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Journal ArticleDOI

Characteristics of response of renal vascular bed to contrast media. Evidence for vasoconstriction induced by renin-angiotensin system.

01 Nov 1970-Investigative Radiology (Invest Radiol)-Vol. 5, Iss: 6, pp 539-547
TL;DR: The vasoconstrictor response to contrast media apparently is related to the hyper tonicity of these agents, activation of the renin-angiotensin system and the local conversion of angiotens in I to ang Elliotensin II within the kidney.
Abstract: Three contrast media (mcglumine diatrizoate, meglumine iothalamate and sodium diatrizoate) produced a characteristic biphasic renal hemodynamic response in dogs. An initial transient vasodilatation, which is the common response to contrast media of all vascular beds, was followed by a more prolonged period of vasoconstriction, which is unique to the kidney. Phenoxybenzamine blocked the renal vasoconstriction produced by norepinephrine and 5–hydroxytryptamine but did not influence the biphasic response to the contrast media. The vasoconstriction caused by a bolus of angiotensin or by the contrast media was completely abolished during angiotensin tachyphylaxis, however. Thus, neither norepinephrine nor 5–hydroxytryptamine was involved in mediating the vasoconstriction, whereas angiotensin was implicated. The vasoconstrictor response to contrast media apparently is related to the hyper tonicity of these agents, activation of the renin-angiotensin system and the local conversion of angiotensin I to angiotensin II within the kidney.
Citations
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Journal ArticleDOI
TL;DR: The current evidence on the causes, pathogenesis and clinical course of contrast-medium nephropathy as well as therapeutic approaches to its prevention evaluated in clinical trials are reviewed.
Abstract: WITH THE INCREASING USE OF CONTRAST MEDIA in diagnostic and interventional procedures, nephropathy induced by contrast media has become the third leading cause of hospital-acquired acute renal failure. It is also associated with a significant risk of morbidity and death. The current understanding of the pathogenesis indicates that contrast-medium nephropathy is caused by a combination of renal ischemia and direct toxic effects on renal tubular cells. Patients with pre-existing renal insufficiency, diabetes mellitus and congestive heart failure are at highest risk. Risk factors also include the type and amount of contrast medium administered. Therapeutic prevention strategies are being extensively investigated, but there is still no definitive answer. In this article, we review the current evidence on the causes, pathogenesis and clinical course of contrast-medium nephropathy as well as therapeutic approaches to its prevention evaluated in clinical trials.

356 citations

Journal ArticleDOI
TL;DR: A 64-year-old man was admitted to the hospital for evaluation of progressive dyspnea and increasing angina and showed normal sinus rhythm and evidence of an old, anteroseptal myocardial infarction.

292 citations

Journal ArticleDOI
TL;DR: The intravascular administration of the ionic radiocontrast agent sodium iothalamate and iohexol stimulated endothelin release from cultured bovine endothelial cells, suggesting a direct effect of ionic and nonionic agents on vascular endothelium.
Abstract: The intravascular administration of the ionic radiocontrast agent sodium iothalamate (2.9 g of iodine/kg body wt) to rats induced an increase in plasma concentration of immunoreactive endothelin from 21.3 +/- 1.2 to 36 +/- 3 fmol/mL, preceded by a transient rise in the plasma level of atrial natriuretic peptide and associated with a fall in RBF. Equi-iodine amounts of the nonionic agents ioxaglate and iohexol elicited similar or more marked changes in plasma endothelin, but hypertonic solutions of NaCl, mannitol, or glucose did not. Comparable levels of endothelin produced by infusions of endothelin-1 induced a reduction of up to 29% in RBF. Iothalamate and iohexol stimulated endothelin release from cultured bovine endothelial cells, suggesting a direct effect of ionic and nonionic agents on vascular endothelium. The data invite speculation that under some circumstances endothelin release might play a role in the circulatory changes caused by these compounds and in the pathogenesis of radiocontrast nephropathy.

204 citations

Journal ArticleDOI
TL;DR: The ratio of iodine atoms to dissolved particles is an important characteristic of contrast media and is a commonly used term in the literature and describes the important relationship between the imaging effect (attenuation of x rays) and the osmotoxic effect of the media.
Abstract: All currently used x-ray contrast media are based on the triiodinated benzene ring (Fig 1), acetrizoate being the parent triiodinated contrast medium first in clinical use (3-6). Contrast media are characterized as ionic or nonionic and as monomers or dimers (6-14). Ionic media dissociate in water; the iodinated benzene ring contains the ionizing carboxyl group (valence, -1) with a cation (valence, +1), usually sodium or meglumine. Nonionic contrast agents have the desirable property of being soluble in water (hydrophilic) and yet do not dissociate in solution. The ratio of iodine atoms to dissolved particles is an important characteristic of contrast media and is a commonly used term in the literature. This describes the important relationship between the imaging effect (attenuation of x rays) and the osmotoxic effect of the media. Since the ratio represents the number of iodine atoms divided by the numbers of particles of the contrast medium in solution, a higher ratio is more desirable, since more iodine means better opacification and fewer particles of contrast medium means a lower osmotoxic effect (6). Agents with a ratio of 1.5 (ratio 1.5 agents) have been termed high-osmolar contrast media (HOCM), agents with a ratio of 3 have been termed low-osmolar contrast media (LOCM), and agents with a ratio of 6 have been termed isotonic contrast media (10CM).

188 citations

Journal ArticleDOI
TL;DR: An immediate GFR decline proportional to the osmolarity of CM and secondary to the renal hypoperfusion that is neither caused by hypovolemia nor mediated by ET-1, an early tubular dysfunction at the level of the proximal nephron, and a protective effect of single-dose pretreatment with either captopril or nifedipine on D-induced acute and short-term GFR changes are found.
Abstract: The pathophysiology and prevention of contrast media (CM)-induced nephropathy in chronic renal failure (CRF) are still ill defined. GFR, RPF, endothelin-1 (ET-1) levels, urinary sodium concentration, and fractional excretion of sodium were measured in CRF patients undergoing water diuresis in basal conditions and 20 to 120 min after an iv bolus of either the high-osmolar CM diatrizoate (D) or the low-osmolar CM iopamidol (I). The two CM induced an immediate and progressive decline of both GFR and RPF in the absence of hypovolemia, more pronounced in D (-36% at 120 min) than after I (-19% at 120 min; P < 0.05 versus D). Both CM determined a marked and steady increase of the fractional excretion of sodium. The natriuresis could not be totally ascribed to a CM-induced osmotic diuresis as because the urinary sodium concentration markedly increased. In two further groups of patients receiving D, we studied the effects of pretreatment with a single dose of either captopril or nifedipine. Both drugs, although not preventing the increase of natriuresis, partially antagonized D-induced renal hypoperfusion: GFR and RPF were equally reduced by 20% in D/captopril and D/nifedipine (P < 0.05 versus D). In unpretreated patients receiving either D or I, plasma ET-1 did not change but urinary levels increased; these changes were, however, dissociated from those observed in renal hemodynamics. Both plasma and urinary levels of ET-1 did not vary in pretreated groups. The 72-h follow-up evidenced a significant reduction of renal function only in the unpretreated D group. Therefore, the main findings after CM administration in CRF patients are: (1) an immediate GFR decline proportional to the osmolarity of CM and secondary to the renal hypoperfusion that is neither caused by hypovolemia nor mediated by ET-1, (2) an early tubular dysfunction at the level of the proximal nephron, and (3) a protective effect of single-dose pretreatment with either captopril or nifedipine on D-induced acute and short-term GFR changes.

186 citations