Factors relating to consent for organ donation: prospective data on potential organ donors.

BACKGROUND: Obtaining family consent to organ donation is a significant obstacle to improving further Australian deceased organ donation rates. Currently, neither the consent rates for donors eligible to donate after circulatory death, nor factors that influence decision to decline or consent to donation in general are known in Australia. METHODS: This study at four university teaching hospitals in Melbourne, Victoria, examined consecutive patients where organ donation was discussed with the family RESULTS: A total of 123 cases were identified; the family consent rate was 52.8%, and 34.1% proceeded to donation. Consent to donation was related to potential donor factors such as country of birth, cultural background in Australia, a non-religious or Christian background and registration on the Australian Organ Donor Register. Family-related factors included being English speaking and having knowledge of the deceased's wishes about organ donation. Family of donation after circulatory death-eligible donors were less likely to consent to donation than the family of donation after brain death-eligible donors, although not reaching statistical significance. Among consented potential donors, those eligible for donation after brain death and with a shorter length of stay were more likely to proceed to donating organs for transplantation. CONCLUSION: Despite a small sample size, these findings describe current consent and donation rates and associated factors and may assist in improving conversations about organ donation.

Modulation of the vagal bradycardia evoked by stimulation of upper airway receptors by central 5-HT1 receptors in anaesthetized rabbits.

1. The effects of central application of 5-HT1A and 5-HT1B/1D receptor ligands on the reflex bradycardia, apnoea, renal sympathoexcitation and pressor response evoked by stimulating upper airway receptors with smoke in atenolol-pretreated anaesthetized rabbits were studied. 2. Intracisternal administration of the 5-HT1A receptor antagonists WAY-100635 (100 microg kg(-1)) and (-)pindolol (100 microg kg(-1)) significantly reduced the smoke-induced bradycardia, attenuated the pressor response and in the case of (-)pindolol, sympathetic nerve activity. The same dose of WAY-100635 i.v. was without effect. 3. Buspirone (200 microg kg(-1), i.c.) potentiated the reflex bradycardia. This action was prevented if the animals were pretreated with WAY-100635 (100 Hg kg(-1), i.v.) 4. (+)8-OH-DPAT (25 microg kg(-1), i.c.) attenuated the evoked bradycardia, pressor response, apnoea and renal sympathoexcitation. The attenuation of the apnoea and renal sympathoexcitation, but not the bradycardia or pressor response was prevented in animals pretreated with WAY-100635 (100 microg kg(-1), i.v.). The attenuation of the reflex bradycardia and the reduction in the renal sympathoexcitation were reduced by pretreatment with the 5-HT1B/1D receptor antagonist GR127935 (100 microg kg(-1), i.v.). 5. In WAY-100635 (100 microg kg(-1), i.v.) pretreated animals, sumatriptan (a 5-HT1B/1D receptor agonist) reduced the reflex bradycardia and the pressor response. The 5-HT1B/1D receptor antagonist GR127935 (20 microg kg(-1), i.c. or 100 microg kg(-1), i.v.) had no effect on the reflex responses. 6. In conclusion, the present data are consistent with the hypothesis that activation of central 5-HT1A receptors potentiate whilst activation of 5-HT1B/1D receptors attenuate the reflex activation of cardiac preganglionic vagal motoneurones evoked by stimulation of upper airway receptors with smoke in rabbits.

Studies on the roles of ATP, adenosine and nitric oxide in mediating muscle vasodilatation induced in the rat by acute systemic hypoxia.

1. In Saffan-anaesthetized rats, we have further investigated the mechanisms underlying the vasodilatation induced by adenosine in skeletal muscle by acute systemic hypoxia (breathing 8% O2 for 5 min). 2. In eleven rats the nitric oxide (NO) synthesis inhibitor nitro-L-arginine methyl ester (L-NAME, 10 mg kg-1, i.v.) reduced the increase in femoral vascular conductance (FVC) induced by hypoxia by approximately 50%. L-NAME had similar effects on the increase in FVC induced by intra-arterial (I.A.) infusion of adenosine (at 1.2 mg kg-1 min-1 for 5 min via the tail artery) and by ATP (I.A., 1 mg kg-1 min-1 for 5 min). Subsequent administration of the adenosine receptor antagonist 8-sulphophenyl theophylline (8-SPT, 20 mg kg-1, i.v.) virtually abolished the adenosine- and ATP-induced increase in FVC. 3. In a further nine rats, 8-SPT reduced the increase in FVC induced by hypoxia by approximately 50%. This remaining increase in FVC was substantially reduced by L-NAME. 4. In an additional nine rats, alpha,beta-methyleneADP (160 micrograms kg-1, i.v.) which inhibits the 5'-ectonucleotidase that degrades AMP to adenosine, reduced the peripheral vasodilatation (fall in arterial blood pressure, ABP) induced by ATP infusion, but had no effect on the increase in FVC or decrease in ABP evoked by systemic hypoxia. 5. These results provide the first evidence that the muscle vasodilatation induced by adenosine during systemic hypoxia is mainly dependent on NO synthesis. They also suggest that adenosine is released as such rather than being formed extracellularly from AMP. Given evidence that extraluminal adenosine acts in an NO-independent fashion we propose that hypoxia releases adenosine from the endothelium. Our results also indicate that hypoxia induces muscle vasodilatation that is adenosine independent but NO dependent: they allow the possibility that this is partly mediated by ATP released from the endothelium.