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F U Sack

Publications and source records attributed to F U Sack.

26 records · Page 2Linked to original sources
PubMed1991

Performance of dynamic cardiomyoplasty related to the functional state of the heart.

Cardiomyoplasty (CMP) was performed with the left Latissimus dorsi in five beagles (group 1) with intact hearts and seven foxhounds (group 2) in whom the left ventricle was enlarged by 31 +/- 11.9% of cross-sectional area. Ventricular function curves were constructed at filling pressures ranging from 15-40 mmHg (group 2). Myocardial contraction patterns were investigated by epicardial 2-D echocardiography. Skeletal muscle contraction caused a significant increase in aortic pressure, dP/dt, stroke volume, work and performance in all animals. Function curves were shifted upward in a parallel manner. Echocardiography showed an increase of the LV cross-sectional delta area of 14.8% +/- 5.8% (group 1) and of 39.5% +/- 15.1%, and approximation of the edges of the wall defects (group 2). In conclusion, dynamic CMP as applied in this acute model, increased the performance of normal canine hearts and hence, a model of cardiac failure may not be a prerequisite for the investigation of certain technical aspects of CMP. In the failing heart, a parallel upward shift of myocardial function curves suggested increased performance of the heart/skeletal muscle complex over a wide range of filling pressures. However, the descending limb of the function curve with increasing filling pressures was observed despite skeletal muscle contraction. Hence, similar to other assist systems, the residual function of the heart may be of considerable importance in the overall performance of dynamic CMP.

Acute Disease↗
PubMed1991

Reduction of postischemic reperfusion injury by the vasoactive drug buflomedil.

The effect of buflomedil on postischemic reperfusion injury was studied in the dorsal skin fold chamber preparation of awake hamsters. Microvascular events were investigated in the striated skin muscle by means of intravital fluorescence microscopy prior to 4 h of pressure-induced ischemia and 30 min, 2 and 24 h after reperfusion. In untreated control animals, ischemia and reperfusion provoked marked leukocyte sticking and macromolecular leakage while functional capillary density was reduced. Treatment with buflomedil (3 mg/kg b.w. in 0.3 ml saline, administered as bolus of 0.1 ml 10 min prior to release of ischemia followed by i.v. infusion of 0.2 ml during the first 20 min of reperfusion) significantly reduced leukocyte sticking and macromolecular leakage, while functional capillary density was effectively preserved. No differences in macro- and microhemodynamic parameters were observed between buflomedil-treated and untreated animals. These findings support the concept that activated leukocytes are involved in the microvascular manifestation of reperfusion injury and indicate that leukocyte sticking and its sequelae can be efficiently prevented by treatment with buflomedil.

Animals↗
PubMed1989

Tissue oxygenation after prolonged ischemia in skeletal muscle: therapeutic effect of prophylactic isovolemic hemodilution.

Prolonged ischemia is known to cause severe damage in skeletal muscle and skin as a result of reperfusion failure. Isovolemic hemodilution has been suggested as a modality to reverse microcirculatory disorders by improving flow properties and flow conditions of the blood. The aim of the present study was to investigate whether prophylactic isovolemic hemodilution could improve tissue oxygenation after 4h of pressure induced ischemia in skeletal muscle. In 17 Syrian golden hamsters a dorsal skin fold chamber and two permanent arterial and venous catheters were implanted. Following a recovery period of 48h ischemia was induced for 4h by means of a transparent stamp compressing the tissue within the chamber. In 9 animals (control, hct 43%) measurements of tissue PO2 (platinum multiwire electrode) were performed prior to and 15 min, 2h and 24h after release of ischemia. In 8 animals isovolemic hemodilution with Dextran 60 (hct 29%) was carried out prior to ischemia and measurements of local tissue PO2 were performed as reported for the control group with an additional measurement 30 min after hemodilution. In control animals tissue PO2 decreased significantly (p less than 0.01) from 20.7 +/- 2.4 mmHg prior to ischemia to 8.8 +/- 3.1 mmHg after 15 min of reperfusion; after 24h tissue PO2 was 15.6 +/- 6.1 mmHg. In hemodiluted animals tissue PO2 increased due to hemodilution from 20.9 +/- 1.6 mmHg to 23.5 +/- 2.5 mmHg (p less than 0.05); after 15 min of reperfusion tissue PO2 was 19.8 +/- 6.8 mmHg and remained unchanged for 24h (20.0 +/- 2.5 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Computer assisted leukocyte adhesion measurement in intravital microscopy.

The pathogenetic role of the leukocytes in the development of postischemic injury is not yet understood. Therefore a model was developed which allows for in vivo quantification of leukocyte-endothelium interaction in the awake animal. The velocity of leukocytes was measured by means of intravital microscopy and interactive digital image analysis. An adhesion coefficient (AC) was calculated which characterizes the degree of the leukocyte-endothelium interaction. A special procedure of automatically taking image samples for the leukocyte velocity measurement reduces observer bias. As shown in a validation experiment, this procedure yields reproducible results and therefore allows to quantify the influence of prophylactic and therapeutic measures on postischemic leukocyte-endothelium interaction.

Animals↗
PubMed1988

Quantitative analysis of microcirculatory disorders after prolonged ischemia in skeletal muscle. Therapeutic effects of prophylactic isovolemic hemodilution.

Reperfusion injury following prolonged ischemia is thought to be caused primarily by microvascular failure. The aim of the present study was to investigate whether prophylactic isovolemic hemodilution with Dextran 60 (hct 30%) could improve microvascular perfusion after 4 h of pressure-induced ischemia in skeletal muscle. In 28 Syrian golden hamsters (6-8 weeks/60-80 g b. wt.) a dorsal skinfold chamber and permanent arterial and venous catheters were implanted under Nembutal anesthesia (50 mg/kg b. wt.). Following a recovery period of 48 h pressure-induced ischemia was applied to the skeletal muscle within the skinfold chamber by means of a transparent stamp. Quantitative analyses of microhemodynamics were performed in the awake animal prior to and 15 min, 1, 2, 4 and 24 h after ischemia using vital fluorescence microscopy. In non-treated animals, functional capillary density decreased after 4 h of ischemia to 30% of the initial values (P less than 0.001); after 24-h reperfusion only 50% of the initially perfused capillaries were reperfused (P less than 0.001). The heterogeneity of functional capillary density increased after ischemia to a maximum of 2.19 +/- 0.94 as compared to 0.48 +/- 0.11 prior to ischemia. Capillary RBC-velocity suffered a marked reduction in the early reperfusion phase and did not recover up to the 24-h observation time. In contrast, prophylactic isovolemic hemodilution was associated with only a small and reversible reduction of functional capillary density after 4-h ischemia. At 24-h reperfusion 90% of the initially perfused capillaries were reperfused. Capillary RBC-velocity was reduced in the early reperfusion phase, but returned to normal values within 24 h. Thus, prophylactic isovolemic hemodilution resulted in a marked reduction of microvascular reperfusion failure in skeletal muscle. A hematocrit lower than normal prior to ischemia provides better conditions for capillary reperfusion after prolonged ischemia.

Animals↗
PubMedDate not supplied

Endothelin plasma levels in acute graft rejection after heart transplantation.

BACKGROUND: Endothelin is an oligopeptide of endothelial origin with potent vasoconstrictive and mitogenic properties, implicated in the pathogenesis of cyclosporine-induced hypertension, graft vasculopathy, and renal failure. Experimental animal data suggest a role for endothelin in allograft rejection also. METHODS: To determine the role of endothelin in acute graft rejection after heart transplantation, we determined endothelin plasma levels in 165 blood samples from 79 cardiac allograft recipients (2 to 81 months after the operation) with normal graft function and correlated our findings with the histologic severity of acute graft rejection according to International Society for Heart and Lung Transplantation grading. For comparison endothelin levels were determined in 30 healthy controls and in 22 early postoperative transplant recipients (< 2 months after the operation). RESULTS: Endothelin plasma levels were significantly higher in transplant recipients than in controls (early postoperative: 7.97 = 7.53 pg/ml; late postoperative: 3.68 +/- 1.72 pg/ml; controls: 1.55 +/- 0.89 pg/ml). Endothelin plasma levels were not significantly different between groups of rejection grades 0 to 4. In the comparison of two groups of no rejection or lower (International Society for Heart and Lung Transplantation grade 0 and 1, n = 134) and higher (International Society for Heart and Lung Transplantation grade > or = 2, n = 31) rejection severity or comparing patients requiring rejection therapy (n = 20) with those not requiring therapy (n = 145), endothelin levels did not differ significantly between the groups. In 22 patients with three to six available consecutive biopsy scores and endothelin levels, intraindividual longitudinal analysis did also not show any significant correlation. The only positive correlation of endothelin levels with other laboratory parameters was found with serum creatinine concentrations (p < 0.001). In the early postoperative recipients, no correlation of endothelin plasma levels with rejection severity was seen; furthermore the only significant association was found with time after operation. CONCLUSIONS: In this study endothelin plasma levels were not influenced by acute allograft rejection after heart transplantation. Therefore endothelin levels do not appear to be a useful marker for noninvasive rejection diagnosis. Furthermore, a relevant pathogenetic role of endothelin in the rejection process cannot be derived from these data.

Acute Disease↗