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Arteriographic demonstration of collateral arterial supply to the liver after hepatic artery ligation.

Eight patients were studied arteriographically after hepatic artery ligation (done to control bleeding in 6). Sources of arterial flow to the liver after ligation were (a) replaced or accessory hepatic artery; (b) interlobar collaterals in the liver; (c) right inferior phrenic artery; (d) through the gastroduodenal artery from arterial branches in the pancreas, duodenum, and omentum; (e) fine collateral branches of the gastroduodenal artery as they pass into the porta hepatis; and (f) recanalization of the ligated hepatic artery. Collateral vessels, seen as early as four hours after ligation, increase in size and number during the following six months.

Adult↗

Right common carotid artery ligation for extracorporeal membrane oxygenation: cerebral blood flow velocity measurement with Doppler duplex US.

Duplex Doppler ultrasound (US) provides a noninvasive method of monitoring cerebral blood flow velocity in newborns. The authors observed the changes in cerebral blood flow velocity in the right middle cerebral artery (RMCA) in 15 neonates during right common carotid artery (RCCA) ligation for extracorporeal membrane oxygenation. Antegrade flow in the RMCA continued uninterrupted in all patients at the moment of ligation. Peak systolic velocity decreased initially and then increased to 70% of baseline levels in the following 3-5 minutes. End diastolic velocity remained relatively unchanged at the time of ligation and rose slightly above baseline during the following 3-5 minutes. This study demonstrates that at the time of RCCA ligation, collateral flow is immediately established in the RMCA distribution and is further augmented within minutes.

Blood Flow Velocity↗

Roles of insulin-like growth factor II in cardiomyoblast apoptosis and in hypertensive rat heart with abdominal aorta ligation.

Although IGF-II activating the IGF-II receptor signaling pathway has been found to stimulate cardiomyocyte hypertrophy, the role of IGF-II in cardiac cell apoptosis remains unclear. This study aimed to identify the roles of IGF-II and/or IGF-II receptors (IGF-II/IIR) in cardiomyoblast apoptosis and in hypertensive rat hearts with abdominal aorta ligation. Cultured rat heart-derived H9c2 cardiomyoblasts and excised hearts from Sprague-Dawley rats with 0- to 20-day complete abdominal aorta ligation, a model of ANG II elevation and hypertension, were used. IGF-II/IIR expression, caspase activity, DNA fragmentation, and apoptotic cells were measured by RT-PCR, Western blot, agarose gel electrophoresis, and TUNEL assay following various combinations of ANG II, IGF-II/IIR antibody, CsA (calcineurin inhibitor), SP-600125 (JNK inhibitor), SB-203580 (p38 inhibitor), U-0126 (MEK inhibitor), or Staurosporine (PKC inhibitor) in H9c2 cells. ANG II-induced DNA fragmentation and TUNEL-positive cells were blocked by IGF-II/IIR antibodies and antisense IGF-II, but not by IGF-II sense. IGF-II-induced apoptosis was blocked by IGF-IIR antibody and CsA. The increased gene expressions of IGF-II and -IIR induced by ANG II were reversed by U-0126 and Sp600125, respectively. Caspase 8 activities induced by ANG II were attenuated by U-0126, SP-600125, and CsA. DNA fragmentation induced by ANG II was totally blocked by SP-600125, and CsA and was attenuated by U-0126. In rats with 0- to 20-day complete abdominal aorta ligation, the increases in IGF-II/IIR levels in the left ventricle were accompanied by hypertension as well as increases in caspase 9 activities and TUNEL-positive cardiac myocytes. ANG II-induced apoptosis was reversed by IGF-II/IIR blockade and coexisted with increased transactivation of IGF-II and -IIR, which are mediated by ERK and JNK pathways, respectively, both of which further contributed to cardiomyoblast apoptosis via calcineurin signaling. The increased cardiac IGF-II, IGF-IIR, caspase 9, and cellular apoptosis were also found in hypertensive rats with abdominal aorta ligation.

Angiotensins↗

Intrinsic factor receptor activity and cobalamin transport in bile duct-ligated rats.

The intrinsic factor (IF)-cobalamin (Cbl) receptor activity in the mucosal homogenates progressively decreased after bile duct ligation in the rat, and 80% of the receptor activity was decreased in 96 h after ligation. The activity was restored to normal values of 5.5-6 pmol of IF-[57Co]Cbl bound/g mucosa when the assays were performed with both conjugated and unconjugated bile acids. When [57Co]Cbl bound to intrinsic factor was orally administered, the tissue levels of [57Co]Cbl were decreased by 75-80% in bile duct-ligated rats. The apical membrane receptor activity was also decreased after bile duct ligation; however, the activity was stimulated twofold by the addition of ileal cytosol and threefold with the addition of both ileal cytosol and taurocholate (1 mM). Enhanced binding of IF-[57Co]Cbl to the apical ileal brush-border membrane occurred with the use of dialyzed ileal cytosol but not with cytosol isolated from duodenal or proximal jejunal mucosa. The enhanced binding obtained with ileal cytosol was abolished after its treatment with trypsin. These results suggest that luminal bile acids optimize the binding of IF-Cbl by the ileal membrane receptor via interactions with a cytosolic factor and thus influence the gastrointestinal absorption of cobalamin.

Animals↗

Nonuniformity of axial and circumferential remodeling of large coronary veins in response to ligation.

The pressure-induced remodeling of coronary veins is important in coronary venous retroperfusion. Our hypothesis is that the response of the large coronary veins to pressure overload will depend on the degree of myocardial support. Eleven normal Yorkshire swine from either sex, weighing 31-39 kg, were studied. Five pigs underwent ligation of the left anterior descending (LAD) vein, and six served as sham-operated controls. The ligation of the coronary vein caused an increase in pressure intermediate to arterial and venous values. After 2 wk of ligation, the animals were euthanized and the coronary vessels were perfusion-fixed with glutaraldehyde. The LAD vein was sectioned, and detailed morphometric measurements were made along its length from the point of ligation near the base down to the apex of the heart. The structural remodeling of the vein was circumferentially nonuniform because the vein is partially embedded in the myocardium; it was also axially nonuniform because it is tethered to the myocardium to different degrees along its axial length. The wall area was significantly larger in the experimental group, whereas luminal area in the proximal LAD vein was significantly smaller in the same group compared with sham-operated controls. The wall thickness-to-radius ratio was also significantly larger in the experimental group in proportion to the increase in pressure. The major conclusion of this study is that the response of the vein depends on the local wall stress, which is, in part, determined by the surrounding tissue. Furthermore, the geometric remodeling of the coronary vein restores the circumferential stress to the homeostatic value.

Anatomy, Cross-Sectional↗

Cerebral hemodynamics following internal maxillary artery ligation in the goat.

Changes in cerebral and extracerebral blood flow in the goat after ligation of the internal maxillary artery and deliberate thrombosis of the extracerebral arteries (buccinator, ethmoidal, and ophthalmic) with thrombin were compared to changes seen in animals after internal maxillary artery ligation only and in normal animals where no surgical manipulations were performed. Blood flow was measured by injecting 51-Cr-labeled microspheres into the internal maxillary artery via a catheter placed into the temporal artery. Analysis of the radioactivity in extracerebral and intracerebral tissues indicated that when the internal maxillary artery is ligated and the extracerebral arteries are thrombosed, virtually all of the blood flow from the carotid artery is destined from the brain. However, if only the internal maxillary artery is ligated nearly one-fourth of the blood flow from the maxillary travels to extra-cerebral tissues. In normal animals, it was determined that only one-fourth of the blood flow in the internal maxillary is destined for the cerebral circulation. Results from this study indicate that if the former method is employed an accurate measure of cerebral blood flow is possible without the complications of extra-cerebral flow. If the latter technique is used care must be taken in evaluating cerebral blood flow since a large component of extra-cerebral blood flow is present.

Animals↗

Pulmonary microvascular permeability after coronary arterial ligation in dogs.

Recent studies have indicated that pulmonary microvascular permeability may be increased after coronary arterial ligation. We tested this by estimating the pulmonary microvascular reflection coefficient (delta) in six anesthetized control dogs and in six dogs in which we ligated the left anterior descending coronary artery. We cannulated lung lymph vessels and measured the lymph and plasma protein concentrations (CL and CP, respectively). The left atrial pressure was increased to decrease CL to a minimum. We used the minimum CL to estimate delta as 1 -CL/CP. delta for the control [0.70 +/- 0.03 (SD)] and coronary artery ligated groups (0.70 +/- 0.04) were almost identical. This data indicates that coronary artery ligation does not increase pulmonary microvascular permeability.

Animals↗

Band ligation or sclerotherapy as endoscopic treatment for oesophageal varices in schistosomotic patients: results of a randomized study.

Endoscopic sclerotherapy and banding ligation are the two preferred methods to treat oesophageal variceal bleeding. There are many reports dealing with such treatment in cirrhotic patients but we do not know how good they are to treat varices secondary to other forms of portal hypertension. Schistosomiasis mansoni is the main cause of portal hypertension and oesophageal varices in Brazil. We performed a prospective randomised study to compare: 1) the efficacy of both treatments in eradicating oesophageal varices, and 2) complications secondary to both treatments. Forty patients were divided in two groups. Both sclerotherapy and banding ligation were performed until variceal eradication. There were no severe complications. Variceal eradication was faster obtained with banding ligation than sclerotherapy although there was no statistical difference (mean number of sessions 3.05 vs 3.72, p = 0.053). Benign complications were equally frequent in both groups, although additional sedation was more common in the sclerotherapy group. We concluded that both treatments are equally effective in the eradication of oesophageal varices, although banding ligation is better tolerated by the patient and probably faster.

Adult↗

[Secondary prophylaxis with elastic band ligation in esophageal-gastric varices].

The aim of the present study was to determine the usefulness of elastic band ligation in the prevention of hemorrhage recurrence due to esophageal-gastric varices. Sixty-five patients who survived an episode of variceal hemorrhage were included in the study. Twenty-nine patients (45%) were Child-Pugh class A, 25 (38%) were class B, and 11 (17%) were class C. The cause of cirrhosis was hepatitis C virus and alcohol in 45% and 31% of the patients, respectively. The first ligation session was performed between the third and fifth day after the hemorrhagic episode and subsequent sessions were carried out at intervals of 3-4 weeks. The ligation sessions were performed with antibiotic prophylaxis. A mean of 2.7 bands were placed per session (range 1-5), and the mean number of sessions required per patient to achieve variceal eradication was 2.5 (range 1-6). The rate of bleeding recurrence was 24.6% (16 episodes). In conclusion, endoscopic elastic band ligation is a useful technique for the eradication of esophageal varices and for the prevention of bleeding recurrence.

Adult↗

Hepatic blood flow in rats with portal branch ligation.

Hepatic arterial blood flow (HABF) in the liver lobes and splanchnic nonhepatic arterial blood flow were measured in rats with and without right portal branch ligation for 1 month using 57Co microspheres. Portal branch ligation led to 60% atrophy of the ligated lobe and to hypertrophy of the nonligated lobe. In nonligated lobes of the portal branch ligation model and in the lobes of controls, HABF expressed per gram liver was comparable. In both models splanchnic non-HABF was also comparable. In the atrophic lobe, HABF remained constant; expressed per gram liver, it increased. In this lobe the net result was a significant decrease in total hepatic blood flow (ml/min/g liver).

Animals↗

Hepatic adenine nucleotides and DNA synthesis during the regenerative and atrophic process of the liver lobes after selective portal vein ligation.

Selective portal vein occlusion prior to aggressive hepatic resection is now an alternative way to decrease postoperative morbidity and mortality rates. However, the detailed changes in the hepatic energy status and DNA synthesis rate in both portal vein ligated (PVL) and nonligated (PVNL) lobes of the liver are not clear. In rats, the portal branch that supplies 70% of the liver volume was ligated, and changes in arterial ketone body ratio (AKBR), liver weight, histology, DNA synthesis rate and adenine nucleotides of the PVL and PVNL liver lobes were determined before and 1, 2, 4 and 7 days after portal vein ligation, and compared with those in sham-operated rats. The weight of the PVL lobes decreased, while that of the PVNL lobes increased depending on time. The DNA synthesis rates of the PVNL lobes were significantly higher than those in sham-operated control liver during the first 4 days with the maximal value on the 2nd day, while those of PVL lobes were essentially similar to the control values. Energy charge (EC) in both PVL and PVNL lobes significantly decreased on day 1 and recovered gradually, but with less extent in the regenerating PVNL lobes. The concentrations of total adenine nucleotides (TAN) in both the PVL and PVNL lobes were essentially similar during the first 2 days, but became significantly lower in PVL lobes after day 4. A decrease in EC preceded an increase in DNA synthesis only in the PVNL lobes, in contrast to the PVL lobes. Mitosis of hepatocytes on day 2 and subsequently enlarged lobules with an increased number of hepatocytes were histologic features in the PVNL liver. The AKBR was not correlated with hepatic energy charge of the liver. In conclusion, PVNL liver regenerates preceded by a decrease in EC and a subsequent increase in DNA synthesis keeping TAN constant, while PVL liver becomes atrophic, with a similar change in EC of the PVNL liver but ultimately decreased TAN without any change in DNA synthesis. AKBR is not a parameter reflecting the hepatic EC after portal branch ligation.

Adenine Nucleotides↗

Inhibitory effect of trimetazidine on utilization of myocardial glycogen during coronary ligation in dogs.

The left anterior descending coronary artery (LAD) of the dog was ligated completely for 1.5 min, and immediately after LAD ligation the heart was taken for determination of the glycogen phosphorylase and glycogen. Trimetazidine was injected intravenously 20 min before LAD ligation. LAD ligation increased the activity of glycogen phosphorylase and decreased the level of glycogen in both ischemic (LAD) and nonischemic (circumflex) areas. Trimetazidine at the dose of 0.3 or 1.0 mg/kg, being the dose that did not affect blood pressure and heart rate markedly, inhibited the ischemia-induced changes in glycogen phosphorylase and glycogen level. It is concluded that trimetazidine inhibits the ischemia-induced increase in the utilization of glycogen in the dog myocardium.

Animals↗

Physiological effects of portal ligation on the longitudinal and circular muscles of the dog portal tree.

We studied physiological effects of portal vein ligation on the longitudinal and circular muscles of the dog portal tree. Portal venous blood pressure after portal ligation was higher in dogs that died than in those that survived. The portal veins isolated from dogs that died after portal ligation exhibited both lower rate of onset and decreased intensity of spontaneous activity, compared with those from dogs that survived. Responsiveness of longitudinal muscles of each of the four portal segments to noradrenaline, acetylcholine, histamine and KCl was markedly reduced in dogs that died, compared with those that survived, although the responsiveness of circular muscle was nearly equal in both groups of dogs. The longitudinal muscle of the truncal portal vein from dogs that died responded less strongly to electrical transmural stimulation than that from surviving dogs. The nonadrenergic, noncholinergic response was almost abolished in dogs that died rapidly. The degree of spontaneous activity or responsiveness to various stimulations in smooth muscles of the portal tree is considered to reflect muscular development. The degree of development of the longitudinal muscle of the portal tree may determine the survival of dogs after portal ligation.

Acetylcholine↗

Placental blood flow and fetal weight following uterine artery ligation. Temporal aspects of intrauterine growth retardation in the guinea pig.

Placental blood flow (microsphere distribution), placental weight and fetal weight were examined at three stages of gestation following unilateral uterine artery ligation at days 30-32 in 23 guinea pigs. Placental blood flow and placental weight were reduced in the ligated horn at days 45, 55, and 65. The fetal weight was decreased at days 55 and 65. We suggest that ligation of the uterine artery reduces placental blood flow which, in turn, restricts placental growth without any significant effect on fetal weight before day 45. At this stage of gestation no correlation was found between fetal weight and placental blood flow. Later in gestation, however, fetal growth becomes limited by placental blood flow, and between days 45 and 55 ligation impedes the increase in blood flow, and consequently the fetal growth rate declines.

Animals↗

Venous surgery in erectile dysfunction. The role of dorsal-penile-vein ligation and spongiosolysis for impotence.

We report here on our surgical experience with venous leakage of the cavernous bodies. Out of 159 patients operated on, 134 were available for long-term follow-up. Depending on the cavernosographic findings, one of three different surgical procedures was carried out: ligation of the deep dorsal vein of the penis, spongiosolysis, or ligation of the crura. 18% of the patients undergoing ligation of the deep dorsal vein, postoperatively attained spontaneous erections, while 35% needed adjuvant corpus cavernosum autoinjection therapy. Spongiosolysis gave a more favourable result: spontaneous erections in 30% and vasoactive drug-dependent erections in 35%. Crural ligation did not prove successful. No serious complications were encountered postoperatively. Our data suggest that venous surgery should only be offered to a selected group of patients comprising young impotent men with venous leakage, maybe in combination with arterial disease, and patients suffering from distal venous leakage. Old age, neurogenic disorders causing erectile dysfunction, and diabetes mellitus should represent exclusion criteria for venous surgery.

Combined Modality Therapy↗

Laparoscopic ligation of bilateral spermatic varices under epidural anesthesia.

Feasibility and safety of laparoscopic ligation of bilateral internal spermatic varices under epidural anesthesia were assessed in 11 patients. Another 11 patients undergoing the same procedure under ventilation-assisted anesthesia served as controls. Patients in both groups belonged to the American Society of Anesthesia functional class I. Arterial blood analyses were obtained (1) in the horizontal supine position; (2) in the 15 degrees Trendelenburg position; (3) at 15 min after carbon dioxide pneumoperitoneum insufflation, and (4) at 15 min after desufflation in the supine position. In the epidural anesthesia group arterial blood parameters and respiratory rate remained stable in the Trendelenburg position. After intraperitoneal insufflation of carbon dioxide for 15 min, the arterial carbon dioxide level increased from 40.1 +/- 2.2 to 42.1 +/- 2.6 mm Hg, the respiratory rate increased from 17.0 +/- 1.4 to 20.6 +/- 1.2/min, the blood pH value decreased from 7.386 +/- 0.027 to 7.355 +/- 0.034, all values showing statistically significant differences. These changes returned to the preinsufflation level 15 min after release of the pneumoperitoneum. The above-mentioned parameters remained unchanged under the pneumoperitoneum by assisted ventilation in the control group. The mean time of surgery was similar in both groups: 82 and 90 min for the groups having general and epidural anesthesia, respectively. All laparoscopic procedures were accomplished successfully under general anesthesia. However, failure to ligate the internal spermatic varices occurred in 3 patients under epidural anesthesia, mainly due to patient intolerance to abdominal distension. The operation was continued under intubated general anesthesia for relaxing the abdominal muscle to provide an adequate working space. In 8 patients being successfully operated under epidural anesthesia, 5 experienced mild but tolerable abdominal distension; 2 complained of shoulder pain intraoperatively. Although laparoscopic ligation of internal spermatic varices could be accomplished in some patients under epidural anesthesia, it carried a high failure rate, more intraoperative morbidity, and significant arterial blood gas alterations. Routine ventilation-assisted anesthesia is suggested for therapeutic laparoscopy even for an easy procedure such as the ligation of the internal spermatic varices.

Anesthesia, Epidural↗

Beta3-integrin mediates smooth muscle cell accumulation in neointima after carotid ligation in mice.

BACKGROUND: Pharmacological blockade of beta3-integrins inhibits neointimal lesion formation in nonmouse animal models of arterial injury. In contrast, beta3-integrin-deficient (beta3-/-) mice are not protected from neointimal lesion formation after arterial injury. We investigated this discrepancy in beta3-/- and wild-type (beta3+/+) mice using different models of injury. METHODS AND RESULTS: After disruption of the carotid with a transluminal probe, there was no significant difference in neointimal thickening between beta3-/- and beta3+/+ mice. However, after ligation of the carotid without medial disruption, there was reduced neointimal thickening in beta3-/- mice compared with beta3+/+ mice at intervals up to 3 months. Lesion reduction in beta3-/- mice was associated with fewer intimal smooth muscle cells (SMCs) without a difference in SMC apoptosis or proliferation rate compared with beta3+/+ mice, consistent with reduced SMC migration from the media into the intima of beta3-/- mice. Moreover, combined eccentric medial disruption and ligation of the carotid in beta3-/- mice resulted in neointimal lesion formation only at the site of medial disruption. Transplantation of bone marrow cells harvested from beta3+/+ mice into irradiated beta3-/- mice resulted in reduced neointimal lesion formation after carotid ligation injury, confirming the importance of alpha(v)beta3 and not alpha(IIb)beta3 in the attenuated response. CONCLUSIONS: The alpha(v)beta3-integrin mediates intimal SMC accumulation that contributes to neointimal thickening in the setting of arterial ligation.

Animals↗

Effects of therapy on maximal walking time following femoral ligation in the rat.

Maximal walking times at a constant rate of 10 m/min were compared in normal rats, normal rats that had been exercised daily for 6 weeks, and rats that had undergone bilateral femoral artery ligation followed by 6 weeks of either an oral vasodilator, absence of sympathetic impulses to the extremities, cold exposure, or daily exercise. Rats maintained on the vasodilator could walk no farther than untreated, ligated rats. Both chronic cold exposure and sympathectomy significantly increased maximal walking distances of ligated rats and daily exercise increased maximal walking distances 7-fold. Rats that had received 6 weeks of exercise training following femoral artery ligation could walk longer than normal untrained rats; therefore, the increased exercise tolerance could not be explained solely by the restoration of normal large artery conductance by enlargement of collaterals bypassing the femoral occlusion.

Animals↗