(-)15-Deoxyspergualin, originally discovered as an antitumoral drug, was shown to have different immunosuppressive effects, when pancreas and orthotopic allogeneic liver transplantations in rats were compared. In the strong rejection model dark agouti----Lewis (RT1a----RT1(1)) we could only show a minor immunosuppressive effect, as far as pancreaticoduodenal and pancreas segment transplantations are concerned: graft survival was prolonged by 9 days in pancreas segment allografts (p less than 0.01) and by 6 days in pancreaticoduodenal allografts (p less than 0.01), when recipients were treated by ten doses of 2.5 mg/kg deoxyspergualin. Pretreatment of recipients with 15-deoxyspergualin was not efficient. On the contrary, in orthotopic liver transplantation done by the cuff technique, a remarkable prolongation of allograft survival could be demonstrated: about half of the animals showed prolongation of allograft survival for more than 80 days, compared with about 11 days in the control group (p less than 0.01). The substance is considered to be valuable for clinical application.

Zur Untersuchung der pathophysiologischen Entstehung von Spätfolgen eines Schocks, z.B. einer Schocklunge, entwickelten wir ein neues tierexperimentelles Modell des protrahierten traumatisch-hämorrhagischen Schocks.

Durch langfristige Beobachtung im traumatisch-hämorrhagischen Schock des Hundes wird geprüft, ob sich frühzeitig für den weiteren Verlauf richtungsweisende Gerinnungsveränderungen zeigen.

The distribution of myocardial blood flow (MBF) was evaluated in pressure-induced LV hypertrophy of foxhounds. At the early stage of developing hypertrophy, i.e., 3 months after aortic banding (+ 53% LV weight) resting MBF and flow reserve were not significantly different from control hearts. One year after banding (+94% LV weight) myocardial flow reserve had clearly decreased. Acute coronary stenosis of 60 and 70% cross-sectional area resulted in a moderate fall of flow reserve in controls and hearts with early hypertrophy. In hearts with extensive hypertrophy the drop of poststenotic MBF was considerably greater affecting preferentially the subendocardium. The data suggest that myocardial blood flow was impaired before any signs of heart failure were observed. Furthermore a decrease of MBF may not be confined to forms of hypertrophy induced by renal and idiopathic hypertension.

Erhühte Infarktgefahrdung (1) und gesteigerte Flimmerbereitschaft stellen ein besonderes Problem bei chirurgischer Intervention am hypertrophierten Herzen dar. Besünders ischamiegefährdet sind offenbar die Herzinnenschichten (2). Da Angaben über die Myokarddurchblutung (MBF) bei der Hypertrophie weitgehend fehlen, wird die regionale Durchblutungsverteilung in den vorliegenden Experimenten untersucht. Urn der Frage nach der Ischamiegefährdung der Innenschichten nachzugehen, wurde bei den Versuchstieren zusätzlich eine akute Coronarstenose erzeugt, welche die Durchblutungsreserve der Innenschichten bereits unabhangig von der Myokardhypertrohpie einschränkt (2).

In moderate hypertrophy (+35%) of the canine left ventricle (LV), resting myocardial blood flow (MBF, tracer microspheres) was not significantly altered when compared with controls. The endo/epi flow ratio of the LV was, however, significantly smaller (0.82-0.9) than in controls (1.02-1.17). After coronary dilatation with dipyridamole, coronary flow reserve was smaller in hypertrophied hearts. This became particularly obvious when acute coronary constriction (70%) was induced. There was, however, no indication that after coronary constriction in early hypertrophy the subendocardium was more jeopardized than in controls.

Durch Langzeitbeobachtung der Blutgerinnung im experimentellen protrahierten Schock werden neben den akuten Gerinnungsstörungen Gerinnungsveränderungen der Spätphase untersucht, um Aufschluß über Pathogenese, Verlauf und Prognose zu erhalten.

Twenty mongrel dogs are subjected to a standardized traumatic hemorrhagic shock. After reinfusion of the dogs' own blood the animals are continuously observed for the 72 hr. Deterioration of general hemodynamics and activation of intravascular coagulation is more pronounced in the nonsurviving animals. Correspondingly, histologic alterations particularly of the liver and intestine are more marked in the nonsurvivors. Increase of partial thromboplastin time and long-lasting increase of the prothrombin time (Quick) appear to be early signs of a fatal prognosis.

Ergebnisse experimenteller Schockforschung wurden überwiegend an akuten Modellen gewonnen, welche den klinischen Verlauf des traumatisch-hämorrhagischen Schocks ungenügend berücksichtigen.

Experimental trauma and hemorrhage acutely reduce capillary blood flow in all organs except the heart. After reinfusion of the withdrawn blood a long-lasting increase of pulmonary bronchial blood flow and hepatic and renal blood flow is observed parallel to a rise in cardiac output. However, blood flow in the intestines, pancreas, and spleen remains significantly reduced. Particularly, renal and pulmonary bronchial blood flow is significantly higher in animals surviving for 72 hr than in animals succumbing after an average of 32 hr.