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PubMed1989

Growth response of tetraploid smooth muscle cells to balloon embolectomy-induced vascular injury in the spontaneously hypertensive rat.

Previous studies in this laboratory have demonstrated that smooth muscle hypertrophy in large arteries of hypertensive animals is accompanied by development of polyploidy in a large fraction of the smooth muscle cell population. The present studies address whether there is an inherent loss in the ability of tetraploid cells to respond to proliferative stimuli by examining whether these cells initiate DNA replication after balloon catheter-induced vascular injury. Left carotid arteries of 5- to 7-month-old spontaneously hypertensive rats were subjected to balloon injury, and the animals were perfused intravenously with [3H]thymidine for 32 h. The animals were killed, and smooth muscle cells were isolated from carotid medial preparation by enzymatic digestion. Cells were processed for simultaneous autoradiographic analysis of [3H]thymidine incorporation and fluorometric analysis of cellular DNA content as a means of simultaneously assessing both the ploidy level of a cell and whether or not it had initiated DNA replication in response to balloon injury. Results demonstrated the presence of [3H]thymidine-labeled cells with DNA contents that were greater than 4C but less than 8C (p less than 0.01), indicating that they are cycling tetraploid cells. These data demonstrate that tetraploid smooth muscle cells in vivo are capable of initiating DNA synthesis in response to balloon injury. Results indicate that there is not an inherent loss in the capacity of tetraploid cells to respond to a proliferative stimulus, although it remains to be determined whether the polyploid cells that initiate DNA replication after balloon injury actually go on to divide.

Animals↗
PubMedDate not supplied

Survival following massive pulmonary hemorrhage complicating pulmonary embolectomy: a case report.

Continued employment of extracorporeal circulation provides for adequate oxygenation despite massive pulmonary hemorrhage. However, this modality requires continuing heparinization, which seems to preclude control of the hemorrhage. The longer bleeding persists, the more the pulmonary damage. Further, the problems of massive volume replacement will be added to this catastrophe. The authors believe that rapid discontinuance of extracorporeal bypass, reversal of heparinization with protamine, aggressive pulmonary suctioning, and alternate ventilation with 100% O2 were responsible for their good result. Arterial hypoxemia was avoided despite pulmonary suction yielding 1500 ml in 17 minutes.

Adult↗
PubMed1991

Pulmonary embolectomy by catheter device in massive pulmonary embolism.

From 1982 to 1989, ECD was performed on 18 patients suffering from poorly-tolerated massive pulmonary embolism, for whom classic treatments (fibrinolytics and surgery) were impossible. Eleven of these 18 patients immediately improved (S group). This procedure was unsuccessful in other seven patients (F group). Thirteen patients survived (72 percent). The time lag between the first episode of pulmonary embolism and ECD was significantly shorter in the S group than in the F group (4.7 +/- 5.4 days vs 18.3 +/- 6.9 days, p = 0.0004). So was the elapsed time between the onset of hemodynamic impairment and ECD (13 +/- 12 hours vs 59 +/- 38 hours, p = 0.003). We conclude that ECD should be considered when other treatments are impossible especially when the first symptoms date back less than 15 days and the hemodynamic impairment less than 48 h.

Adult↗