Microvascular pressure, surface area, and permeability in isolated hindquarters of SHR

1985 ◽  
Vol 249 (3) ◽  
pp. H498-H504
Author(s):  
R. J. Korthuis ◽  
C. R. Kerr ◽  
M. I. Townsley ◽  
A. E. Taylor
Keyword(s):  
Skeletal Muscle ◽  
Capillary Pressure ◽  
Surface Area ◽  
Convective Transport ◽  
Microvascular Permeability ◽  
Spontaneously Hypertensive ◽  
Pressure Surface ◽  
Total Plasma Protein ◽  
Wistar Kyoto ◽  
Osmotic Reflection Coefficient

The transvascular escape rate (TER) of labeled albumin is reported to increase in essential hypertension. However, the mechanism for this augmented rate of protein efflux is uncertain and may be related to increased microvascular permeability, surface area, and/or pressure. To determine the possible contributions of these mechanisms to increased TER of protein, the osmotic reflection coefficient for total plasma protein, capillary filtration coefficient, and effective capillary pressure were estimated in isolated hindquarters of age-matched (12-13 wk) spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), and Wistar (WR) rats. Estimates of the reflection and filtration coefficients were not significantly different in SHR, WKY, and WR. However, capillary pressure was significantly greater in SHR than in normotensive controls. These results indicate that 1) skeletal muscle microvascular permeability and surface area are similar in SHR, WKY, and WR; 2) effective capillary pressure is greater in SHR than WKY or WR; and 3) if TER for protein is elevated in hypertensive skeletal muscle, the primary mechanism for this process may be increased convective transport of protein secondary to elevated microvascular hydrostatic pressure.

Microvascular rarefaction in spontaneously hypertensive rat cremaster muscle

1981 ◽  
Vol 241 (3) ◽  
pp. H306-H310 ◽  
Author(s):  
I. I. Chen ◽  
R. L. Prewitt ◽  
R. F. Dowell
Keyword(s):  
Surface Area ◽  
Fourth Order ◽  
Unit Volume ◽  
Spontaneously Hypertensive Rat ◽  
Absolute Number ◽  
Cremaster Muscle ◽  
Vascular Effects ◽  
Spontaneously Hypertensive ◽  
Vessel Length ◽  
Wistar Kyoto

We have investigated the neural and local vascular effects on vessel length and surface area per unit volume in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) by quantitative stereology. Fourteen SHR and 14 KWY (70-130 g) were anesthetized with chloralose-urethan, and the cremaster muscle was exposed for microscopic observation. The large arterioles entering the muscle were termed the first order, and consecutive branches were termed second-, third-, and fourth-order arterioles. The data were collected in three consecutive states: innervated, denervated, and vasodilated with nitroprusside. The third- and fourth-order arteriole and capillary lengths per unit volume in the SHR were less than those of the WKY in all three states. The vessel surface area per unit volume was also reduced in the SHR. Denervation and sodium nitroprusside (Nipride) resulted in larger percent increases in vessel length and surface area in the SHR than in the WKY. We conclude that in the SHR cremaster muscle there are fewer terminal arterioles and capillaries anatomically present, and, under resting conditions, a greater percentage but similar absolute number of them are closed to flow.

Regional transcapillary albumin exchange in rodent endotoxaemia: effects of fluid resuscitation and inhibition of nitric oxide synthase

2000 ◽  
Vol 100 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Suveer SINGH ◽  
Peter B. ANNING ◽  
C. Peter WINLOVE ◽  
Timothy W. EVANS
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Surface Area ◽  
Blood Volume ◽  
Fluid Resuscitation ◽  
Volume Ratio ◽  
Capillary Density ◽  
Microvascular Permeability ◽  
Capillary Perfusion ◽  
Dual Isotope

Sepsis is characterized by increased microvascular permeability and regional variations in capillary perfusion, which may be modulated by nitric oxide (NO) and reversed by fluid resuscitation (FR). The effects of saline FR and NO synthase blockade [by NG-nitro-L-arginine methyl ester (L-NAME)] on microvascular albumin transport and perfused capillary density were assessed in anaesthetized Wistar rats with acute normodynamic endotoxaemia. Separate dual-isotope techniques were employed to measure the permeability index (PIA) and the permeability×surface area product index (PIB), which provide different and complementary information regarding blood–tissue albumin exchange. PIA represents the tissue/blood distribution volume ratio of albumin. PIB is a composite measure of endothelial permeability and the vascular surface area available for albumin exchange, and therefore takes into account the effect of altered blood volume. Capillary density was quantified by fluorescence microscopy following circulation of Evans Blue-labelled albumin. Compared with controls, PIA was reduced significantly in lipopolysaccharide (LPS)-treated animals in skeletal muscle and skin, probably due to blood volume redistribution rather than to changes in permeability. PIB was increased significantly in LPS-treated animals in the kidney, mesentery, skeletal muscle, skin and lung, and in the small bowel following FR. FR also improved the LPS-induced metabolic base deficit, but did not alter capillary density. L-NAME significantly attenuated the LPS-induced rise in PIB in the lung. In conclusion, acute endotoxaemia induces tissue-dependent variations in microvascular albumin exchange. FR improves acid–base disturbance in endotoxaemia, through mechanisms other than microvascular recruitment. NO appears to increase microvascular permeability in endotoxaemia, an effect that may be attenuated by L-NAME, particularly in the lung.

scholarly journals Tyrosine hydroxylase immunoreactivity as indicator of sympathetic activity: simultaneous evaluation in different tissues of hypertensive rats

2011 ◽  
Vol 300 (2) ◽  
pp. R264-R271 ◽  
Author(s):  
Katia Burgi ◽  
Marina T. Cavalleri ◽  
Adilson S. Alves ◽  
Luiz R. G. Britto ◽  
Vagner R. Antunes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Tyrosine Hydroxylase ◽  
Sympathetic Activity ◽  
High Performance ◽  
Hypertensive Rats ◽  
Regional Patterns ◽  
Spontaneously Hypertensive ◽  
Direct Recording ◽  
Wistar Kyoto ◽  
Different Tissues

Vasomotor control by the sympathetic nervous system presents substantial heterogeneity within different tissues, providing appropriate homeostatic responses to maintain basal/stimulated cardiovascular function both at normal and pathological conditions. The availability of a reproducible technique for simultaneous measurement of sympathetic drive to different tissues is of great interest to uncover regional patterns of sympathetic nerve activity (SNA). We propose the association of tyrosine hydroxylase immunoreactivity (THir) with image analysis to quantify norepinephrine (NE) content within nerve terminals in arteries/arterioles as a good index for regional sympathetic outflow. THir was measured in fixed arterioles of kidney, heart, and skeletal muscle of Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (123 ± 2 and 181 ± 4 mmHg, 300 ± 8 and 352 ± 8 beats/min, respectively). There was a differential THir distribution in both groups: higher THir was observed in the kidney and skeletal muscle (∼3–4-fold vs. heart arterioles) of WKY; in SHR, THir was increased in the kidney and heart (2.4- and 5.3-fold vs. WKY, respectively) with no change in the skeletal muscle arterioles. Observed THir changes were confirmed by either: 1) determination of NE content (high-performance liquid chromatography) in fresh tissues (SHR vs. WKY): +34% and +17% in kidney and heart, respectively, with no change in the skeletal muscle; 2) direct recording of renal (RSNA) and lumbar SNA (LSNA) in anesthetized rats, showing increased RSNA but unchanged LSNA in SHR vs. WKY. THir in skeletal muscle arterioles, NE content in femoral artery, and LSNA were simultaneously reduced by exercise training in the WKY group. Results indicate that THir is a valuable technique to simultaneously evaluate regional patterns of sympathetic activity.

scholarly journals Evidence for functional alterations in the skeletal muscle mechanoreflex and metaboreflex in hypertensive rats

2008 ◽  
Vol 295 (4) ◽  
pp. H1429-H1438 ◽  
Author(s):  
Anna K. Leal ◽  
Maurice A. Williams ◽  
Mary G. Garry ◽  
Jere H. Mitchell ◽  
Scott A. Smith
Keyword(s):  
Skeletal Muscle ◽  
Cardiovascular Response ◽  
Cardiac Events ◽  
Spontaneously Hypertensive ◽  
Afferent Fibers ◽  
Hindlimb Muscle ◽  
Wide Range ◽  
Muscle Mechanoreflex ◽  
Wistar Kyoto ◽  
Stimulation Of

Exercise in hypertensive individuals elicits exaggerated increases in mean arterial pressure (MAP) and heart rate (HR) that potentially enhance the risk for adverse cardiac events or stroke. Evidence suggests that exercise pressor reflex function (EPR; a reflex originating in skeletal muscle) is exaggerated in this disease and contributes significantly to the potentiated cardiovascular responsiveness. However, the mechanism of EPR overactivity in hypertension remains unclear. EPR function is mediated by the muscle mechanoreflex (activated by stimulation of mechanically sensitive afferent fibers) and metaboreflex (activated by stimulation of chemically sensitive afferent fibers). Therefore, we hypothesized the enhanced cardiovascular response mediated by the EPR in hypertension is due to functional alterations in the muscle mechanoreflex and metaboreflex. To test this hypothesis, mechanically and chemically sensitive afferent fibers were selectively activated in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) decerebrate rats. Activation of mechanically sensitive fibers by passively stretching hindlimb muscle induced significantly greater increases in MAP and HR in SHR than WKY over a wide range of stimulus intensities. Activation of chemically sensitive fibers by administering capsaicin (0.01–1.00 μg/100 μl) into the hindlimb arterial supply induced increases in MAP that were significantly greater in SHR compared with WKY. However, HR responses to capsaicin were not different between the two groups at any dose. This data is consistent with the concept that the abnormal EPR control of MAP described previously in hypertension is mediated by both mechanoreflex and metaboreflex overactivity. In contrast, the previously reported alterations in the EPR control of HR in hypertension may be principally due to overactivity of the mechanically sensitive component of the reflex.

Leukocyte depletion attenuates vascular injury in postischemic skeletal muscle

1988 ◽  
Vol 254 (5) ◽  
pp. H823-H827 ◽  
Author(s):  
R. J. Korthuis ◽  
M. B. Grisham ◽  
D. N. Granger
Keyword(s):  
Skeletal Muscle ◽  
Reflection Coefficient ◽  
Capillary Pressure ◽  
Vascular Permeability ◽  
Vascular Resistance ◽  
Vascular Injury ◽  
Whole Blood ◽  
Ischemia Reperfusion ◽  
Autologous Whole Blood ◽  
Osmotic Reflection Coefficient

To determine whether leukocytes play an important role in the pathogenesis of the vascular injury (increased vascular permeability and resistance) associated with ischemia-reperfusion, isolated canine gracilis muscles were perfused with autologous whole blood or with whole blood that had been depleted of leukocytes (primarily granulocytes) using Leukopak filters. The osmotic reflection coefficient for total plasma proteins, isogravimetric capillary pressure, and total vascular resistance was determined for the following conditions: control, ischemia (4 h inflow occlusion) plus reperfusion with whole blood, and ischemia plus reperfusion with granulocyte-depleted whole blood. Reperfusion with whole blood was associated with a reduction in the osmotic reflection coefficient from 0.96 to 0.61, whereas isogravimetric capillary pressure was reduced by 40%, indicating a dramatic increase in vascular permeability. Total vascular resistance was increased approximately twofold. Reperfusion with leukocyte-depleted blood largely prevented the increases in vascular permeability and resistance. These data suggest that leukocytes play a major role in the pathogenesis of ischemia-reperfusion injury in skeletal muscle.

Enhanced response of arterioles to oxygen during development of hypertension in SHR

1986 ◽  
Vol 250 (5) ◽  
pp. H761-H764 ◽  
Author(s):  
J. H. Lombard ◽  
M. E. Hess ◽  
W. J. Stekiel
Keyword(s):  
Skeletal Muscle ◽  
Vascular Resistance ◽  
Local Control ◽  
Fourth Order ◽  
Spontaneously Hypertensive Rat ◽  
Control Mechanisms ◽  
Cremaster Muscle ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

The goal of this study was to assess the possible role of O2-related local control mechanisms in contributing to an elevated skeletal muscle resistance during the development of hypertension in the spontaneously hypertensive rat (SHR). Diameters of first- (1A), second- (2A), third- (3A), and fourth-order (4A) arterioles were measured by television microscopy in the cremaster muscle of SHR in the early (4- to 6-wk-old) and rapidly developing (8- to 9-wk-old) stages of hypertension and in age-matched normotensive Wistar-Kyoto (WKY) controls. Active neurogenic tone was blocked by superfusing the tissue with 0.1 microgram/ml tetrodotoxin. When superfusion solution PO2 was elevated by changing the gas equilibration mixture from 0 to 5% O2, neurally blocked 3A and 4A of SHR exhibited a significantly greater constriction and a higher incidence of complete closure than those of their age-matched WKY controls. However, there were no significant differences in the constriction of larger arterioles (1A and 2A) in response to elevated superfusion solution PO2. The results suggest that O2-related local control mechanisms could contribute to constriction and closure of small arterioles and to an elevated skeletal muscle vascular resistance early in the development of hypertension in SHR

Altered carnitine metabolism in spontaneously hypertensive rats

1985 ◽  
Vol 249 (2) ◽  
pp. E183-E186 ◽  
Author(s):  
K. A. Foster ◽  
B. O'Rourke ◽  
D. K. Reibel
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Spontaneously Hypertensive Rats ◽  
Elevated Serum ◽  
Total Serum ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Fatty Acid Utilization ◽  
Carnitine Metabolism ◽  
Wistar Kyoto

Carnitine metabolism was examined in spontaneously hypertensive rats (SHR). Carnitine levels were elevated by 25% in hypertrophied hearts of 10- and 15-wk-old SHR when compared with Wistar-Kyoto (WKy) controls. This elevation was associated with a greater than 25% increase in total serum carnitine. The elevated serum carnitine does not appear to be due to increased mobilization from skeletal muscle because carnitine levels were elevated by 25% in gastrocnemius and diaphragm of SHR. Elevated serum carnitine is also not a result of reduced urinary excretion because daily urinary carnitine output was increased by 150% in SHR. These findings suggest that the most likely mechanism for increased serum carnitine is increased carnitine synthesis by the liver. The changes in carnitine metabolism in SHR appear to occur between 5 and 10 wk of age, because the carnitine levels in serum and organs were comparable in 5-wk-old WKy and SHR. The observed alterations in tissue and serum carnitine levels may result in altered fatty acid utilization in SHR.

Abnormal insulin metabolism by specific organs from rats with spontaneous hypertension

1989 ◽  
Vol 257 (4) ◽  
pp. E491-E498 ◽  
Author(s):  
C. E. Mondon ◽  
G. M. Reaven ◽  
S. Azhar ◽  
C. M. Lee ◽  
R. Rabkin
Keyword(s):  
Skeletal Muscle ◽  
Oral Glucose ◽  
Metabolic Clearance ◽  
Insulin Metabolism ◽  
Spontaneously Hypertensive ◽  
Insulin Resistant ◽  
Wky Rats ◽  
Suppression Test ◽  
Wistar Kyoto ◽  
Shr And Wky Rats

Spontaneously hypertensive rats (SHR) have been shown to be both insulin resistant and hyperinsulinemic after oral glucose administration or infusion of exogenous insulin during an insulin suppression test. To determine if this hyperinsulinemia may be due to decreased removal of insulin, the metabolic clearance (k) of insulin was measured in isolated perfused liver, kidney, and hindlimb skeletal muscle from SHR and Wistar-Kyoto (WKY) control rats. The data indicate that the k for insulin removal by liver was similar in SHR and WKY rats, averaging 287 +/- 18 and 271 +/- 10 microliters.min-1.g-1 liver, respectively. In contrast, the k for insulin removal by hindlimbs from SHR was decreased 37% (P less than 0.001) compared with WKY rats (8.6 +/- 0.5 vs. 13.7 +/- 0.7 microliters.min-1.g-1 muscle), and this decrease was not accompanied by decreased binding of insulin to its receptor in plantaris muscle. Although the removal of insulin by glomerular filtration was similar in SHR and WKY rats (653 +/- 64 microliters/min vs. 665 +/- 90 microliters.min-1.kidney-1), total insulin removal by kidney was significantly lower (P less than 0.05) in SHR (710 +/- 78 microliters/min) compared with WKY rats (962 +/- 67 microliters/min), due to decreased peritubular clearance of insulin in SHR (56 +/- 73 vs. 297 +/- 59 microliters/min, P less than 0.05). These findings suggest that the decreased clearance of insulin in SHR rats was possibly not due to impaired hepatic removal of insulin but rather to decreased removal by skeletal muscle and kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

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