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At least 865 records · Page 48Linked to original sources

Clip migration after 11-gauge vacuum-assisted stereotactic biopsy: case report.

A 68-year-old woman underwent stereotactic biopsy of a small cluster of calcifications. The post-biopsy mammograms showed the biopsy-marking clip to be located correctly at the biopsy site. Follow-up mammograms 1 year later showed that the clip migrated to another quadrant of the breast. Findings in this case demonstrate that at long-term follow-up a biopsy-marking clip may not be accurately marking the biopsy site.

Aged↗

Clip or marker migration 5-10 weeks after stereotactic 11-gauge vacuum-assisted breast biopsy: report of two cases.

Two women, aged 50 and 51 years, underwent stereotactic, 11-gauge vacuum-assisted biopsy from the cranial approach of small lesions in the upper outer quadrant of the right breast with removal of lesions that were detected with mammography. Postbiopsy mammograms showed the metal clip or marker at the biopsy sites in both patients. Histologic analysis of both lesions indicated atypical hyperplasia. Mammograms obtained prior to surgical excision showed caudal z-axis migration of the clip or marker to be 6.5 cm at 5 weeks and 4.5 cm at 10 weeks, respectively. By ignoring the clip or marker that had migrated to an inaccurate location and by using internal and external breast landmarks to guide presurgical excision needle localization, the biopsy sites were successfully excised in both patients.

Biopsy↗

Percutaneously applied ureteral clips: treatment of vesicovaginal fistula.

Percutaneous techniques to manage urinary fistulas have had limited success. To overcome this, self-closing metallic clips were developed to occlude the ureter. The clips are applied through a percutaneously placed 30-F Teflon sheath. A case is reported in which the clips and new technique were successfully used.

Aged↗

Breast-conserving surgery for primary breast cancer: necessity for surgical clips to define the tumor bed for radiation planning.

Radiographs obtained at definitive and boost irradiation in 50 patients with stage I-II breast cancer were retrospectively examined. Tangent target fields planned on the basis of surgical clips placed at excision biopsy were evaluated with simulation radiographs. Four (8%) of 50 tangent target fields would have been inadequate without clips, and 23 (46%) of the boost targets would have been missed (12 [24%], totally; 11 (22%), marginally). Radiopaque surgical clips placed at excision biopsy help plan boost-irradiation target fields.

Adult↗

Displacement of microcalcifications during stereotactic 11-gauge directional vacuum-assisted biopsy with marking clip placement: case report.

A 53-year-old woman with right breast microcalcifications of intermediate concern underwent stereotactic directional vacuum-assisted biopsy with marking clip placement. Postbiopsy mammograms showed displacement of a few of the targeted microcalcifications adjacent to misplaced marker clips. Mammography following stereotactic breast biopsy is important to document the location and number of residual calcifications and to determine the adequacy and location of clip placement.

Biopsy↗

Naloxone attenuates development of hypertension in two-kidney one-clip Goldblatt rats.

The present experiments were designed to determine if an opiate antagonist affects blood pressure in two-kidney one-clip Goldblatt rats. Male Sprague-Dawley rats were divided into three groups. Group 1 received an infusion of saline intraperitoneally via an osmotic pump and left renal artery constriction (RAC). In group 2, rats were treated the same as group 1, except that they received an intraperitoneal infusion of naloxone (100 micrograms/h). Group 3 received the same infusion of naloxone without RAC. Naloxone-infused Goldblatt rats showed a significantly lower systolic blood pressure (SBP) than saline-infused Goldblatt rats (132 +/- 7 vs. 160 +/- 9 mmHg at day 14), but a higher SBP than control (132 +/- 7 vs. 106 +/- 1 mmHg). Infusion of naloxone did not significantly change SBP in normotensive rats. Renal renin activity in the clipped kidney was higher than in the nonclipped kidney in groups 1 and 2. Plasma renin activity (PRA) in both groups of Goldblatt rats was higher than in group 3, but no significant difference was found between the two groups of Goldblatt rats (groups 1 and 2). Naloxone (1.5 microM) did not affect the basal secretion of renin by isolated cortical slices from untreated rats. The present data demonstrate that naloxone significantly attenuates the development of hypertension in two-kidney one-clip rats. The attenuation of blood pressure was not associated with the changes in PRA, renal renin activity, or plasma aldosterone concentrations. The data support the hypothesis that the endogenous opioid system may be involved in the development of renovascular hypertension.

Aldosterone↗

Hypotensive effect of water restriction in the two-kidney one-clip hypertensive rat.

In two-kidney one-clip hypertensive rats we evaluated the effect of water restriction on the development and maintenance of severe hypertension (systemic blood pressure 200-230 mmHg). After application of renal arterial clips in rats allowed access to water for 1 or 2 h daily, BP stabilized at 180-190 mmHg. No increase in water intake occurred and plasma renin activity(PRA) (measured before the drinking period) was significantly below the levels observed in ad libitum-drinking hypertensive rats. In rats administered 4 ml water/100 g body weight twice daily by gavage, development of hypertension was more clearly suppressed. Blood pressure increased slowly and reached levels of only 150-170 mmHg. Furthermore, PRA was significantly lower in this group compared with ad libitum-drinking hypertensive animals. In rats with established (4-5 wk) renal hypertension, restriction of water intake to 1 or 2 h daily resulted in a rapid decrease in BP of about 30 mmHg. Daily administration of Pitressin tannate to hypertensive rats allowed free access to water induced a similar decrease in BP as well as suppression of PRA. These results indicate that the hypotensive effect of water restriction in the two-kidney one-clip hypertensive rat model may be mediated, at least in part, through elevated circulating levels of vasopressin that subsequently inhibit renin release.

Animals↗

The role of thromboxane in two-kidney, one-clip Goldblatt hypertension in rats.

Impaired contralateral kidney (CLK) function is important in the maintenance of hypertension in the two-kidney, one-clip (2K, 1C) Goldblatt rat model. Since glomerular filtration rate (GFR) is influenced by the products of arachidonic acid metabolism, we investigated the potential role of eicosanoids as mediators of impaired CLK pressure-volume regulation. At 4 wk following right renal artery clipping, GFR of hypertensive rats was significantly reduced. This decrease was due to the fixed reduction in GFR of the clipped kidney and failure of the CLK to increase its GFR. Thromboxane (Tx) production by isolated perfused CLK was significantly elevated, whereas prostacyclin production remained unchanged. Furthermore, CLK GFR was inversely proportional to Tx production. Treatment of 4-wk hypertensive animals with either the Tx synthase inhibitor UK-38,485 or the Tx receptor antagonist GR 32191 produced a significant increase in CLK GFR. In addition, treatment with either the Tx synthase inhibitor or the Tx receptor antagonist significantly reduced systemic blood pressure. Thus, in this 2K, 1C model of hypertension, increased renal Tx production prevents functional hypertrophy of the contralateral kidney. As a result, CLK pressure-volume regulation is impaired and systemic hypertension is maintained. Furthermore, Tx antagonists restore CLK function and acutely lower systemic blood pressure. Therefore, increased renal Tx production by the CLK appears to be an important mediator of hypertension in the 2K, 1C model.

6-Ketoprostaglandin F1 alpha↗

Role of tissue renin angiotensin system in two-kidney, one-clip hypertensive rats.

To investigate the molecular pathology of two-kidney, one-clip (2K-1C) rats, we examined the gene expressions of the renin-angiotensin system (RAS) and angiotensin II (ANG II) concentration in various tissues in the early (4 wk) and chronic (16 wk) phases of hypertension. Four weeks after clipping, the brain renin mRNA level was lower in 2K-1C rats than in control rats (P < 0.05). On the other hand, the levels of brain and renal angiotensinogen mRNA were not significantly different in the two groups. The brain and adrenal ANG II concentrations were significantly higher in 2K-1C rats than in control rats. Sixteen weeks after clipping, there was no significant difference in the brain renin mRNA levels in the two groups, and renal and brain angiotensinogen mRNA levels were normal. Moreover, the ANG II concentrations in the adrenals and brain (except the cortex) of 2K-1C rats were not significantly higher than those in control rats. These results show a differential pattern of tissue RAS gene expression in rats during the development of 2K-1C hypertension, which is regulated in a tissue-specific manner. Furthermore, the data suggest that brain ANG II may be affected by circulating ANG II, but not by the brain renin angiotensin system, and may regulate brain renin, probably by negative feedback through its own receptor.

Actins↗

Renal tissue and urinary kallikrein activity in two-kidney, one-clip hypertensive rats.

Renal tissue and urinary kallikrein activity were studied to assess the role of the renal kallikrein-kinin system in two-kidney, one-clip hypertensive rats. Body weight, urine volume, systolic blood pressure and urinary kallikrein activity were measured in 11 hypertensive rats and 6 normotensive rats 1, 4, 8 and 12 weeks after clipping or sham operation. The hypertensive rats used in the present study had systolic blood pressures of over 180 mm Hg 12 weeks after the operation and presented polyuria with a reduction in weight gain, which placed them in the malignant hypertension category. Urinary kallikrein activity in hypertensive rats significantly decreased from 21.7 +/- 13.3 nkat/day at 1 week to 11.6 +/- 5.5 nkat/day at 12 weeks after clipping (p less than 0.05), while urinary kallikrein activity in normotensive rats significantly increased from 23.6 +/- 8.9 nkat/day at 1 week to 43.7 +/- 16.2 nkat/day at 4 weeks after the sham operation. Significant differences were observed in urinary kallikrein activity between hypertensive rats and normotensive rats 4 and 12 weeks after the operation (p less than 0.05). Renal tissue kallikrein activity from bilaterally nephrectomized kidneys was investigated 12 weeks after the operation. No significant difference in tissue kallikrein activity was found between the two kidneys of the hypertensive rats. However, tissue kallikrein activity was significantly lower in the contralateral kidney of hypertensive rats as compared to the same kidney of normotensive rats (2.13 +/- 0.73 nkat/g in hypertensive rats vs. 3.05 +/- 0.69 nkat/g in normotensive rats, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of nifedipine on renal cortical and medullary blood flow in two-kidney, one-clip renovascular hypertension in rabbits.

The effects of nifedipine, a calcium antagonist, on blood pressure and renal regional blood flow were investigated in two-kidney, one-clip renovascular hypertensive rabbits. At 1 week after left renal artery constriction, in the constricted group, systemic blood pressure (BP) significantly rose with the elevation of plasma renin activity (PRA). In both kidneys, renal vascular resistance (RVR on the constricted group was significantly increased as compared to that in the control group. In the clipped kidney, total renal blood flow (RBF) and renal cortical blood flow (RCBF) of the constricted group were significantly decreased, while renal medullary blood flow (RMBF) remained at the control value. In the nonclipped kidney, RBF and RCBF of the constricted group did not significantly change, and RMBF was significantly increased as compared to that of the control group. After administration of nifedipine for 1 week (1.0 mg/kg/day), BP in the constricted group was decreased to the control level and PRA in both groups was increased. The percent change of BP in the constricted group was significantly decreased and the percent change of PRA in the constricted group was significantly increased as compared to those in the control group. Nifedipine increased RBF, RCBF and RMBF and decreased RVR of both kidneys in each group. In the nonclipped kidney, the percent change of RBF, RCBF and RMBF of the constricted group was significantly increased and the percent change of RVR was significantly decreased as compared to those of the control group. In the clipped kidney, only the percent change of RBF of the constricted group was significantly lower than that in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Role of the kallikrein-kinin system in two-kidneyed and one-clipped hypertensive rats.

The influence of aprotinin as a kallidinogenase inactivator on the antihypertensive effect of angiotensin I converting enzyme inhibitor (CEI) was studied in two-kidneyed and one-clipped hypertensive rats. Sixteen two-kidneyed and one-clipped hypertensive rats and sham-operated normotensive rats were prepared for this experiment. They were divided into two groups: those with the aprotinin infusion and those without. The effects of the oral administration of CEI were compared as regards mean arterial pressure (MAP) and urinary kallikrein activity (UKA). In 8 hypertensive rats under glucose infusion, MAP fell from 184.4 +/- 4.5 to 106.3 +/- 5.2 mm Hg, and UKA changed from 1.37 +/- 0.18 nkat/12 h to 0.61 +/- 0.11 nkat/12 h after the administration of CEI. In the remaining hypertensive rats under aprotinin infusion, MAP decreased from 175.0 +/- 3.0 to 140.6 +/- 5.1 mm Hg, and UKA slightly changed from 0.72 +/- 0.25 nkat/12 h to 0.59 +/- 0.12 nkat/12 h. Thus, the decrease of MAP after the administration of CEI was suppressed by the aprotinin infusion, and this significant difference was supported by the decrease of UKA. As for 16 normotensive rats, CEI did not alter MAP, nor did aprotinin have any effect on it. However, UKA tended to decrease after the administration of CEI. These results suggest that both the kallikrein-kinin system and the renin-angiotensin system play an important role in the maintenance of high blood pressure in two-kidneyed and one-clipped chronically hypertensive rats.

Animals↗

Prevention of hypertension and organ damage in 2-kidney, 1-clip rats by tetradecylthioacetic acid.

Dietary lipids are reported to affect the blood pressure in both humans and experimental animal models with hypertension. In the present study, 2-kidney, 1-clip (2K1C) hypertensive rats were treated with the modified fatty acid tetradecylthioacetic acid (TTA) from the time of clipping or after hypertension was established. TTA treatment attenuated the development of hypertension and reduced established 2K1C hypertension. The mRNA level of renin in the clipped kidney and the plasma renin activity were markedly reduced, and the plasma angiotensin II level tended to decrease after TTA treatment. In addition, TTA reduced the mRNA level of angiotensinogen in white adipose tissue. Prevention of organ damage was demonstrated by normal urinary excretion of protein, maintained serum albumin, lower heart weight, and clearly reduced vascular, glomerular, and tubulointerstitial damage in the nonclipped kidney. Renal function was not affected as estimated by unchanged plasma creatinine. Furthermore, the serum levels of triacylglycerol and cholesterol were reduced by TTA. The serum fatty acid composition was changed, resulting in a favorable increase of oleic acid. However, the levels of all of the omega-3 fatty acids and of linoleic acid were reduced, and no change was seen in the level of arachidonic acid, but the urinary excretion of 8-iso-prostaglandin F2alpha was declined. In conclusion, TTA attenuated the development of hypertension, reduced established hypertension, and prevented the development of organ damage in 2K1C rats, possibly by reducing the amounts of the vasoconstrictors angiotensin II and 8-iso-prostaglandin F2alpha and by inducing a favorable increase of oleic acid in serum.

Albuminuria↗

Gene expression of brain nitric oxide synthase and soluble guanylyl cyclase in hypothalamus and medulla of two-kidney, one clip hypertensive rats.

Nitric oxide may act at autonomic sites in the brain to regulate arterial blood pressure. Our goal was to determine whether gene expressions of the brain isoform of nitric oxide synthase and of the beta subunit of soluble guanylyl cyclase, the target of nitric oxide, were altered in discrete autonomic brain regions after induction of hypertension in rats. The two-kidney, one clip model was used to induce hypertension, and measurements were made 3 and 6 weeks after the left renal artery was clipped. Only experimental rats with blood pressures elevated by at least 25 mm Hg were used. Total RNA was purified from microdissected tissue blocks containing hypothalamus, dorsal medulla, rostral ventrolateral medulla, and caudal ventrolateral medulla. Changes in nitric oxide synthase and guanylyl cyclase mRNA were semiquantified in each region by use of reverse transcription-polymerase chain reactions in which known concentrations of deletion mutants of the two genes were coamplified as internal standards. Compared with controls, significant decreases and increases in nitric oxide synthase mRNA were found in the hypothalamus (x 2.2) and caudal ventrolateral medulla (x 6.4), respectively, of hypertensive rats 3 weeks after clipping. These alterations were reversed in hypertensive rats at 6 weeks; levels increased (x 4.6) in the hypothalamus and decreased (x 5.5) in the caudal ventrolateral medulla. Changes in guanylyl cyclase expression paralleled those for nitric oxide synthase in some but not all areas at both time points.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗

Change in pressor responsiveness to angiotensin II as a determinant of blood pressure after unclipping in two-kidney, one clip hypertensive rats.

The hypotensive effect of correction of renal artery stenosis in humans or experimental animals with renovascular hypertension is commonly attributed to decreasing renin secretion from the formerly stenotic kidney. However, plasma renin activity is normal in 50% of individuals with renovascular hypertension. We studied conscious, chronically instrumented two-kidney, one clip (2K1C) rats. The renal artery clip was removed and mean arterial pressure measured for 3 days. The majority of the fall in blood pressure occurred between 2 and 48 hours after unclipping. Measurement of water balance and urinary sodium excretion revealed no effect of unclipping. In another experiment, 2K1C hypertensive rats were chronically treated with enalapril and concomitant infusion of angiotensin II (3.8 pmol/min [4 ng/min] IV) to maintain blood pressure at hypertensive levels and prevent a fall in angiotensin II levels on unclipping. After 5 days, the clip was removed or sham removed, and treatment was continued. Blood pressure was recorded for 7 days. Blood pressure remained elevated in the sham unclipped rats. Unclipped rats exhibited a dichotomous response; blood pressure fell significantly within 48 hours in the majority of rats (responders) but remained elevated in a minority (nonresponders). All treatment was then withdrawn for 2 days. Sham unclipped rats remained hypertensive, and responders exhibited a further small decline in blood pressure. Blood pressure fell to normal in the nonresponders. Blood pressure falls after correction of renal artery stenosis in renovascular hypertension in part because of a decrease in pressor responsiveness to angiotensin II.

Angiotensin II↗

Effect of potassium chloride on the blood pressure in two-kidney, one clip Goldblatt hypertensive rats.

The effects of potassium loading on blood pressure (BP) and the renin-angiotensin-aldosterone system were investigated in two-kidney, one clip Goldblatt hypertensive rats. Two series of experiments were performed: one was begun just after renal artery constriction, and the other, after hypertension had developed. Potassium loading significantly attenuated the development of hypertension, and was also able to abate existing renovascular hypertension. In both studies, potassium loading increased fluid intake and urine volume, which were accompanied by increased excretion of sodium and potassium. In spite of the massive diuretic effect, potassium loading significantly attenuated the increased plasma renin activity (PRA) induced by renal artery constriction, while it further enhanced the increased plasma aldosterone concentration (PAC) in two-kidney, one clip Goldblatt hypertensive rats. There was no significant difference in the values of serum sodium and potassium between the two groups with or without potassium loading. These results suggest that potassium may attenuate the development of hypertension and reduce the elevated BP by diuresis and natriuresis and by suppression of the PRA in two-kidney, one clip Goldblatt rats.

Animals↗

Increased availability of nitric oxide leads to enhanced nitric oxide dependency of tubuloglomerular feedback in the contralateral kidney of rats with 2-kidney, 1-clip Goldblatt hypertension.

The contralateral kidney of 2-kidney, 1-clip hypertensive (2K1C) rats is unable to escape the renal vasoconstrictive and sodium-retaining effects of increased circulating angiotensin II levels. Evidence is accumulating that renal function is relatively preserved by enhanced influence of NO in the contralateral kidney. In this study, we investigated (1) whether the high NO dependency of renal hemodynamics in the contralateral kidney is due to increased availability of NO or increased sensitivity to NO and (2) whether elevated NO activity dampens the actions of angiotensin II to enhance tubuloglomerular feedback (TGF) responses in the nonclipped kidney of 2K1C rats. To estimate whether the available NO is increased, the NO clamp technique was applied in rats that underwent sham operation (n=6) and in the contralateral kidney of 2K1C Sprague-Dawley rats (3 weeks old; 0.25-mm silver clip; n=6). During systemic infusion of nitro-L-arginine (L-NNA; 50 microg/kg. min(-1)), sodium nitroprusside (SNP) was infused in the renal artery and the rate was adjusted so that renal vascular resistance (RVR) was restored to baseline levels. In sham rats, RVR increased during L-NNA treatment from 17.2+/-2.0 to 33.0+/-3.6 U (P<0.01) and was restored to baseline values during SNP infusion (17.1+/-2.3 U); 9. 2+/-1.8 nmol/min of SNP was needed to restore RVR to baseline values. In 2K1C rats, RVR increased during L-NNA treatment from 16.7+/-1.1 to 53.4+/-3.5 U (P<0.01). This increase of RVR was significantly larger than in sham rats. RVR was restored to baseline values during SNP infusion (17.4+/-0.9 U); 26.0+/-4.3 nmol/min of SNP was needed to restore RVR to baseline values (P<0.05 versus sham). Furthermore, maximum TGF responses were assessed before and during late proximal tubular infusion of L-NNA in the kidneys of sham rats and the nonclipped kidneys of 2K1C rats. Control maximum TGF responses were 4.7+/-0.7 and 5.1+/-0.4 mm Hg in sham and 2K1C rats, respectively. During intraluminal L-NNA infusion, maximum TGF responses were 15. 4+/-0.9 mm Hg in sham rats and 22.2+/-2.5 mm Hg in 2K1C rats (P<0.05 versus sham). Finally, urinary NO(2)+NO(3) excretion in the nonclipped kidney was significantly higher than in the clipped kidney (P<0.05). In conclusion, (1) as assessed using the NO clamp, ambient intrarenal NO levels are increased in the contralateral kidney of 2K1C rats and (2) the NO dependency of the TGF system is enhanced. These experiments indicate that adaptations in NO activity lead to relatively low TGF responsiveness, which will offset the simultaneous sodium-retaining actions of angiotensin II on proximal tubular reabsorption and TGF responsiveness.

Analysis of Variance↗

Antisense inhibition of brain renin-angiotensin system decreased blood pressure in chronic 2-kidney, 1 clip hypertensive rats.

The systemic renin-angiotensin system (RAS) plays an important role in blood pressure (BP) regulation during the development of 2-kidney, 1 clip (2K1C) hypertension. Its contributions decrease with time after constriction of the renal artery. During the chronic phase, the peripheral RAS returns to normal, but the hypertension is sustained for months. We hypothesized that in this phase the brain RAS contributes to the maintenance of high BP. To test the hypothesis, we studied the role of brain RAS by decreasing the synthesis of angiotensinogen (AGT) and the angiotensin II (Ang II) type 1a receptor (AT(1)R) with intracerebroventricular injections of antisense oligonucleotides (AS-ODNs). The response of systolic BP (SBP) to AS-ODNs to AGT mRNA was studied in 2K1C rats at 6 months after clipping, and the response to AS-ODNs to AT(1)R mRNA was studied at 10 months after clipping. Intracerebroventricular injection of AS-ODN-AGT (200 microgram/kg, n=5) significantly decreased SBP (-22+/-6 mm Hg, P<0.05) compared with the sense ODN (n=5) and saline (n=3) groups. Intracerebroventricular injection of AS-ODN-AGT reduced the elevated hypothalamic Ang II level. The hypothalamic Ang II content in sense ODN and saline groups was significantly (P<0.05) higher than in the nonclipped group. Compared with inverted ODN, intracerebroventricular injection of AS-ODN-AT(1)R (250 microgram/kg, n=6) significantly decreased SBP (-26+/-8 mm Hg, P<0.05) for 3 days after injection. This was a brain effect because intravenous AS-ODN-AT(1)R at a dose of 250 to 500 microgram/kg did not affect SBP. These results suggest that the brain RAS plays an important role in maintaining the elevated SBP in chronic 2K1C hypertension.

Angiotensin II↗