Skin microvascular alterations in patients with chronic congestive heart failure.
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Biomedical subjects
J L le Noble
Publications and source records attributed to J L le Noble.
The microcirculation and hypertension.
AIM: To review published evidence on the effects of arteriolar changes in primary and secondary hypertension. BACKGROUND: Pressure profile analyses have shown that the microcirculation is a major site of vascular resistance. With the recent refinement of intravital microscopy techniques detailed information has become available on mechanisms of the microvascular resistance increase in hypertension. Three mechanisms play an important role: (1) a decrease in arteriolar diameter; (2) arteriolar vessel wall hypertrophy; and (3) small arteriolar and capillary rarefaction. METHOD: The evidence was synthesized into a hypothesis on the role of the microcirculation in primary forms of hypertension. HYPOTHESIS: The hypothesis formulated contains two important elements in that (1) diminished outgrowth of the microvascular bed in different tissues is seen as an important early pathogenic mechanism; and (2) the decreases in arteriolar diameter and vessel wall hypertrophy are seen as adaptive mechanisms that maintain a constant wall stress. The three factors together maintain the increase in vascular resistance that is common to all established forms of primary hypertension.
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A functional morphometric study of the cremaster muscle microcirculation in young spontaneously hypertensive rats.
Increased vascular resistance in spontaneous hypertension has been attributed to a reduced arteriolar lumen and a decrease in the number of arterioles and capillaries. In the present study, microvascular mechanisms for increased resistance were investigated in the cremaster muscle of 5-6-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY) using intravital microscopy. Vessels were classified on the basis of their location in the network relative to their branching order and function (A1-A4). In each preparation, one vessel of each category was observed for its side-branches, using bright-field microscopy. By comparing the number of side-branches seen under control conditions and after maximal vasodilatation (10(-3) mol/l adenosine, topically) we assessed their functional reserve. Capillary density was investigated using incident fluorescence microscopy. Both under control conditions and after vasodilatation, mean arterial pressure and heart rate were increased in SHR (mean arterial pressure: SHR 103 +/- 4 mmHg, WKY 89 +/- 3 mmHg, P less than 0.05; heart rate: SHR 380 +/- 16 beats/min, WKY 343 +/- 12 beats/min, P less than 0.05). Arterioles (A1-A4) of SHR and WKY were equal in diameter (SHR: 75.8 +/- 3.2, 48.7 +/- 1.1, 21.4 +/- 0.9, 10.0 +/- 0.04 microns; WKY: 71.6 +/- 2.4, 48.9 +/- 1.1, 18.5 +/- 0.9, 9.8 +/- 0.3 microns; A1-A4, respectively). After adenosine, the relative increase in diameter was similar in both groups. The number of side-branches under control conditions was similar in A1 and A2 vessels. SHR had fewer A3 vessels per A2 and fewer A4 vessels per A3 (per unit length), indicating a diminished arteriolar reserve.(ABSTRACT TRUNCATED AT 250 WORDS)
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Microvascular alterations in adult conscious spontaneously hypertensive rats.
The dorsal skin flap technique was used to study skeletal muscle microcirculation in conscious 10-12-week-old spontaneously hypertensive rats and normotensive Wistar-Kyoto control rats. Videorecordings were made for off-line analysis of consecutive segments of the vascular bed. Resting diameters were significantly smaller in spontaneously hypertensive rats than in Wistar-Kyoto rats at the first-order (-28%) and second-order arteriolar (-21%) levels. Precapillary third-order and fourth-order arterioles of spontaneously hypertensive rats had normal diameters, whereas postcapillary small venule diameters were slightly larger in spontaneously hypertensive rats. Thirty percent and 41% of the spontaneously hypertensive rat and Wistar-Kyoto rat third-order arteriolar vessels and 63 and 45% of the fourth-order arteriolar vessels exhibited vasomotion. Vasomotion amplitude, but not frequency, was significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto rats. It is concluded that, in the established phase of spontaneous hypertension in the rat, a decreased diameter of large arterioles is the major mechanism underlying the increased vascular resistance in cutaneous skeletal muscle.
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Hypertension, the microcirculation and serotonin.
Essential hypertension in humans and most experimental animal models of hypertension is hemodynamically characterized by an increased vascular resistance. The site of resistance increase has been localized by recent intravital microscopic studies in most vascular beds primarily in the microcirculation, i.e. in arterioles smaller than 150 microns. Three mechanisms are held responsible for the resistance increase: (1) a rarefaction of the smallest arterioles and capillaries, (2) an increased wall to lumen ratio and (3) a decreased internal diameter. The latter two effects have been localized primarily in the larger arterioles and arteries. The contribution of each of the three factors to the rise in total peripheral resistance depends on the vascular bed, the model of hypertension and its stage of development. Serotonin is one of the endogenous mediators of vascular tone. Its effects have thus far been mostly studied in relation to alterations of internal vascular diameter. Larger arterioles and arteries constrict, but resistance-sized smaller arterioles dilate in response to the exogenous application of serotonin.
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Microcirculatory changes in cremaster muscle during early spontaneous hypertension in the rat.
The microcirculatory control of flow was studied in the cremaster muscle of 5- to 6-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) using intravital microscopic techniques. Arterioles were classified according to a functional branching order from A1-A4 vessels. Capillary architecture was measured in a separate series of experiments. No significant differences were found in the WKY or SHR vessel diameters, with the exception of third-order arterioles, which were slightly, but significantly, larger in SHR. However, the number of A3 and A4 vessels as well as the capillary density was significantly lower in SHR than in WKY. The differences were even more pronounced during maximal vasodilation induced by local application of 10(-3) mol/l adenosine. The data show that rarefaction of small blood vessels rather than decreased arteriolar diameter is an early characteristic of spontaneous hypertension in the rat.
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Pharmacological evidence for rapid destruction of efferent renal nerves in rats by intrarenal infusion of 6-hydroxydopamine.
In a previous study we reported that intrarenal (i.r.) infusion of 1 mg 6-hydroxydopamine (6-OHDA) in rats resulted in selective efferent denervation of the infused kidney. Although the vasoconstrictor response to electrical stimulation of the posterior hypothalamus (PH) was already abolished 24 h after infusion, norepinephrine (NE) content of the kidney was reduced by only approximately 50% at that time. In the present study, the status of renal nerves 45 min after infusion of 6-OHDA by i.r. application of scorpion venom (SV), a NE releasing agent, was investigated. In saline pretreated rats, 10 micrograms SV i.r. caused a rapid increase (+355 +/- 80%) in vascular resistance in the injected kidney, whereas only minor changes were observed in resistances of the non-injected kidney, mesentery and hindquarters. Pretreatment of animals with phentolamine (1 mg/kg i.v.) largely abolished the vasoconstrictor response (+57 +/- 20%), confirming dependence of the effect of SV on release of NE from nerve terminals. Finally, pretreatment with 1 mg 6-OHDA i.r. also resulted in abolition of renal vasoconstriction following SV (+7 +/- 6%). The results indicate that as early as 45 min after i.r. infusion of 1 mg 6-OHDA in rats, efferent renal nerve endings are no longer functional.
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Candidemia in intensive care unit patients: risk factors for mortality.
Aim of this study was to evaluate whether risk factors which predict the development of candidemia may also predict death in ICU patients with candidemia. During an 8-year-period all ICU patients whose blood cultures yielded Candida species (n = 40) were retrospectively evaluated in a case-control fashion. The average incidence of Candida bloodstream infections was 5.5 per 10,000 patient days, ranging from 2.4 in 1990 to 7.4 in 1994. C. albicans was the most common pathogen in candidemic patients, but the proportion of non-C. albicans strains showed an increasing trend during 1989-1993, with a major shift towards non-C. albicans species in 1994. The overall mortality of patients with candidemia was 58%. Mortality was highest in the group of patients with multi-organ dysfunction syndrome, especially among those in need of hemodialysis. Risk factors for the development of candidemia, such as age, malignancy, steroid use, i.v. catheterization, and the use of broad-spectrum antibiotics were not correlated with mortality in the ICU patients studied.
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