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Mechanisms causing the death of 8 calves surviving with implanted artificial heart from 31 to 173 days
Exp. Path. 26,
~~1~-~~5
(1984)
Research Center of the Regional Institute of National Realth (KUNZ), Brno, CSSR; Slovak Academy of Sdences, Centre of Physiological Sciences, Institute of Normal and Pathological Physiology, Bratislava, OSSR 2) Institute of Pathological Anatomy, l\iedical FatuIty, J. E. Purkyne University, Rrno, CSSR 1
Mechanisms causing the death of 8 calves surviving with implanted artificial heart from 31 to 173 days By B. RARTMANNOVA, J. VASKl;, S. DOLEZEL1 ), Eo URBANEK, J. FILKUKA2), T. SLADEK, L. KRCEK, P. GUBA, M. DOSTAL, J. CERNY, E. SOTAKOVA, P. URBANEK, P. RANZELKA and JAN VASKU
With 3 figures (Received October 25, 1983)
Address for correspondence: Prof. Dr. JAROMJR VASKU, Institute of Pathophysiology, University of J. E. Purkyne, Komenskeho mim 2, 662-43 Brno, OSSR Key words: heart implantation; artificial heart; death causes; calf
Summary Causes of the death of four animals from the total of eight were technical failures (diaphragm perforations, disconnection of the quick-connector, and a failure of the supply of electric current which could not be prevented). Causes of the death of the remaining four animals were embolisation in the brain stem, embolisation in the superior mesenteric artery leading to diffuse peritonitis, ruptures of aorta and hemocoagulation disorder causing fatal gastrointestinal bleeding. Introduction
A considerable progress in the research on the replacement of the heart with a total artificial heart (TAR) was achieved in the last few years. Reports of the leading research groups show that calves with the TAR had survived already more than 100 days (1, 3, 6, 7, 10, 8). The contributions of our group to this research were reported by 12, 2, 4, 11, 5. The present report brings a short survey of mechanisms leading to the death of eight animals surviving from 31 to 173 days.
Materials and Methods TAR was implanted to 8 calves of both sexes, weighing from 73 to 98 kg, 2-4 months old. The implantation was carried out by means of right-side thoracotomy. The heart ventricles were removed together with the atrioventricular valves. Atrial stumps and distal parts of the aorta and pulmonary artery were sutured with polyester cuffs provided with a quick-connector. The atrial connectors and conneetors of the aorta and of the pulmonary artery were coupled to the mouthpieces of the TAR (for details see: 2). The implanted TAR of the type BRNO-II was fabricated from polymethylacrylate with exception of the diaphragm, which was made of segmented poly ether-urethane (7 implantations); type BRNO-III was made totally of segmented polyurethane (1 implantation). The whole device, i.e. TAR including valves, the pneumatic driving, and control unit was developed by our research group (4) . . The dead animals were routinely autopsied. The thoracic cavity was opened in such a way that the position of the artificial heart, atrial stumps, and great blood vessels joined to TAR were not changed. The technical state of TAR was tested postmortally. The amount of thrombotic deposits inside TAR was evaluated. The organs were dissected in the conventional manner; the vessels wer cut
221
Fig. 1. The view in the left atrium. The semilunar fibrous outgrowth ("pannus") partially occludes the inflow orifice of the TAH (calf No. 51 surviving 142 d). lengthwise so that the adhering thrombi could be found. Histological material was taken from all parenchymatous organs. Special attention was paid to samples of both atria, the aorta and the pulmonary artery excised in sites of the sutures. Slices of tissues were prepared from paraffin blocks and stained by standard histological methods. In addition to the morphological findings, biochemical, hematological, hemodynamical, bacteriological and respirological findings were considered.
Results and Discussion Cause of the death of the calf No. 54, "Waldemar" (surviving for 31 d) was the thromboembolic occlusion of the stem of the superior mesenteric artery with subsequent infarction of the gut. This accident led to the diffuse peritonitis with lethal outcome. The occluding embolus was derived from thrombotic vegetations localized on the inflow valve in the left artificial ventricle. The calf No. 55, "Kamil" (surviving for 35 d), died in consequence of aorta rupture. Hemomediastinum and right-side hemothorax resulted. The cause of the aortic perforation was a chronic necrotizing aortitis localized around the suture of the aorta with the aortic quickconnector; multiple voluminous thrombotic vegetations growing on the ulcerated endothelium of the aorta were observed [s.c. vegetative endocarditis or aortitis according to OLSEN (9)]. A chronic infection localized in the site of the suture seems to be responsible for these changes. Technical failures were causes of the death of calves No. 52, "Samson", and No. 60 "Fatima" (surviving for 105 d and 75 d respectively). In both cases a perforation of the diaphragm of right artificial ventricle occurred. The blood was pumped into the pneumatic part of TAR. The gradual occlusion of the pneumatic driving tube with dried coagulated blood resulted and ultimately led to the blocking of pumping. Negligible amounts of deposits were found inside T AH in both cases.
222
Fig. 2. The fibrous capsule covering the outer surface of TAR forming "pseudo cardium" (calf No. 53 surviving 155 d).
The calf No. 51, "Dalibor" survived for 142 d; its hematological, hemodynamicaL biochemical and respiratory data were within physiological range. The termination of this experiment was caused by a failure in the supply of electric current which could not be prevented. The semilunar fibrous outgrowth, called pannus, partially occluded the inflow orifice (fig. 1); the left-side pannus was somewhat greater than the right one. The other pathological changes were negligible and could not cause the death of the animal. The cause of death of the calf No. 50, "Hasan" (surviving for 150 d), was a hemocoagulation disorder developed during the anticoagulation therapy. The massive bleeding in the bowels caused a severe posthemorrhagic anemia; the cerebral anoxia led ultimately to the death. Moreoever, a clinical state was influenced by a chronic sepsis occurring during the last 50 d. Klebsiella aerobacter was identified by hemocultivation. Calf No. 53, "Florian", survived 155 d. The cause of death was embolisation in the brain stem by calcified thrombi, originating as mineralized deposits on the inner surface of the polyetherurethane diaphragm. The repeated contact of the inflow flap valves with the diaphragm caused the gradual removing of the calcified deposits in the form of the minisplits, which were the cause of the embolism. Calf No. 59, "Omar", survived for 173 d in very good clinical state. The death of this calf was caused by a disconnection of the quick-connector of the left-hand mouthpiece of the blood pump. The left inflow tract was thus opened. Two factors were important here. First, possible disintegration of the material of the quick-connector, and second, the enormous weight of the calf, which caused an enlargement of the mediastinal cavity. Thus, a strain traction was induced at the site of the connection which could be a cause of the failure. The opened left inflow tract caused the peculiar state of the "tamponade of the artifical heart". Because this calf reached a body weight of 200 kg it became a world champion if
223
TNS
Fig. 3. Mineralised dpposits on thl' innn surface of the polyurethane diaphragm of TAH (calf No. 53 surviving 155 dl.
the relationship between the animal body weight and the size of TAR, which had a blood chamber of a volume of 100 ml on each side, is considered. The following findings were common for all animals of this "long-surviving" group. A fibrous capsule covered the outer surface of the TAR in all cases (fig. 2). It originated from the blood clots adhering to one outer surface of TAR immediately after the implantation. These clots were gradually replaced by the granulation tissue which changed to the fibrotic one during the course of the postoperative period. This development could be observed histologically in those tissue samples, where initial phases of this growth were intercepted. The so-called pseudointima originates by a similar process from white thrombotic layer formed in streaming blood on the inner surface of TAR. The calcifications were found on the inner surface of the polyurethane diaphragm of TAR. The extent of these mineralised deposits among individual calves was compared. Different amounts of deposits were found even though the survival time was taken into consideration. The deposits were most developed in calf No. 53, "Florian", where both diaphragms of the artifical ventricle were similarly affected (fig. 3). Contrary to this finding, the calves No. 52, "Samson", and No. 60, "Fatima", did not show any marked mineralisation process inside TAR. Thrombi adhering to the valves were also absent. It remains to be elucidated whether the different pictures of the mineralised deposits on the diaphragm were caused by various properties of its surface resulting from variations in the technology of their fabrication, or whether it was caused by differences in disposition for calcification in individual calves. These differences may result from an enhanced calcifying potency or from an enhanced suppressive mechanism decreasing the intensity of the calcium and phosphate movements
224
between thl' ti,sue, and bod~' fluids. III this easp we can also suppose that the deposits are formed by a calciphylactic mechanism. The picture of the chronic venostasis of various degree was found. It was most pronounced in calves surviving for the longest time and reaching the highest increase in weight. It was characterised e.g., by the "nutmeg liver". The above-described venostatic changes especially in the liver, are a consequence of the gradually increasing central venous pressure (CYP). The increased CYP correlated with the growth of the animals. The inadequacy between the size of the blood pump and its pumping capacity on the one hand and the increasing weight of the body on the other hand can be only partially corrected by the control and driving regimen. Thus, the liver microcirculatory disturbance due to venostasis could not be prevented in the course of the entire experiment. The above-described change with the subsequent liver enlargement and increased hepatic index (the liver weight related to the body weight) were final outcome of this process. In conclusion eight calves surviving 31-173 d (mean survival 108.1 d) were investigated by autopsy with TAR. The achieved lifespan of experimental calves maintained by artificial circulation reaches the level obtained by other groups working in this field. Moreover, no death on the operation table oecurred in the last three years.
Literature 1. ATSUMI, K., FUJIMASA, K. IMACHI, T. NISHISAKA, I. MANO, H. OHMISHI, N. IWAI and A. KONO, Analysis of long survivals (over one month) in the total artifical heart replacement. ESAO Proc~edings 3, 44-48 (1976). 2. CEl{XY, J., M. DOSTAL, J. VASKl:, V. KORisTEK and B. BEDNARiK, Chirurgiceskije aspekty implantace iskusstvennogo serdca. Scripta medica 53, 535-538 (1980). 3. FliKuMAse, H., D. B. OLSEN, J. H. LAWSON, T. MOCHIZUKI, N. DAITOH and F. IWAYA, Reopcrative surgery in calves with a total artificial heart. Int. J. Artif. Organs 3, 24-30 (1980). 4. HAl\ZELKA, P., JAN VASKl:, P. URBANEK, V. KRCMA, .J. VASKU and E. URBANEK, Development of artificial heart in Czechoslovakia. Bioengineering aspects. Scripta medica 53, 539-542 (1980). 5. H.\RTMAXNOyA, B., J. VASKU, S. DOLEZEL, E. URBANEK, .J. FILKULKA, T. SLADEK, L. KRCEK, P. GUBA, M. DOSTAL, J. CERNY, E. SOTAKOYA, P. URBANEK, P. HANZELKA and JAN VASKU, Patomorfologicky rozbor pticin umrti zvifat dlouhodobe prezivajicich po totalni nahrade srdcc. Cs. fysiologie 29,176-177 (1980). 6. HASTINGS, W., J. L. AARON, J. DE:'!ERIS, T. R. KESSLER, A. B. PONS, K. J. RAZZECA, D. B. OLSEN and W. J. KOLFF, A retrospective study of nine calves surviving five months on the pneumatic total artificial heart. Trans. Am. Soc. Artif. Inter. Organs. 27, 71-76 (1981). 7. KASAl, S., 1. KOSHINO, T. WASHIZP, G. ll. JAKOBS, N. MORINAGA, R. KIR.UY, Y. NOSE, Survival of 145 days with a total artificial heart. J. Thoracic and Cardiovasc. Surg. 73, 637-646 (1977). 8. LAWSON, J. R., H. FrKUMASl:, D. B. OLSEN, R. K. JARVIK, T. R. KESSLER, D. COLEMAN, A. B. PONS, R. BLAYLOCK and W. J. KOLFF, Six months survival of a calf with an artificial heart. Artif. Heart 78, 150-156 (1979). 9. OLSEN, D. B., W. C. DE VlUES, P. OYER, B. REITZ, J. MURASHITA, W. J. KOLFF, N. DAITOH, R. K. J ARVIK and R. GAYKOWSKI, Artificial heart implantation, later cardiac transplantation in the ealf. Trans. Am. SO('. Artif. Inter. Organs 27, 132-135 (1981). 10. TSUSHIMA, N., S. K.\XSAI, 1. KOSHI)[O, G. B. JACOBS, N. MORINAGA, T. WASIIIZU, R. R. KIRALY and Y. NOSE, 145 days surYival of calf with total artificial heart (TAR). Trans. Am. Soc. Artif. Inter. Organs 23, 52G--533 (1977). 11. VASK1':, .[., J. CERNY, P. HANZELKA, ;\1. DOSTAL, P. GUBA, E. URBANEK, T. SLADEK, P. URBANEK, O. SOTOLOV A, L. KRCEK and J A:'! VASKl:, First experiences with the short and long term survival with Cr,('('hoslovak 'fA H-'fNS-BRNO I. Proc('edings of the V. Congress of ESAO V, 99-103, 1978. 12. - - - JAN VASK1\ E. URILhEK, 11. DOSTAL, P. URBANEK, P. GUBA, V. PAvLiCEK, 1. KRCEK, T. SLADEK, B. HARTMANNOVA, J. FIKULKA, H. JANECKOVA, O. ~OTOLOVA, E. SOTAK OVA, S. DOLEZEL, V. KRC:lrA, K. CIDL, and B. BEDNARIK, 150-days survival of a calf with a polymethylmethacrylate total artifitial heart: TNS-RRNO-II. Artif. Organs 5, 388-400 (1981).
16 Exp. Path. 26, H. 4
225
~~1~-~~5
(1984)
Research Center of the Regional Institute of National Realth (KUNZ), Brno, CSSR; Slovak Academy of Sdences, Centre of Physiological Sciences, Institute of Normal and Pathological Physiology, Bratislava, OSSR 2) Institute of Pathological Anatomy, l\iedical FatuIty, J. E. Purkyne University, Rrno, CSSR 1
Mechanisms causing the death of 8 calves surviving with implanted artificial heart from 31 to 173 days By B. RARTMANNOVA, J. VASKl;, S. DOLEZEL1 ), Eo URBANEK, J. FILKUKA2), T. SLADEK, L. KRCEK, P. GUBA, M. DOSTAL, J. CERNY, E. SOTAKOVA, P. URBANEK, P. RANZELKA and JAN VASKU
With 3 figures (Received October 25, 1983)
Address for correspondence: Prof. Dr. JAROMJR VASKU, Institute of Pathophysiology, University of J. E. Purkyne, Komenskeho mim 2, 662-43 Brno, OSSR Key words: heart implantation; artificial heart; death causes; calf
Summary Causes of the death of four animals from the total of eight were technical failures (diaphragm perforations, disconnection of the quick-connector, and a failure of the supply of electric current which could not be prevented). Causes of the death of the remaining four animals were embolisation in the brain stem, embolisation in the superior mesenteric artery leading to diffuse peritonitis, ruptures of aorta and hemocoagulation disorder causing fatal gastrointestinal bleeding. Introduction
A considerable progress in the research on the replacement of the heart with a total artificial heart (TAR) was achieved in the last few years. Reports of the leading research groups show that calves with the TAR had survived already more than 100 days (1, 3, 6, 7, 10, 8). The contributions of our group to this research were reported by 12, 2, 4, 11, 5. The present report brings a short survey of mechanisms leading to the death of eight animals surviving from 31 to 173 days.
Materials and Methods TAR was implanted to 8 calves of both sexes, weighing from 73 to 98 kg, 2-4 months old. The implantation was carried out by means of right-side thoracotomy. The heart ventricles were removed together with the atrioventricular valves. Atrial stumps and distal parts of the aorta and pulmonary artery were sutured with polyester cuffs provided with a quick-connector. The atrial connectors and conneetors of the aorta and of the pulmonary artery were coupled to the mouthpieces of the TAR (for details see: 2). The implanted TAR of the type BRNO-II was fabricated from polymethylacrylate with exception of the diaphragm, which was made of segmented poly ether-urethane (7 implantations); type BRNO-III was made totally of segmented polyurethane (1 implantation). The whole device, i.e. TAR including valves, the pneumatic driving, and control unit was developed by our research group (4) . . The dead animals were routinely autopsied. The thoracic cavity was opened in such a way that the position of the artificial heart, atrial stumps, and great blood vessels joined to TAR were not changed. The technical state of TAR was tested postmortally. The amount of thrombotic deposits inside TAR was evaluated. The organs were dissected in the conventional manner; the vessels wer cut
221
Fig. 1. The view in the left atrium. The semilunar fibrous outgrowth ("pannus") partially occludes the inflow orifice of the TAH (calf No. 51 surviving 142 d). lengthwise so that the adhering thrombi could be found. Histological material was taken from all parenchymatous organs. Special attention was paid to samples of both atria, the aorta and the pulmonary artery excised in sites of the sutures. Slices of tissues were prepared from paraffin blocks and stained by standard histological methods. In addition to the morphological findings, biochemical, hematological, hemodynamical, bacteriological and respirological findings were considered.
Results and Discussion Cause of the death of the calf No. 54, "Waldemar" (surviving for 31 d) was the thromboembolic occlusion of the stem of the superior mesenteric artery with subsequent infarction of the gut. This accident led to the diffuse peritonitis with lethal outcome. The occluding embolus was derived from thrombotic vegetations localized on the inflow valve in the left artificial ventricle. The calf No. 55, "Kamil" (surviving for 35 d), died in consequence of aorta rupture. Hemomediastinum and right-side hemothorax resulted. The cause of the aortic perforation was a chronic necrotizing aortitis localized around the suture of the aorta with the aortic quickconnector; multiple voluminous thrombotic vegetations growing on the ulcerated endothelium of the aorta were observed [s.c. vegetative endocarditis or aortitis according to OLSEN (9)]. A chronic infection localized in the site of the suture seems to be responsible for these changes. Technical failures were causes of the death of calves No. 52, "Samson", and No. 60 "Fatima" (surviving for 105 d and 75 d respectively). In both cases a perforation of the diaphragm of right artificial ventricle occurred. The blood was pumped into the pneumatic part of TAR. The gradual occlusion of the pneumatic driving tube with dried coagulated blood resulted and ultimately led to the blocking of pumping. Negligible amounts of deposits were found inside T AH in both cases.
222
Fig. 2. The fibrous capsule covering the outer surface of TAR forming "pseudo cardium" (calf No. 53 surviving 155 d).
The calf No. 51, "Dalibor" survived for 142 d; its hematological, hemodynamicaL biochemical and respiratory data were within physiological range. The termination of this experiment was caused by a failure in the supply of electric current which could not be prevented. The semilunar fibrous outgrowth, called pannus, partially occluded the inflow orifice (fig. 1); the left-side pannus was somewhat greater than the right one. The other pathological changes were negligible and could not cause the death of the animal. The cause of death of the calf No. 50, "Hasan" (surviving for 150 d), was a hemocoagulation disorder developed during the anticoagulation therapy. The massive bleeding in the bowels caused a severe posthemorrhagic anemia; the cerebral anoxia led ultimately to the death. Moreoever, a clinical state was influenced by a chronic sepsis occurring during the last 50 d. Klebsiella aerobacter was identified by hemocultivation. Calf No. 53, "Florian", survived 155 d. The cause of death was embolisation in the brain stem by calcified thrombi, originating as mineralized deposits on the inner surface of the polyetherurethane diaphragm. The repeated contact of the inflow flap valves with the diaphragm caused the gradual removing of the calcified deposits in the form of the minisplits, which were the cause of the embolism. Calf No. 59, "Omar", survived for 173 d in very good clinical state. The death of this calf was caused by a disconnection of the quick-connector of the left-hand mouthpiece of the blood pump. The left inflow tract was thus opened. Two factors were important here. First, possible disintegration of the material of the quick-connector, and second, the enormous weight of the calf, which caused an enlargement of the mediastinal cavity. Thus, a strain traction was induced at the site of the connection which could be a cause of the failure. The opened left inflow tract caused the peculiar state of the "tamponade of the artifical heart". Because this calf reached a body weight of 200 kg it became a world champion if
223
TNS
Fig. 3. Mineralised dpposits on thl' innn surface of the polyurethane diaphragm of TAH (calf No. 53 surviving 155 dl.
the relationship between the animal body weight and the size of TAR, which had a blood chamber of a volume of 100 ml on each side, is considered. The following findings were common for all animals of this "long-surviving" group. A fibrous capsule covered the outer surface of the TAR in all cases (fig. 2). It originated from the blood clots adhering to one outer surface of TAR immediately after the implantation. These clots were gradually replaced by the granulation tissue which changed to the fibrotic one during the course of the postoperative period. This development could be observed histologically in those tissue samples, where initial phases of this growth were intercepted. The so-called pseudointima originates by a similar process from white thrombotic layer formed in streaming blood on the inner surface of TAR. The calcifications were found on the inner surface of the polyurethane diaphragm of TAR. The extent of these mineralised deposits among individual calves was compared. Different amounts of deposits were found even though the survival time was taken into consideration. The deposits were most developed in calf No. 53, "Florian", where both diaphragms of the artifical ventricle were similarly affected (fig. 3). Contrary to this finding, the calves No. 52, "Samson", and No. 60, "Fatima", did not show any marked mineralisation process inside TAR. Thrombi adhering to the valves were also absent. It remains to be elucidated whether the different pictures of the mineralised deposits on the diaphragm were caused by various properties of its surface resulting from variations in the technology of their fabrication, or whether it was caused by differences in disposition for calcification in individual calves. These differences may result from an enhanced calcifying potency or from an enhanced suppressive mechanism decreasing the intensity of the calcium and phosphate movements
224
between thl' ti,sue, and bod~' fluids. III this easp we can also suppose that the deposits are formed by a calciphylactic mechanism. The picture of the chronic venostasis of various degree was found. It was most pronounced in calves surviving for the longest time and reaching the highest increase in weight. It was characterised e.g., by the "nutmeg liver". The above-described venostatic changes especially in the liver, are a consequence of the gradually increasing central venous pressure (CYP). The increased CYP correlated with the growth of the animals. The inadequacy between the size of the blood pump and its pumping capacity on the one hand and the increasing weight of the body on the other hand can be only partially corrected by the control and driving regimen. Thus, the liver microcirculatory disturbance due to venostasis could not be prevented in the course of the entire experiment. The above-described change with the subsequent liver enlargement and increased hepatic index (the liver weight related to the body weight) were final outcome of this process. In conclusion eight calves surviving 31-173 d (mean survival 108.1 d) were investigated by autopsy with TAR. The achieved lifespan of experimental calves maintained by artificial circulation reaches the level obtained by other groups working in this field. Moreover, no death on the operation table oecurred in the last three years.
Literature 1. ATSUMI, K., FUJIMASA, K. IMACHI, T. NISHISAKA, I. MANO, H. OHMISHI, N. IWAI and A. KONO, Analysis of long survivals (over one month) in the total artifical heart replacement. ESAO Proc~edings 3, 44-48 (1976). 2. CEl{XY, J., M. DOSTAL, J. VASKl:, V. KORisTEK and B. BEDNARiK, Chirurgiceskije aspekty implantace iskusstvennogo serdca. Scripta medica 53, 535-538 (1980). 3. FliKuMAse, H., D. B. OLSEN, J. H. LAWSON, T. MOCHIZUKI, N. DAITOH and F. IWAYA, Reopcrative surgery in calves with a total artificial heart. Int. J. Artif. Organs 3, 24-30 (1980). 4. HAl\ZELKA, P., JAN VASKl:, P. URBANEK, V. KRCMA, .J. VASKU and E. URBANEK, Development of artificial heart in Czechoslovakia. Bioengineering aspects. Scripta medica 53, 539-542 (1980). 5. H.\RTMAXNOyA, B., J. VASKU, S. DOLEZEL, E. URBANEK, .J. FILKULKA, T. SLADEK, L. KRCEK, P. GUBA, M. DOSTAL, J. CERNY, E. SOTAKOYA, P. URBANEK, P. HANZELKA and JAN VASKU, Patomorfologicky rozbor pticin umrti zvifat dlouhodobe prezivajicich po totalni nahrade srdcc. Cs. fysiologie 29,176-177 (1980). 6. HASTINGS, W., J. L. AARON, J. DE:'!ERIS, T. R. KESSLER, A. B. PONS, K. J. RAZZECA, D. B. OLSEN and W. J. KOLFF, A retrospective study of nine calves surviving five months on the pneumatic total artificial heart. Trans. Am. Soc. Artif. Inter. Organs. 27, 71-76 (1981). 7. KASAl, S., 1. KOSHINO, T. WASHIZP, G. ll. JAKOBS, N. MORINAGA, R. KIR.UY, Y. NOSE, Survival of 145 days with a total artificial heart. J. Thoracic and Cardiovasc. Surg. 73, 637-646 (1977). 8. LAWSON, J. R., H. FrKUMASl:, D. B. OLSEN, R. K. JARVIK, T. R. KESSLER, D. COLEMAN, A. B. PONS, R. BLAYLOCK and W. J. KOLFF, Six months survival of a calf with an artificial heart. Artif. Heart 78, 150-156 (1979). 9. OLSEN, D. B., W. C. DE VlUES, P. OYER, B. REITZ, J. MURASHITA, W. J. KOLFF, N. DAITOH, R. K. J ARVIK and R. GAYKOWSKI, Artificial heart implantation, later cardiac transplantation in the ealf. Trans. Am. SO('. Artif. Inter. Organs 27, 132-135 (1981). 10. TSUSHIMA, N., S. K.\XSAI, 1. KOSHI)[O, G. B. JACOBS, N. MORINAGA, T. WASIIIZU, R. R. KIRALY and Y. NOSE, 145 days surYival of calf with total artificial heart (TAR). Trans. Am. Soc. Artif. Inter. Organs 23, 52G--533 (1977). 11. VASK1':, .[., J. CERNY, P. HANZELKA, ;\1. DOSTAL, P. GUBA, E. URBANEK, T. SLADEK, P. URBANEK, O. SOTOLOV A, L. KRCEK and J A:'! VASKl:, First experiences with the short and long term survival with Cr,('('hoslovak 'fA H-'fNS-BRNO I. Proc('edings of the V. Congress of ESAO V, 99-103, 1978. 12. - - - JAN VASK1\ E. URILhEK, 11. DOSTAL, P. URBANEK, P. GUBA, V. PAvLiCEK, 1. KRCEK, T. SLADEK, B. HARTMANNOVA, J. FIKULKA, H. JANECKOVA, O. ~OTOLOVA, E. SOTAK OVA, S. DOLEZEL, V. KRC:lrA, K. CIDL, and B. BEDNARIK, 150-days survival of a calf with a polymethylmethacrylate total artifitial heart: TNS-RRNO-II. Artif. Organs 5, 388-400 (1981).
16 Exp. Path. 26, H. 4
225