Mesenteric shunting decreases visceral ischemia during thoracoabdominal aneurysm repair.

PURPOSE: A technique to decrease visceral ischemic time during thoracoabdominal aneurysm (TAA) repair is reported. METHODS: A 10 mm Dacron side-arm graft is attached to the aortic prosthesis and positioned immediately distal to the planned proximal thoracic aortic anastomosis. On completion of the anastomosis, a 16 to 22 Fr perfusion catheter is attached to the side-arm graft and inserted into the orifice of the celiac axis or superior mesenteric artery. The cross-clamp is then placed on the aortic graft distal to the mesenteric side-arm graft. Pulsatile arterial perfusion is thus established to the visceral circulation while intercostal anastomoses or reconstruction of celiac, superior mesenteric, and right renal arteries is performed. Visceral ischemic time and the rise in end-tidal Pco2 after reconstruction of the visceral vessels in patients with mesenteric shunting was compared with a control group matched for aneurysm extent and treated immediately before use of the mesenteric shunt technique. RESULTS: Between July and Oct, 1996, the technique was applied in 15 patients undergoing type I, II, or III TAA repair with a clamp and sew technique. The mean decrease in systolic arterial pressure was 12.5 +/- 8.5 mm Hg, with a concomitant rise in end-tidal Pco2 (mean, 6.9 +/- 5.8 mm Hg), after perfusion was established through the mesenteric shunt. Mean time to establishment of visceral perfusion through the shunt was 25.5 +/- 4.4 minutes; the resultant decrement in visceral ischemic time averaged 31.3 minutes (i.e., until celiac, superior mesenteric, and right renal arteries were reconstructed). Compared with controls, patients with shunts had a significantly decreased (6.9 +/- 5.8 versus 21.6 +/- 8.4 mm Hg; p = 0.0003) rise in end-tidal CO2 on completion of visceral vessel reconstruction. CONCLUSIONS: In-line mesenteric shunting is a simple method to decrease visceral ischemia during TAA repair, and it is adaptable to clamp and sew or partial bypass and distal perfusion operative techniques.

Prevention of spinal cord ischaemic complications after thoracoabdominal aortic surgery.

Since the publication of prior reviews on this topic, substantial clinical experience with a variety of operative strategies to prevent ischaemic cord complications has been reported. The available data on angiographic localisation of critical intercostal vessels, and, in particular, the evoked potential response to cross-clamping in patients indicates that risk of paraplegia varies considerably even among patients with equivalent TAA extent. Factors such as individual development of the ASA, patent critical intercostals, and the particulars of collateral circulation when intercostal aortic ostia are already occluded likely account for this variability. Information available from SSEP monitoring relative to the dynamic course of cord ischaemia with cross-clamping, and the parallel, if not, frustrating experience with angiographic localisation and intercostal vessel reconstruction indicates that a narrow temporal threshold of cord ischaemia with clamping is present in many patients. This reinforces the importance of both expeditious clamp intervals, critical intercostal re-anastomoses, and the desirability of neuroprotective manoeuvres during cross-clamp induced cord ischemia. As suggested in compelling experimental work our contemporary clinical experience, and predicted by prior reviewers, regional cord hypothermia provides significant promise for limiting or eliminating, in particular, immediate perioperative deficits. Avoidance of postoperative hypotension, spinal cord oedema, and preservation of critical intercostal vessels are additional strategies necessary to impact the development of delayed deficits favourably.

Systemic pressor response during hindlimb ischemia is inversely related to femoral artery pressure and fractional inspired oxygen.

BACKGROUND: Delayed-onset reflex increases in mean arterial pressure (MAP) occur during clamping of the infrarenal aorta. This study investigated the afferent limb of the reflex by independently altering femoral artery blood pressure (FBP) or fractional concentration of inspired oxygen (FIO2) while monitoring systemic arterial blood pressure. METHODS: The infrarenal aorta was divided, and an occlusive roller pump delivered incremental flow to the distal aorta thus controlling FBP. In six dogs the FBP was reduced in random order to 50, 40, 30, 20, and 10 mm Hg and held constant for 30 minutes. In another six dogs the FBP was held at 20 mm Hg, whereas the FIO2 was randomly varied among 0.13, 0.21, and 1.0 for 30-minute intervals. RESULTS: Under these conditions MAP was significantly and inversely correlated with FBP (MAP was 172 +/- 8 mm Hg when FBP was 10 mm Hg, p < 0.0001; MAP was 158 +/- 8 mm Hg when FBP was 20 mm Hg, p = 0.0001; MAP was 138 +/- 7 mm Hg when FBP was 30 mm Hg, p = 0.0048; and MAP was 130 +/- 7 mm Hg when FBP was 40 mm Hg, p = 0.0045). MAP was significantly and inversely related to the FIO2 value when FBP was fixed at 20 mm Hg (MAP of 186 +/- 9 mm Hg at FIO2 of 0.13 and was significantly higher than MAP of 163 +/- 11 mm Hg at FIO2 of 0.21, p = 0.01; and MAP of 157 +/- 10 mm Hg at FIO2 of 1.0, p = 0.0001). CONCLUSIONS: The magnitude of the delayed systemic pressor response is inversely proportional to the FBP. We suggest that this pressor response is also particularly sensitive, in part, to arterial blood oxygen tension when hindlimb perfusion pressure is low.

Infrarenal aortic clamp hypertension is exacerbated by baroreceptor blockade.

Aortic clamp-induced hypertension has long been implicated in the cardiovascular mortality and morbidity following infrarenal aortic operations. We studied the physiologic mechanisms leading to clamp-induced hypertension. Mean arterial pressure (MAP), cardiac output, heart rate, and left ventricular pressure were measured in alpha-chloralose-anesthetized dogs. Animals received alpha, beta, both alpha and beta, or no adrenergic blockade (n = 3, 4, 12 and 7, respectively). The infrarenal aorta was clamped following ligation of the infrarenal collateral vessels (lumbar, circumflex iliac, and tail arteries). Statistical analysis used paired t tests within groups, and ANOVA and unpaired t tests between groups, with Bonferroni's correction as indicated. Following placement of the clamp, MAP increased immediately in all groups, with magnitude of the increase related to the extent of adrenergic blockade. MAP increased 5.6 +/- 0.8 mm Hg with no blockade (P = 0.0005), 6.7 +/- 0.8 mm Hg with alpha blockade (P = 0.0153), 15 +/- 3.1 mm Hg with beta blockade (P = 0.0163), and 16.7 +/- 1.3 mm Hg with combined alpha and beta blockade (P < 0.0001). The increase in MAP immediately following infrarenal aortic clamping was most pronounced with combined alpha and beta blockade. We suggest that acute intraoperative hypertension associated with infrarenal aortic clamping is caused by the attenuation of compensatory baroreceptor reflex mechanisms.

Prevention of paraplegia during thoracic aortic cross-clamping: importance of patent internal mammary arteries.

PURPOSE: Unexplained anatomic and physiologic factors account for the unacceptably high rate of paraplegia/paresis after thoracoabdominal aortic reconstruction. We assessed the neurologic significance of patent internal mammary arteries (IMAs) in a novel rat model of aortic clamping in which the aortic origins of the intercostal arteries (ICAs) were occluded. METHODS: Twenty anesthetized, intubated, and halothane-ventilated adult male rats had catheters placed in the carotid and femoral arteries. ICAs arising from the aorta were divided at their origins through a left thoracotomy. IMAs were either divided (IMA-OUT, n = 10) or left intact (IMA-IN, n = 10). Proximal and distal descending aortic clamps were placed for 7 minutes. A neurologic deficit score (NDS) was assigned at 1, 4, 18, 24, and 48 hours by use of an established scoring system. RESULTS: The mean IMA-IN NDS was statistically better than the mean IMA-OUT NDS at 1, 4, 18, and 24 hours with p = 0.0005, 0.0014, 0.0098, and 0.0151, respectively. Moreover, the mortality rate in the IMA-OUT group was statistically greater than in the IMA-IN group (p = 0.0036). CONCLUSION: In this model, patent IMAs prevent paraplegia when the ICAs are occluded at their aortic origin and the aorta is clamped for 7 minutes.

Isolation of mouse T-cell lymphoma lines from different long-term interleukin 2-dependent cultures.

A number of different biological properties have been ascribed to the hormone-like protein interleukin 2 (IL-2). However, the most salient feature of this lymphokine is its ability to sustain the long-term proliferation of T-cells from humans and mice. Reported herein are the results of studies demonstrating the isolation of growth factor-independent cell lines from the long-term IL-2-dependent murine T-cell line CTLL-2 that is used frequently as the source of target cells in IL-2 bioassays. Sustained log-phase growth of these T-cells in vitro has been achieved using Petri dishes of polymethylpentene; growth could not be sustained in similar dishes of glass, untreated polystyrene, polystyrene that had been treated for cell culture, or polycarbonate. The IL-2-independent line grew as a T-cell lymphoma when injected i.p. into pristane-treated, but not untreated, syngeneic C57BL/6 mice. In contrast, cells from the IL-2 parental line CTLL-2 did not grow in vivo. Characterization of the IL-2-independent lines propagated in vitro (denoted as line CEC) or in vivo (denoted as line CEP) demonstrated that they retained their dependency for 2-mercaptoethanol and expressed phenotypic profiles of their parental line CTLL-2 (Thy 1.2+, Lyt-1-; Lyt-2-). Isolation of an IL-2-independent T-cell lymphoma from a CTLL-2 line obtained from another investigator using a protocol that has proven reproducible under carefully controlled laboratory conditions and defined phenotypic traits of the syngeneic T-cell isolates provided evidence that the tumors were not a cross-culture contaminant arising as a result of a laboratory accident. Moreover, karyotypic analysis using a quinacrine:Hoechst banding technique revealed similar marker chromosomes in the IL-2-dependent and -independent lines. IL-2-independent lines have also been established from the IL-2-dependent murine T-cell line CT-6. Accordingly, the results of these studies suggest that, during prolonged cultivation that has included exposure to crude IL-2 preparations known to contain phorbol ester, possibly viruses, and other contaminants, the IL-2-dependent lines have developed subpopulations that are thought to have undergone malignant transformation of unknown etiology to generate IL-2-independent murine T-cell lymphomas that can be passaged repetitively either in vitro or in vivo.