Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 6231010

[Immune complex diseases].

P S Gurevich
View original source ↗Export metadata ↓

Abstract

Immune complex diseases (ICD) include different diseases of infectious and noninfectious origin in the pathogenesis of which the leading role belongs to immune complexes circulating in the blood stream. Three variants of the ICD course are distinguished: fulminant, acute, and chronic. The main morphological manifestation of ICD is vasculitis (in the fulminant course--microangiothrombopathy) and its consequences in the form of various circulation disorders. Renal glomeruli are frequently involved (glomerulonephritis). Immunopathologic reactions in the form of hypersensitivity reaction or inhibition of immune response are important in ICD.

Explore related subjects

ArteriolesBlood CoagulationCapillariesGlomerulonephritisHumansImmune Complex DiseasesThrombosisWaterhouse-Friderichsen SyndromeEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P S Gurevich. 1983. [Immune complex diseases].. https://pubmed.ncbi.nlm.nih.gov/6231010/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Effect of familial hypertension on glomerular hemodynamics and tubulo-glomerular feedback after uninephrectomy.

Familial hypertension, glomerular hemodynamic alterations, and dysregulation of tubulo-glomerular feedback (TGFB) have all been associated with the development of chronic renal failure. In the present study we evaluated renal and glomerular hemodynamics and TGFB responses in healthy kidney donors either with or without familial hypertension, before and after nephrectomy. Para-amino-hippurate plasma clearance (CPAH) and inulin plasma clearance (CInu) were measured in 15 kidney donors before and 1 year after nephrectomy. All subjects were normotensive and were kept in a sodium-replete state. Both clearances were measured after 40 min of constant infusion of PAH and Inu, as well as 20, 30, 50, and 60 min after the intravenous administration of acetazolamide (5 mg/kg). Glomerular hemodynamics were calculated by means of the Gomez formulae. Nephrectomy caused the expected decreases in CPAH and CInu and increase in the filtration fraction (all P < .0001). The decrease in renal resistances of the remaining kidney was greater at the afferent (-24%, P = .0075) than at the efferent arteriolar level (-17%, P < .0001). The TGFB activation was not altered by nephrectomy or by familial hypertension. Effective renal plasma flow (ERPF) decrease after TGFB activation appeared earlier than glomerular filtration rate (GFR) decrease before (P = .01), but not after, nephrectomy (P = .48). The presence of familial hypertension was associated with increased glomerular pressure (P = .0004). This study suggests that uninephrectomy in healthy human subjects causes a greater decrease in afferent arteriolar resistances, but that TGFB responses are not quantitatively altered. Familial hypertension is associated with a tendency toward higher glomerular pressures.

Arterioles↗
PubMed2000

Regulation of coronary vasomotor tone under normal conditions and during acute myocardial hypoperfusion.

Ischemia generally has been assumed to cause maximal vasodilation of the coronary resistance vessels. However, recent observations have demonstrated that during ischemia, the coronary microvessels can retain some degree of vasodilator reserve and remain responsive to vasoconstrictor stimuli. Traditional understanding of coronary blood flow regulation envisioned an array of resistance vessels that respond homogeneously to local myocardial metabolic needs. Although coronary arterioles (<100 microm) do respond to myocardial metabolic activity, recent studies have demonstrated that up to 40% of total coronary resistance resides in small arteries 100-400 microm in diameter. Vasoconstriction of these small arteries is capable of decreasing blood flow, but they are minimally responsive to the metabolic effects of the resultant flow reduction. The lack of metabolic vasoregulation of the resistance arteries explains, at least in part, the observation that myocardial ischemia does not predictably cause maximal resistance vessel dilation. In addition, vasoconstrictor influences can compete with metabolic vasodilator activity in coronary arterioles. These findings suggest that pharmacologic vasodilators acting at the microvascular level might be therapeutically useful in patients with ischemic heart disease. Unfortunately, when myocardial ischemia results from a flow-limiting coronary stenosis, nonselective pharmacologic vasodilation of the resistance vessels can worsen subendocardial ischemia by decreasing intravascular pressure to produce coronary steal and by worsening of stenosis severity. Selective dilation of small arteries in ischemic regions might have potential for enhancing blood flow. A critical property of an effective agent is that it not interfere with metabolic vasoregulation at the arteriole level, so that dilation of small arteries in adequately perfused regions would be countered by compensatory vasoconstriction of the arterioles to prevent coronary steal.

Arterioles↗