significant decrease in both mean arterial pressure (MAP) and hepatic tissue flow (HTF), and an increase in serum AST and cytokines such as tumor necrosis factor (TNF)-α and cytokine-induced neutrophil chemoattractant (CINC). An increase in the number of sequestered neutrophils and enhanced expressions of intercellular adhesion molecules (ICAM)-1 and CINC were also noted in the liver. The treatment with UTI significantly restored HTF to basal level without affecting MAP, and decreased the number of sequestered neutrophils in the hepatic sinusoids, suppressed the expression of ICAM-1 and CINC in the sinusoids, inhibited the production of serum TNF-α and CINC, and inactivated Kupffer cells. Conclusion: Intravenous administration of UTI is likely to ease unfavorable effects on the hepatic microvasculature evoked by brain death.

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Acute Increase of Myocardial Workload, Hemodynamic Instability, and Myocardial Histological Changes Induced by Brain Death in the Cat

Bruinsma¹,

Nederhoff²,

Geertman³

et al. 1997

Journal of Surgical Research

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Energy Metabolism of the Heart and the Liver in Brain-Dead Dogs as Assessed by 31P NMR Spectroscopy

Cited by 10 publications

References 0 publications

Peritransplant Cardiometabolic and Mitochondrial Function: The Missing Piece in Donor Heart Dysfunction and Graft Failure

Peritransplant Cardiometabolic and Mitochondrial Function: The Missing Piece in Donor Heart Dysfunction and Graft Failure

Protective Effects of Urinary Trypsin Inhibitor (UTI) on Hepatic Microvasculature in Hypotensive Brain-Dead Rats

Acute Increase of Myocardial Workload, Hemodynamic Instability, and Myocardial Histological Changes Induced by Brain Death in the Cat

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