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Transplantation. 1992 Jun;53(6):1211-4.
Breakdown of hepatic tight junctions during reoxygenation injury.

Konno H, Lowe PJ, Hardison WG, Miyai K, Nakamura S, Baba S.

Second Department of Surgery, Hamamatsu University School of Medicine, Japan.

We investigated whether reoxygenation following anoxia increased biliary permeability and whether or not allopurinol had a protective effect. Isolated rat livers were perfused for 30 min in a one-pass system with buffer equilibrated with 100% nitrogen after stabilization, and then for 60 min with the oxygenated buffer. Hepatic tight junction permeability was assessed by quantifying the early appearance in the bile of horseradish peroxidase (HRP) injected with the perfusate. This early peak represents paracellular passage of HRP, whereas a later second peak results from transcellular passage. In the control livers, 7% of the total HRP passage (93 +/- 50 pg/g liver) was paracellular and 93% was transcellular. After 30 min of reoxygenation following anoxia, however, 516 +/- 20 pg/g liver of HRP passed paracellularly. Addition of allopurinol (5 micrograms/ml) to the perfusate from the start of perfusion reduced paracellular passage of HRP to 219 +/- 49 pg/g liver after anoxia and reperfusion (P less than 0.01). Allopurinol also reduced the cumulative lactate dehydrogenase (LDH) release during the first 30 min of reoxygenation from 2.1 +/- 0.3 x 10(4) to 1.4 +/- 0.4 x 10(4) units/g liver (P less than 0.01). Reduction of the anoxic period from 30 min to 25 min significantly reduced the change in tight junction permeability and the extent of cellular injury: Paracellular passage of HRP was 336 +/- 20 pg/g and LDH release was 0.7 +/- 0.1 x 10(4) units/g liver, both significantly lower than those at 30 min (P less than 0.01). No significant difference in hepatic ATP levels after 60 min of reoxygenation was noted among the experimental groups, but all had lower levels than the control group. The protective effect of allopurinol suggests that the mechanism of biliary reoxygenation injury involves free radical generation. Susceptibility of tight junctions suggests a pattern of injury similar to that involved in anoxic damage of the vascular endothelium.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1604475&dopt=Abstract




East Afr Med J. 1994 Jul;71(7):453-9.
Is one year follow-up justified in kala-azar post-treatment?

Nyakundi PM, Wasunna KM, Rashid JR, Gachihi GS, Mbugua J, Kirigi G, Muttunga J.

Clinical Research Centre, Kenya Medical Research Institute, Nairobi.

Sixty-five patients, 51 males and 14 females, with clinical and parasitological evidence of visceral leishmaniasis were initially treated as follows: 44.6% were on intravenous sodium stibogluconate (pentostam) 20 mg/kg/d for 30 days, 35.4% was on a combination of pentostam as above and allopurinol 21 mg/kg/d in three divided doses for 30 days while 20% was on pentostam 10 mg/kg thrice/d intravenously for 10 days. All patients were parasitologically negative by the end of their respective treatment regimen. All patients were reviewed at 2 months, 6 months, and 12 months periods in order to evaluate the relapse rates and optimal follow-up period. Thirteen patients (20%) relapsed at 2 months and one patient (1.5%) relapsed at 6 months follow-up periods respectively. There was no relapse between 6 months and 12 months follow-up period. The mean liver and spleen sizes in responders showed a dramatic reduction at 2 months follow-up and thereafter a gradual reduction occurred in the next 10 months. Weight gain continued throughout the year. Apart from platelet count which showed a sustained high level from discharge to 12 months follow-up, the peripheral blood indices stabilized from 2 months follow-up. Relapses were retreated until parasitologically negative twice and then followed up, for a period of 12 months. At follow-up the liver and spleen sizes reduced gradually in the next 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7828500&dopt=Abstract




Am J Trop Med Hyg. 1984 May;33(3):357-61.
The response of Kenyan kala-azar to treatment with sodium stibogluconate.

Rees PH, Kager PA, Wellde BT, Hockmeyer WT.

Of 16 patients with kala-azar treated with sodium stibogluconate (0.1 ml/kg body weight a day), one died on the 12th day of treatment and nine were cured by a 30-day course, although two subsequently relapsed. Extending the course cured a further five patients, and in one patient allopurinol was used in addition before a cure was achieved. Clinical and hematological recovery began within a few days of the start of treatment, but parasites continued to be seen in splenic aspirates for 3 weeks or more.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6329010&dopt=Abstract












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