Association of a summary index of child feeding with diet quality and growth of 6-23 months children in urban Madagascar.

BACKGROUND/OBJECTIVES: The assessment of child feeding practices has received renewed attention through the development of an infant and child feeding index (ICFI). However, the advantages and shortcomings of such a summary index are still not well known. The aim of this study was to assess the usefulness of ICFI as an analytical tool (1) by studying its association with complementary food energy intake and mean micronutrient density adequacy (MMDA) and (2) by testing whether ICFI and its components are associated with length-for-age z-score (LAZ) of 6-23 months children in urban Madagascar. SUBJECTS/METHODS: ICFI was constructed using data from questionnaires on feeding practices and quantitative 24-h recalls (n=1589). Multivariate analysis was used to control for household wealth and other confounding factors. RESULTS: ICFI was positively correlated with complementary food energy intake (P<0.0001) and MMDA (P<0.0001). ICFI was associated with LAZ among 6-8 months children (P=0.02). For all ages combined, there was a tendency towards an association that did not reach statistical significance (P=0.08). Among feeding practices that formed ICFI, breastfeeding was associated with LAZ (P=0.03) but not in the expected direction with +0.16 z-score difference in favour of non-breast-fed children. When breastfeeding was removed and introduced separately into the multivariate model, the relationship between the modified ICFI and LAZ became significant (P=0.02). CONCLUSIONS: Findings suggest that the ICFI could be a useful analytical tool, which needs however to be constructed according to its final use and which should be adapted to each context.

Saratin, an inhibitor of von Willebrand factor-dependent platelet adhesion, decreases platelet aggregation and intimal hyperplasia in a rat carotid endarterectomy model.

PURPOSE: Post-carotid endarterectomy, thrombosis, and intimal hyperplasia may be decreased by the inhibition of platelet adhesion and activation. In this study, a novel agent, saratin, was used to inhibit platelet-to-collagen adhesion in a rat carotid endarterectomy model. Saratin is a recombinant protein isolated from the saliva of the medicinal leech Hirudo medicinalis, which is thought to act by binding to collagen, and inhibits von Willebrand factor-collagen interaction under conditions of increased shear and therefore, the adherence and activation of platelets at the vessel wall. Saratin has the advantage of being a nonsystemic, site-specific topical application. METHODS: A rat carotid endarterectomy model was used in which an open technique with arteriotomy and intimectomy was used. Saratin was applied to the endarterectomized surface of the carotid artery before arterial closure. End point measurements included platelet adhesion, thrombosis rate, intimal hyperplasia development, bleeding times, and platelet counts. Electron micrographs of carotid arteries were used for quantitative analysis of platelet aggregation and platelet counts. Intimal hyperplasia and thrombosis were assessed with computer-assisted morphometric analysis of elastin-stained carotid artery sections with direct measurement of the intimal hyperplasia area. RESULTS: The topical application of saratin significantly decreased platelet adhesion compared with controls at 3 hours after carotid endarterectomy (64 +/- 17 vs 155 +/- 33 platelets per grid, P = .05), and 24 hours after carotid endarterectomy (35 +/- 11 vs 149 +/- 37 platelets per grid, P = .0110), respectively. A percent luminal stenosis, as a measure of intimal hyperplasia, was significantly decreased with saratin application compared with controls (10.9% +/- 1.8% vs 29.8% +/- 6.8%, P = .0042). This decrease in intimal hyperplasia formation correlated with the inhibition of platelet adhesion. Thirty-three percent of control arteries were found to be thrombosed 2 weeks after carotid endarterectomy compared with a 0% thrombosis rate in the saratin-treated group (P = .0156). No increased bleeding was encountered along the arterial suture line in the saratin group. Bleeding times and systemic platelet counts were not found to change significantly in the saratin-treated rats compared with control rats at 3 and 24 hours after endarterectomy. CONCLUSION: Saratin significantly decreased platelet adhesion, intimal hyperplasia, luminal stenosis, and thrombosis after carotid endarterectomy in rats. Saratin did not increase suture line bleeding or bleeding times, and did not decrease platelet counts. Saratin may serve as a topical agent to be used for the site-specific inhibition of thrombosis and intimal hyperplasia after vascular manipulation.

Increased intimal hyperplasia after carotid endarterectomy in spontaneously hypertensive rats.

This study evaluated the effects of hypertension on postoperative intimal hyperplasia using a rat carotid endarterectomy (CEA) model with spontaneously hypertensive rats (SHR) and normotensive Sprague-Dawley rats (SD). SHR and SD rats underwent left carotid exposure and CEA via an arteriotomy, scoring and removal of the intima, followed by arteriotomy closure. The rats were then sacrificed two weeks postoperatively. The left carotid artery was harvested and underwent elastin and double immunohistochemical staining. The percent of lumenal stenosis was calculated using morphometric measurements, and stained cells within the intimal hyperplasia were counted. The means and standard deviation of the means were calculated, and the two groups were compared using a 2-sample t test. The systolic blood pressure was 228 +/-35 mm Hg in the SHR group and 108 +/-8 mm Hg in the SD group (p<0.00001). The percent of lumenal stenosis was 82.6 +/-17.1% in the SHR group and 21.2 +/-13.7% in the SD rats (p value <0.0001). The percentage of cells staining for a-SM actin was equal in the SHR group and the SD group (> 91%) but the percentage of these cells staining for BrdU was 38.2 +/-8.4% in the SHR group and 10.7 +/-5.8% in the SD group (p< 0.00001). Hypertension in the SHR rats was associated with an increased lumenal stenosis due to increased intimal hyperplasia. The increased intimal hyperplasia was due to enhanced and accelerated replication of smooth muscle cells. Hypertension may be associated with increased restenosis rates after CEA.

Folate supplementation inhibits intimal hyperplasia induced by a high-homocysteine diet in a rat carotid endarterectomy model.

OBJECTIVE: Hyperhomocysteinemia has been implicated as a causative factor in intimal hyperplasia development. The addition of dietary folate in a hyperhomocysteinemia, carotid endarterectomy rat model is postulated to decrease plasma homocysteine levels and, in turn, reduce post-carotid endarterectomy intimal hyperplasia. METHODS: Each rat was fed one of six diets: (1) lab chow with no folate (n = 7), (2) lab chow with 10 mg/kg folate added (n = 3), (3) lab chow with 25 mg/kg folate added (n = 3), (4) a homocysteine diet with no folate (n = 7), (5) a homocysteine diet with 10 mg/kg folate added (n = 5), or (6) homocysteine diet with 25 mg/kg folate added (n = 5). Each rat then underwent an open carotid endarterectomy. In 2 weeks, intimal hyperplasia in the carotid artery was measured. Plasma homocysteine and folate levels were measured. RESULTS: Plasma folate levels rose with folate administration. Plasma homocysteine in the lab chow group was 5.4 +/- 0.5 micromol/L and did not change with the addition of folate. In the homocysteine diet group, plasma homocysteine rose 10-fold over the lab chow group (51.9 +/- 6.5 vs 5.4 +/- 0.5, micromol/L, P <.0001). In the group fed a homocysteine diet with 10 mg/kg folate added, a significant decrease in plasma homocysteine was observed (17.5 +/- 8.5 vs 51.9 +/- 6.5, micromol/L, P =.0003). In the group fed a homocysteine diet with 25 mg/kg folate added, plasma homocysteine levels were further reduced to levels seen in the lab chow group (12.6 +/- 2.6 vs 5.4 +/- 0.5, micromol/L, P = not significant). The relationship between plasma folate and homocysteine was inverse (R = 0.39, P =.0036). Luminal stenosis due to intimal hyperplasia was minimal in lab chow groups and unaffected by folate. The homocysteine diet group demonstrated post-carotid endarterectomy luminal stenosis due to intimal hyperplasia (60.9% +/- 9.2%). In the group fed a homocysteine diet with 10 mg/kg folate added, intimal hyperplasia was reduced, compared with the homocysteine diet group (32.6% +/- 7.4% vs 60.9% +/- 9.2%, P =.009). In the group fed a homocysteine diet with 25 mg/kg folate added, intimal hyperplasia was reduced to lab chow group levels (10.8% +/- 0.8% vs 4.8% +/- 1.0%, P = not significant) and was reduced, compared with the group fed a homocysteine diet with 10 mg/kg folate added. CONCLUSION: The use of folate in this hyperhomocysteinemia carotid endarterectomy model and the resultant attenuation of plasma homocysteine elevation and intimal hyperplasia development lend strong support to homocysteine being an independent etiologic factor in post-carotid endarterectomy intimal hyperplasia.

Abdominal aortic aneurysm repair.

Newer, minimally invasive catheter-based endovascular technology utilizing stent grafts are currently being evaluated for abdominal aortic aneurysm (AAA) repair. A retrospective review of all (3 years) consecutive, non-ruptured elective AAA repairs was undertaken to document the results of AAA surgical repair in a modern cohort of patients to allow a contemporary comparison with the evolving endoluminal data. One hundred twenty-one AAAs were identified in a male veteran population. Mean age was 68.5 +/-7.7 years. Medical history review showed hypertension in 55%, heart disease in 73.5%, peripheral vascular disease in 21%, stroke and transient ischemic attacks in 22%, diabetes mellitus in 7%, renal insufficiency in 10%, and smoking history in 80%. The AAA size was documented with ultrasound (5.2 +/-1.3 cm, n=40) and computed tomography (5.6 +/-1.3 cm, n=100). Fifty-nine percent had angiography. Intraoperative end points included an operative time of 165 +/-6.3 minutes from incision to dressing placement. A Dacron tube graft was used in 78%, the remaining were Dacron bifurcated grafts. A suprarenal clamp was used in 8% for proximal aortic control with juxtarenal aneurysms. A pulmonary-artery catheter was placed in 69%. A transverse incision was used in 69% of patients and a midline incision was used in the rest. Estimated blood loss was 1505 +/-103 mL; cell saver blood returned 754 +/-53 mL; crystalloid/Hespan 4771 +/-176 mL; banked packed red blood cells 0.75 +/-0.11 U. Time to extubation was, in the operating room (78.5%), on the day of the operation (5.0%), postoperative day (POD) 1 (12.4%), POD2 (1.7%), POD3 (0.8%), and one case was performed with epidural anesthesia only. Postoperative end points included a 30-day mortality rate of 1.6% (two patients). Postoperative morbidity included wound dehiscence 0.8%; sepsis, urinary tract infection, wound infection, leg ischemia, ischemic colitis, and stroke each had an incidence of 1.6%; myocardial infarction, congestive heart failure, pneumonia, re-operation for suspected bleeding, and ileus or bowel obstruction occurred with an incidence of 3.3%. No significant increase in serum creatinine levels was noted. Time to enteral fluids/nutrition was 3.5 +/-0.08 days. Patients were out of bed to a chair or walking by 1.3 +/-0.06 days postoperatively. The length of stay in the intensive care unit (ICU) was 2.0 +/-0.12 days and postoperative hospital stay was 6.6 +/- 0.33 days. Transfusion requirement for the hospital stay was 1.6 +/-0.2 U per patient. This review highlights a cohort of male veteran patients with significant cardiac co-morbidity who have undergone repair with a conventional open technique and low mortality and morbidity rates. This group had rapid extubation, time to oral intake, and ambulation. In addition, ICU and hospital stays were relatively short.

Increasing levels of dietary homocystine with carotid endarterectomy produced proportionate increases in plasma homocysteine and intimal hyperplasia.

PURPOSE: The role that homocysteine may play in post-carotid endarterectomy (CEA) restenosis due to intimal hyperplasia is not well understood. This study was designed to investigate the effects of different levels of dietary homocystine on: (1) plasma homocysteine; (2) post-CEA intimal hyperplasia; and (3) levels of the methyl donor S-adenosylmethionine (SAM) and its counterpart S-adenosylhomocysteine (SAH) in the homocysteine pathway. METHODS: Male rats were fed specialized diets for 2 weeks pre- and post-CEA. Groups included control (0 homocystine added, n=9), 1.5 (1.5 g/kg homocystine added, n=10), 3.0 (3.0 g/kg homocystine added, n=9), and 4.5 (4.5 g/kg homocystine added, n=11). The rats underwent a surgical carotid endarterectomy. Endpoints included; plasma homocysteine, intimal hyperplasia, replicative index using with alpha-SM actin and BrdU, hepatic SAM levels, SAH levels, and the hepatic activities of methylenetetrahydrofolate reductase (MTHFR) and cystathionine beta-synthase (CBS). RESULTS: Increasing dietary homocystine produced a proportionate increase in plasma homocysteine and an increase in intimal hyperplasia. Regression analysis of plasma homocysteine levels and intimal hyperplasia showed a significant correlation (r=0.71,P=0.003). Plasma homocysteine levels above 15 microM were associated with significant increases in intimal hyperplasia above 6.5% (P=0.04). Elevation of plasma homocysteine levels to moderate levels (5-25 microM) resulted in significant post-CEA intimal hyperplasia. Cellular analysis of the area of intimal hyperplasia in all diet groups showed comparable amounts of cells positive for alpha-SM actin. However, with increasing levels of dietary homocystine and plasma homocysteine there was an increase in replicative index (P<0.001) as determined by BrdU staining. Increasing dietary homocystine increased plasma homocysteine and was followed by increases in the replicative index thus producing increased intimal hyperplasia and lumenal stenosis. In hepatic measurements the 1.5 and 3.0 g/kg homocystine diets caused: increased liver activity of MTHFR (P=0.03) and decreased hepatic levels of SAM, SAH and SAM/SAH ratios compared to controls. Homocystine treatment did not cause significant alterations in CBS levels (P=0.992). These studies also showed no correlation of the MTHFR and CBS enzymes with plasma homocysteine levels or intimal hyperplasia. However, hepatic levels of SAM showed significant negative correlations with plasma homocysteine (r=-0.58; P=0.006) and with BrdU percentages of cellular proliferation (r=-0.69; P=0.06). CONCLUSION: The degree of post-CEA intimal hyperplasia in a rat model is directly related to the plasma level of homocysteine. The hyperplastic effects of homocysteine may be mediated in part by a physiological insufficiency of methyl donors as shown by decreases in SAM. Thus, increasing levels of plasma homocysteine enhanced and accelerated the smooth muscle cell response after CEA which led to increased intimal hyperplasia and lumenal stenosis.

Infectious complications resulting from use of hemostatic puncture closure devices.

BACKGROUND: Femoral access site complications have increased as the fields of invasive cardiology, radiology, and endovascular surgery have emerged. In order to address one of these complications, hemorrhage, the hemostatic puncture closure devices were developed. METHODS: Retrospective review of cardiac catheterizations performed at a single institution to investigate infectious groin complications related to use of the Perclose Prostar and Techstar devices. RESULTS: Infectious groin complications were significantly higher in the Perclose group as compared with manual compression. Three patients had clinical and laboratory evidence of arterial infection whereas 2 had soft tissue infections. All 5 required operative intervention ranging from incision and drainage to arterial reconstruction. Hemorrhagic complications were not significantly different between the two groups. CONCLUSIONS: The Perclose devices provide hemostasis after femoral artery catheterization similar to manual compression. However, infectious groin complications appear to be more common with these devices.

Blue toe syndrome: treatment with intra-arterial stents and review of therapies.

PURPOSE: To determine if intra-arterial stent placement can adequately treat lesions producing microemboli to the lower extremities. MATERIALS AND METHODS: During a 6.5-year period, 15 patients presenting with blue toe syndrome had 16 presumed embolic lesions treated with intra-arterial stents. These patients were evaluated during routine clinical follow-up during a 6-month period. This evaluation included physical and noninvasive arterial examinations. When patients could not return for follow-up, hospital, clinical, vascular laboratory, and radiology records were reviewed to assemble the appropriate information. Outcomes included symptoms of recurrent emboli, amputation, and death. RESULTS: Treated embolic lesions included two aortic stenoses, three bilateral iliac artery stenoses, nine unilateral iliac artery stenoses (one patient received separate treatment of unilateral iliac lesions), and two superficial femoral artery stenoses. Patients were followed-up for a mean of 18 months. Eight of 15 patients (53%) were improved or stable without complications. There were eight negative outcomes experienced in seven patients. Three patients (20%) were deceased at follow-up. Four patients (27%) had undergone amputation; one transmetatarsal amputation and three below-the-knee amputations. Only one of these was related to progressive disease in the treated extremity (7%). One patient (7%) experienced recurrent embolic symptoms. Stents were patent in all patients. CONCLUSION: Patients with blue toe syndrome are at high risk of limb loss and mortality despite treatment. Intra-arterial stent placement provides an alternative to standard surgical treatment. Further studies are needed to define the optimum therapy.

Hyperhomocysteinemia increases intimal hyperplasia in a rat carotid endarterectomy model.

PURPOSE: This preliminary study investigated the ability to elevate the serum homocysteine (H[e]) levels and investigated the increases in postoperative neointimal hyperplasia (IH) in an environment with hyperhomocysteinemia and the resultant restenosis in a rat carotid endarterectomy (CEA) model. METHOD: The 9 rats for the control group were fed rat chow, and the 8 rats for the H(e) group were fed H(e)-supplemented rat chow for 2 weeks before and after CEA. The animals underwent anesthesia, and a left common CEA was performed. After 14 days, the serum H(e) levels were measured and the left carotid artery was harvested and elastin stained. Morphometric measurements were used to calculate the area of stenosis of the lumen. The mean and the standard deviation of the mean were determined. The 2 groups were compared with the Mann-Whitney test and a linear regression model. Three additional rats per group were studied, with carotid artery sectioning with double immunohistochemical staining for 5-bromodeoxyuridine (BrdU) and alpha-smooth muscle (alpha-SM) actin. RESULTS: The serum H(e) level in the H(e) group was 36.32 micromol/L +/- 15.28, and in the control group the level was 5.53 micromol/L +/- 2.06 (P =.0007). IH presented as percent lumen stenosis was 21.89% +/- 4.82% in the H(e) group and 4.82% +/- 1.64% in the control group (P =.0007). The linear regression model of the serum H(e) levels and the percent stenosis showed a linear relationship (r2 =.72). The alpha-SM actin staining revealed that nearly all of the cells in the IH area were of smooth muscle or myofibroblast origin and that 10.1% +/- 2.6% of the cells were stained for BrdU in the control group versus 23% +/- 7.1% in the H(e) group. Also, 9.3% +/- 2.6% of the cells in the IH area were stained for BrdU and for alpha-SM actin versus 19.1% +/- 5. 6% stained for both BrdU and alpha-SM actin in the H(e) group. CONCLUSION: This is the first study to examine IH after CEA and hyperhomocysteinemia in rats. The study shows that the elevation of serum H(e) levels can be obtained by feeding rats modified diets with added H(e). The consistent elevation of serum H(e) levels was associated with more than 4 times the amount of IH after a CEA in a rat model.

Assessment of apparent vena caval penetration by the Greenfield filter.

PURPOSE: To examine and elucidate the mechanisms for apparent "penetration" by Greenfield vena caval filters. METHODS: Two filters were placed in the inferior venae cavae (IVC) of four immature sheep and followed with cavography for 1 year. Two animals underwent computed tomography (CT) and laparoscopic examination. At necropsy, the vena cava and adjacent structures of all four animals were examined grossly and histologically. RESULTS: Based upon cavography and CT imaging, all filters appeared to penetrate the vena cava at 12 months. However, at laparoscopy, no hooks or limbs were exposed, and the pericaval tissues remained intact; each hook or limb was within the adventitia or encapsulated in scar tissue. Histology of the tissue at the hook sites revealed remodeling of the intimal surface of the IVC and thinning of the adventitia. CONCLUSIONS: Based upon these data, we hypothesize that the vena cava gradually adapts by medial and adventitial thinning and myointimal remodeling to the radial force exerted by a filter. This process allows increase in the filter base diameter while maintaining the integrity of the cava and protecting adjacent structures.

Azotemia: gadopentetate dimeglumine as contrast agent at digital subtraction angiography.

In an azotemic patient with suspected renal artery stenosis, undiluted gadopentetate dimeglumine was administered in an aortic bolus to provide contrast at digital subtraction angiography of the aorta and renal arteries. The contrast material (5 mmol/mL) was power injected (rate, 15 mL/sec; total dose, 30 mL). Selective renal arteriography was also performed with 5 mL of undiluted gadopentetate dimeglumine hand injected into each renal artery (total dose, 40 mL). The patient tolerated the procedure without complication or worsening of renal function, and diagnostic angiographic images were obtained.

Inhibition of aortic aneurysm development in blotchy mice by beta adrenergic blockade independent of altered lysyl oxidase activity.

PURPOSE: This study was designed to define the effects of beta-adrenergic blockade on aortic lysyl oxidase (LO), an enzyme responsible for elastin and collagen cross-linking, and aneurysm formation in the blotchy mouse. It was hypothesized that beta-blockade would inhibit the development of aneurysms because of its hemodynamic effect rather than a direct effect on LO activity. METHODS: Three groups of mice were studied: group I--normal littermates of blotchy mice; group II--untreated blotchy mice; group III--blotchy mice given either propranolol, atenolol, or nadolol. Data from the three different beta blocker-treated animals, group III, were statistically identical and were combined for analysis. The study was concluded when the mice were 4 months of age. At that time systolic blood pressure, heart rate, and aortic diameters were measured, and the entire aorta from each mouse was subjected to a bioassay for LO activity. RESULTS: Group I normal mice had an aortic arch diameter of 0.10 +/- 0.02 cm. Group II blotchy mice developed aortic arch aneurysms with a diameter of 0.21 +/- 0.03 cm. In Group III, beta blockade reduced the aortic arch diameter in blotchy mice to 0.11 +/- 0.03 cm. Mean heart rate in group III beta-blocked mice was reduced 25% compared with group I normal mice, and 18% compared with group II untreated blotchy mice. Blood pressures were similar in all three groups. Group II blotchy mice exhibited approximately half of the aortic LO activity (2.43 +/- 0.57 cpm/micrograms protein) noted in group I normal mice (5.82 +/- 1.06 cpm/micrograms protein). Aortic LO activity in group III blotchy mice remained low (2.09 +/- 0.85 cpm/micrograms protein) despite administration of beta-blockers. CONCLUSIONS: This is the first study to document an actual decrease in the level of aortic LO activity in blotchy mouse. beta-Blockade inhibits development of aortic aneurysms in blotchy mice. This is associated with a reduction in heart rate, but not by alterations in LO activity.

Staging of fixation and retrievability of Greenfield filters.

PURPOSE: The purpose of this study was to determine the retrievability of the Greenfield filter, to characterize fixation, and to evaluate the mechanical function of a new retrieval unit. METHODS: Stainless steel, titanium, and two prototype Greenfield filters (n = 82) were placed in 15 sheep at multiple sites and retrieved acutely, and 7, 14, and 21 days after placement. The animals were killed, and appropriate tissues were submitted for histopathologic evaluation. RESULTS: Eighty-two percent of all filters were retrieved. Two animals died during the procedure of cardiac tamponade. Retrieval was easiest immediately after placement, but it was least successful from the right atrium and associated with the highest incidence of damage. By 21 days, the intima around the filter hooks had thickened with myointimal hyperplasia and variable amounts of endothelial regeneration. Guide wire-hook modification was used to improve filter capture. CONCLUSIONS: All models of the Greenfield filter can be retrieved 14 to 21 days after placement, although there is high risk to retrieval from the right atrium and ventricle. The long-term safety of the Greenfield filter in man makes it difficult to justify removal in any but exceptional cases.

Systemic hypertension induced by aortic cross-clamping: detrimental effects of direct smooth muscle relaxation compared with ganglionic blockade.

PURPOSE: Infrarenal aortic cross-clamping performed during vascular reconstructive procedures is often accompanied by systemic supraclamp hypertension. Much of the disease and death that attend aortic cross-clamping centers around hypertension. Many different strategies have been developed to attenuate intraoperative hypertension, and a host of pharmacologic agents are regularly used to lessen the heart-related, cerebral, and systemic effects of clamp-induced hypertension. This study was performed to evaluate two such strategies; the intravenous administration of either trimethaphan camsylate or nitroprusside. METHODS: We used a highly controllable and reproducible model of aortic cross-clamping in which we have previously shown the hypertension associated with clamping to be an active process mediated by means of a reflex arc. Ten dogs, five treated with nitroprusside (NP group) and five treated with trimethaphan camsylate (TC group), underwent 90 minutes of aortic cross-clamping. During this 90-minute period each group received 30 minutes of antihypertensive therapy. RESULTS: Control mean arterial pressure +/- SEM was 80 +/- 5 mm Hg for both groups and increased to 140 +/- 5 mm Hg with clamp application. With antihypertensive treatment the elevation in mean arterial pressure produced by cross-clamping was reduced to preclamp levels in the TC group and only partially (52%) in the NP group, despite very high doses of nitroprusside. Cardiac output (CO) increased in the NP group by 115% and decreased by 36% in the TC group. This increase in CO translates into a large (101%) increase in cardiac minute work for the NP group. CONCLUSIONS: The attenuation of clamp-induced hypertension by nitroprusside is associated with a dramatic increase in CO and cardiac work whereas the use of trimethaphan camsylate is not. The use of this ganglionic blocker may be more appropriate in this setting.

Delayed onset hypertension with infrarenal aortic cross-clamping in dogs.

The time course and mechanism of systemic hypertension associated with infrarenal aortic cross-clamping were investigated in 31 chloralose-anesthetized dogs after ligating the tail artery, the paired infrarenal lumbar arteries, and the circumflex iliac arteries bilaterally. Cardiac output, renal blood flow, and suprarenal and infrarenal mean arterial blood pressure were continuously monitored. Infrarenal aortic clamping (90 min) in the standard group (n = 6) consistently decreased infrarenal blood pressure from 90 +/- 6 to 13 +/- 1 mm Hg within 1 min, while suprarenal blood pressure gradually increased over 20-30 min from 88 +/- 7 to 144 +/- 8 mm Hg, where it remained until declamp. The SHAM group (identical operation and instrumentation, without aortic clamping) (n = 5) showed no statistically significant changes. After 90 min of clamp total peripheral and renal resistance nearly doubled but no statistically significant changes in cardiac output, heart rate, central venous pressure, renal blood flow, renin, or glomerular filtration rate were detected. Upon declamping, pressures returned to control levels within 20 min. Groups with bilateral nephrectomy (n = 9) or unilateral iliac artery clamping (n = 7) produced similar time courses and patterns of hemodynamic change. Ablation of afferent nerves from the left hind limb (n = 4) eliminated the hypertension produced by left iliac artery clamping. The substantial delay (20-30 min) to the onset and full development of suprarenal hypertension, with near immediate infrarenal hypotension, is not consistent with a direct mechanical impedance effect. Hypertension in the presence of a bilateral nephrectomy or unilateral iliac artery clamping combined with its full reversal by nerve section strongly suggests that this is a reflex hypertension. This reflex mechanism of hypertension development has implications for intra- or perioperative events associated with hypertension management.

Renal vasoconstriction and transient declamp hypotension after infrarenal aortic occlusion: role of plasma purine degradation products.

To better understand renal and systemic hemodynamics associated with hindquarter ischemia produced by aortic compression, chloralose-anesthetized dogs were given phentolamine while an external clamp maintained infrarenal aortic pressure below 25 mm Hg for 45 minutes. In four sham-operated dogs, infrarenal pressure was maintained; reinforced cannulas, capable of resisting clamp compression, were placed within the aorta and the inferior vena cava. Suprarenal and infrarenal arterial pressure and renal blood flow were continuously monitored. Blood samples taken before clamp application and at 1, 3, 5, and 10 minutes after clamp removal were assayed for adenosine, inosine, xanthine, and hypoxanthine. On clamp removal suprarenal pressure immediately dropped from a preclamp pressure of 114 to 82 mm Hg but returned to preclamp values within 1 minute. Renal blood flow was significantly reduced after clamp release, reaching a nadir of 39% of preclamp flow. This reduction persisted despite a normalization of arterial pressure. Summed plasma purines were significantly elevated 1 minute after clamp removal. Sham-operated dogs showed no significant alterations in arterial pressure, renal blood flow, or plasma purine levels. This study demonstrates a significant non-alpha-adrenergic receptor-mediated reduction in renal blood flow and a coincident increase in purine degradation products after removal of an infrarenal aortic cross-clamp.

Depressor response during experimental portal hypertension in dog.

Elevation of splanchnic portal pressure in dogs results in an apparently reflexic response manifest as an active reduction in mean arterial pressure (AP). The results from 14 dogs separated into a tachycardic (TACH) heart rate (HR) response (P less than 0.005, n = 6) group and a bradycardic (BRAD) HR response (P less than 0.005, n = 8) group. Both groups showed similar reductions in AP and cardiac output (CO); however, stroke volume (SV) was reduced to a greater extent (P less than 0.029) in the TACH group. Atropine eliminated or reversed the bradycardia in the BRAD group and propranolol blocked the tachycardia in the TACH group. When portal hypertension was repeated in the BRAD group after atropine, similar reductions (P less than 0.01) were observed in AP, SV, and CO but total peripheral resistance (TPR) no longer increased. Reductions in SV or CO due to reduced venous return only partially explain the AP changes. These data suggest the reflex activation of several mechanisms that contribute to rather than completely oppose the reduction in AP anticipated with a reduction in venous return. They include an atropine-sensitive negative chronotropic effect and a negative inotropic effect as well as adjustments in TPR. We thus propose a reflex mechanism that is activated by increased splanchnic pressure and contributes to an active lowering of mean arterial pressure.

Regional blood flow changes in response to mildly pressor doses of triglycyl desamino lysine and arginine vasopressin in the conscious dog.

Arginine vasopressin (AVP) is used to treat esophageal variceal hemorrhage but has the drawbacks of rebleeding and reported coronary insufficiencies. In conscious dogs (n = 23) we compared AVP and an analog, triglycyl desamino lysine vasopressin (TDLVP), for arterial pressor responses and changes in regional blood flow. Dogs were infused with saline (n = 5), AVP (n = 7) or TDLVP (n = 7), and blood flow was measured with microspheres during control, infusion and postinfusion in 46 tissue sections including pieces of the esophagus, stomach, liver, kidney, spleen, heart, skin, muscle and brain. TDLVP (1.0 micrograms/kg/min) and AVP (0.025 micrograms/kg/min) produced a similar mean arterial pressure increase of 23 mm Hg and a heart rate decrease of 38 beats/min. TDLVP sustained the increase in mean arterial pressure and reduction in heart rate at 30 min postinfusion whereas AVP did not. Neither AVP nor TDLVP showed a reduction in brain, kidney or liver flow; however, both produced reductions (73 and 61%, respectively, P less than .01) in mucosal-esophageal flow. Only TDLVP reduced mucosal-fundus blood flow (P less than .01). Endocardial flow was reduced (27%) in both TDLVP and AVP groups; however, heart rate also decreased during this time and a linear correlation between these two measurements yielded a value for r2 of 0.83. Thus, TDLVP offers a therapeutic alternative to AVP in treating gastroesophageal varices due to its longer duration of action as represented by the sustained reduction in esophageal and mucosal-fundus flow.