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G Gollin

Publications and source records attributed to G Gollin.

25 records · Page 2Linked to original sources
PubMed1993

Biochemical detection of small intestinal allograft rejection by elevated circulating levels of serum intestinal fatty acid binding protein.

BACKGROUND: Intestinal fatty acid binding protein (I-FABP) was investigated as a serum marker for acute intestinal allograft rejection. Its behavior was compared with that of another putative marker of intestinal damage, hexosaminidase. METHODS: Transplants were performed in three groups of rats: group 1, Lewis to Lewis; group 2, ACI to Lewis, no immunosuppression; and group 3, ACI to Lewis with cyclosporine given on posttransplant days 0 through 5. Daily serum I-FABP and hexosaminidase levels were quantitated and serial graft biopsy specimens were obtained. RESULTS: Serum I-FABP levels fell to 20 ng/ml or less in all animals between posttransplant days 3 and 4. In group 1, I-FABP levels remained at baseline throughout the experiment. In group 2, I-FABP levels rose dramatically on either day 6 or 7 and declined to baseline within 4 days of the peak. On the day that I-FABP levels increased, findings of biopsy specimens were consistent with early rejection. In group 3 the rise in serum I-FABP levels was delayed 2 to 10 days. Hexosaminidase did not correlate with rejection. CONCLUSIONS: Serum I-FABP content correlated with early histologic manifestations of rejection. Hexosaminidase was insensitive as a marker in this model. I-FABP, which has a human analog, has potential as a biochemical marker for early intestinal allograft rejection.

Animals↗
PubMed1993

Intestinal fatty acid binding protein in serum and urine reflects early ischemic injury to the small bowel.

BACKGROUND: Intestinal fatty acid binding protein (I-FABP) is a 15 kd protein that constitutes 2% to 3% of enterocyte protein. Normally I-FABP is undetectable in serum. The purpose of this study was to determine whether I-FABP could be detected in peripheral serum and/or urine early in the evolution of intestinal ischemic injury. METHODS: I-FABP and two putative biochemical markers of mesenteric ischemia, hexosaminidase and lactate dehydrogenase, were quantitated in the serum of rats subjected to mesenteric ischemia produced by: (1) 0.5 hours, 1 hour, or 3 hours of superior mesenteric artery (SMA) occlusion followed by reperfusion; (2) 1 hour of mesenteric occlusion to a 10 cm segment of jejunum followed by reperfusion; and (3) arterial ligation to a 10 cm segment of jejunum without reperfusion. I-FABP was also quantitated in the urine and intestinal mucosa of these animals. RESULTS: The baseline serum I-FABP level was < or = 4.0 ng/ml in all animals. In control animals, I-FABP remained unchanged throughout the experiment. In the ischemia/reperfusion groups, I-FABP immediately appeared in the serum on reperfusion. With segmental arterial ligation, I-FABP was detected in the serum within 15 minutes. Urinary content of I-FABP rose 60 minutes after its initial appearance in the serum, and its elimination paralleled serum I-FABP levels. Serum hexosaminidase and lactate dehydrogenase levels only rose after 3 hours of SMA occlusion with reperfusion. One hour of SMA occlusion and reperfusion resulted in only mild to moderate mucosal injury, whereas 3 hours of SMA ischemia with reperfusion produced areas of transmural necrosis. CONCLUSIONS: I-FABP is released into the peripheral circulation after reversible intestinal ischemic injury and has potential as a biochemical marker to facilitate the early detection of mesenteric ischemia.

Animals↗
PubMed1985

Does prostacyclin (PGI2) cardioplegic infusion improve myocardial protection after ischemic arrest?

To determine whether prostacyclin (PGI2) plays a beneficial role in the blood-perfused heart undergoing global ischemia, 20 isolated canine hearts were studied after sustaining one hour of cardioplegic arrest under moderate hypothermia (27 degrees to 28 degrees C). Left ventricular function (peak systolic pressure, rate of rise of left ventricular pressure [dP/dt], and compliance change in left ventricular volume), myocardial edema, coronary blood flow, and oxygen content were measured during the preischemic period and at 15 and 30 minutes during reperfusion. Results showed an improved hemodynamic recovery (peak systolic pressure, p = 0.018 at 30 minutes; dP/dt, p = 0.020 at 15 minutes) in the group of hearts treated with PGI2 infusion compared with controls. There was no difference in ventricular compliance or myocardial edema between the two groups. This benefit was attributed to a significant increase in myocardial blood flow (p = 0.028 at 15 minutes) and oxygen delivery (p = 0.021 at 15 minutes) during the reperfusion period with PGI2. These data suggest a potential clinical role for PGI2 when applied to the globally ischemic heart in the improvement of myocardial resuscitation during the early reperfusion period.

Animals↗
PubMed1984

Carbon-13 nuclear magnetic resonance studies of myocardial glycogen metabolism in live guinea pigs.

Myocardial glycogen metabolism was studied in live guinea pigs by 13C NMR at 20.19 MHz. Open-chest surgery was used to expose the heart, which was then positioned within a solenoidal radio frequency coil for NMR measurements. The time course of myocardial glycogen synthesis during 1-h infusions of 0.5 g of D-[1-13C]glucose (and insulin) into the jugular vein was investigated. The possible turnover of the 13C-labeled glycogen was also studied in vivo by following the labeled glucose infusion with a similar infusion of unlabeled glucose. The degree of 13C enrichment of the C-1 glycogen carbons during these infusions was measured in heart extracts by 1H NMR at 360 MHz. High-quality proton-decoupled 13C NMR spectra of the labeled C-1 carbons of myocardial glycogen in vivo were obtained in 1 min of data accumulation. This time resolution allowed measurement of the time course of glycogenolysis of the 13C-labeled glycogen during anoxia by 13C NMR in vivo. With the solenoidal coil used for 13C NMR, the spin-lattice relaxation time of the labeled C-1 carbons of myocardial glycogen could be measured in vivo. For a comparison, spin-lattice relaxation times of heart glycogen were measured in vitro at 90.55 MHz. Natural abundance 13C NMR studies of the quantitative hydrolysis of extracted heart glycogen in vitro at 90.55 MHz showed that virtually all the carbons in heart glycogen contribute to the 13C NMR signals. The same result was obtained in 13C NMR studies of glycogen hydrolysis in excised guinea pig heart.

Animals↗
PubMed1983

In vivo 31P-NMR studies of myocardial high energy phosphate metabolism during anoxia and recovery.

31P NMR spectra of heart in-situ in live guinea pigs were obtained continuously in 20.5 s time blocks during 3 min of anoxia, during subsequent reoxygenation and, in separate animals, during terminal anoxia. Reversible anoxia resulted in rapid degradation of phosphocreatine (t 1/2 = 54.5 +/- 2.5 s) which recovered fully during reoxygenation. Heart Pi increased during anoxia and returned to basal levels after oxygen was restored. During 3 min of anoxia, no significant changes in ATP levels or pH were detected. The results demonstrate that it is feasible to measure rapid fluxes of high energy phosphates by 31P NMR in intact animals during and after anoxic stress to the myocardium.

Animals↗
PubMedDate not supplied

Diagnosis of acute and chronic cardiac rejection by magnetic resonance imaging: a non-invasive in-vivo study.

To evaluate the potential usefulness for characterization of tissue and anatomical changes associated with cardiac transplantation rejection by nuclear magnetic resonance imaging (MRI), sixteen dogs underwent heterotropic cardiac transplantation with six not immunosuppressed serving as controls. Myocardial biopsy and MRI were obtained and compared on a weekly basis. Untreated allografts showed a significant increase in T2 and intensity values by MRI compared to the native heart as early as one week after transplantation. The MRI findings corresponded to the histological progression of acute rejection process in both treated and untreated groups. The linear relationship between histology and MRI was 0.72 while the correlation between T2 and the water content was 0.92. Serial gated MRI correlated with chronic anatomical changes of transplant rejection with evidence of progressive or increasing myocardial wall thickness and decrease in ventricular chamber size.

Animals↗