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H G Bohlen

Publications and source records attributed to H G Bohlen.

At least 37 records · Page 2Linked to original sources
PubMed1993

Evaluation of carbocyanine-labeled erythrocytes for microvascular measurements.

Red blood cells labeled with the carbocyanine dyes, 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) and 3,3'-dioctadecyloxacarbocyanine perchlorate (DiO), were evaluated for use in making microvascular measurements in rat small intestine and spinotrapezius muscle. We determined the minimum concentration of each dye which produced near maximal fluorescent intensity and labeled cell fraction. These dyes, which have excitation and emission spectra similar to fluorescein and rhodamine derivatives, have a number of advantages over the isothiocyanates: (1) the labeling procedure is quicker, easier, and less expensive; (2) the labeled cell fraction and the fluorescent intensity of DiI and DiO cells are stable for long periods of time in the rat circulation; and (3) DiI-labeled cells are brighter and transmit light through overlying erythrocytes better than rhodamine X isothiocyanate. However, in vitro and in vivo evaluations illustrate the potential limiting effects of vessel diameter and cell velocity on the accuracy of microvascular measurements made using this technique. In the small intestine and spinotrapezius muscle preparations, measurements of labeled cell flux were readily reproducible and could be partly automated with image analysis only in capillaries and small venules. Counting labeled cells in larger vessels by human observation or with automation was not reproducible, presumably due to absorption and dispersion of the fluorescent signal by overlying erythrocytes and smearing of the cell image at high cell velocities.

Animals↗
PubMed1993

Topical hyperglycemia rapidly suppresses EDRF-mediated vasodilation of normal rat arterioles.

Arteriolar dilation to endothelium-derived relaxing factor (EDRF) is suppressed early in diabetes mellitus. The purpose of this study was to determine whether acute exposure to a hyperglycemic media can suppress EDRF function of normal arterioles. Dilation of intestinal arterioles to iontophoretically applied acetylcholine (ACh) and nitroprusside was measured in normoglycemic rats before and after 1 h of topical exposure to isotonic solutions containing D-glucose concentrations of 200, 300, and 500 mg/100 ml. Exposure to a D-glucose concentration of 200 mg/100 ml had no effect on vasodilation to ACh. D-Glucose concentrations of both 300 and 500 mg/100 ml caused significant suppression of the responses: for example, at the approximate 50% effective dosage (100 nA), the dilatory response was decreased by 60% at a D-glucose concentration of 300 mg/100 ml and 55% at a D-glucose concentration of 500 mg/100 ml. Responses to nitroprusside were not significantly (P < 0.05) impaired after exposure to D-glucose concentrations of 200, 300, or 500 mg/100 ml. Exposure to an isotonic L-glucose concentration of 500 mg/100 ml for 1 h had no significant (P > 0.05) effect on responses to ACh. Pretreatment with superoxide dismutase, catalase, indomethacin, or meclofenamic acid preserved EDRF-mediated vasodilation during exposure to a D-glucose concentration of 500 mg/100 ml at almost all the ACh dosages tested. These results indicate that oxygen radicals formed in part by increased eicosanoid synthesis during exposure to D-glucose hyperglycemia interfere with the EDRF mechanism before its action on the microvascular smooth muscle.

Acetylcholine↗
PubMed1993

Sodium hyperosmolarity of intestinal lymph causes arteriolar vasodilation in part mediated by EDRF.

This study evaluated 1) the effect of increased submucosal lymph osmolarity on the regulation of first-order (1A) and second-order (2A) intestinal arterioles and 2) the role of endothelium-derived relaxing factor (EDRF) in hypertonic-induced vasodilation. Increasing the submucosal lymph osmolarity from 280 to 400 mosM, in increments of 30 mosM, resulted in a dose-dependent dilation of 1A and 2A. A submucosal lymph tonicity of 340 mosM, as occurs during glucose and oleic acid absorption, caused dilation of 1A (118%) and 2A (124%) equivalent to that during absorptive hyperemia. The dilation caused by 400 mosM mannitol (137%) was similar to that with 340 mosM NaCl (131%) and approximately 70% of that with 400 mosM NaCl (152%). After EDRF blockade, the responses to sodium hypertonicity decreased by about one-half; blockade reduced mannitol-induced dilation by 22%. These results indicate that sodium hypertonicity, as occurs during absorption, can play a major role in absorptive hyperemia, and about one-half of the dilation is related to a sodium-coupled release of EDRF.

Animals↗
PubMed1993

Adrenergic and pressure-dependent vascular regulation in sedentary and trained rats.

In this study, we determined if aerobic exercise training alters adrenergic or pressure-dependent vascular regulation in the rat hindlimb or intestine. Pressor responses to bilateral carotid artery occlusion and systemic phenylephrine (PE) infusion were not altered by training. During occlusion, peak and steady-state changes in hindlimb vascular resistance (HLR) were significantly greater in trained (24 and 13%) than in sedentary (8 and -3%) rats; a similar trend existed for intestinal vascular resistance (IR). The pressure-dependent contribution was consistent between groups (HLR: peak 55-85%, steady state 25-45%; IR: peak and steady state 40-65%). During PE infusion, increases in IR and HLR were similar between groups. The increase in HLR was substantially pressure dependent in both groups (approximately 50% at highest dose) as was the change in IR in trained rats. However, the IR response to PE was not pressure dependent in sedentary rats. The direct effects of PE were similar between sedentary and trained rats in the hindlimb but were suppressed in the intestine of trained rats compared with sedentary rats. Therefore, aerobic exercise training altered adrenergic and pressure-dependent vasoregulatory mechanisms in both skeletal muscle and intestinal tissues.

Animals↗
PubMed1992

Intestinal lymphatic vessels release endothelial-dependent vasodilators.

This study evaluated the possibility that the endothelial cells of microscopic lymphatic vessels can release vasoactive agents which affect the lymphatic vessels and nearby arterioles. Microinotophoresis of acetylcholine (ACh) or bradykinin (BK) onto the wall of quiescent submucosal lymphatic vessels in the rat small intestine had no discernible effects on their diameters but caused spontaneously active mesenteric lymphatic vessels to constrict. Application of ACh or BK to the arteriolar wall caused significant vasodilation. Release of either drug onto the wall of a nearby lymphatic produced arteriolar dilation that was approximately 80% of that observed with direct application to the arteriolar wall; drug application into parenchymal tissue produced a dilation less than 25% of that observed during application to the lymphatic. NG-monomethyl-L-arginine application to the lymphatic blocked all ACh-induced lymphatic-mediated responses but had no effect on the response to direct ACh application to the arteriolar wall or any of the responses to BK application. These results are consistent with the hypothesis that lymphatic endothelial cells are capable of releasing agents that dilate nearby arterioles and cause spontaneously active lymphatic vessels to constrict.

Acetylcholine↗
PubMed1992

Functional adaptations of rat skeletal muscle arterioles to aerobic exercise training.

This study tested the hypothesis that both structural and functional adaptations of arterioles occur within the skeletal muscle of rats aerobically trained for 8-10 wk with treadmill exercise. The training regimen used has been shown to elicit a 37% increase in plantaris citrate synthase activity but did not result in an elevation in citrate synthase activity in the spinotrapezius or gracilis muscles of rats used in this study. In the in vivo resting spinotrapezius muscle, arteriole diameters were similar in sedentary (SED) and trained (TR) rats. However, large- (1A) and intermediate- (2A) sized arterioles dilated proportionately more in TR than in SED rats during 1- to 8-Hz muscle contractions, even though the passive mechanical properties (circumference-passive wall tension relationships) were similar between groups. Vascular casts demonstrated a trend for an increase in the number of small (3A) arterioles and an approximately 20% increase in the passive diameter of 1A and 2A arterioles in the spinotrapezius muscle of TR rats. In contrast, in the gracilis muscle, arteriole diameters and density were identical in SED and TR rats, but the capillary-to-muscle fiber ratio was approximately 15% higher in TR rats. The results suggest that aerobic exercise training can greatly increase functional vasodilation and induce a slight increase in vascular density in skeletal muscle tissues, even if the oxidative capacity of these tissues is not increased by the training regimen.

Adaptation, Physiological↗
PubMed1991

Vascular smooth muscle structure and juvenile growth in rat intestinal venules.

The morphological structure of individual vascular smooth muscle cells from intestinal venules was evaluated with a combination of quantitative scanning (SEM) and transmission (TEM) electron microscopy techniques. In addition, growth of individual venular smooth muscle cells and of the overall vessel wall was compared from measurements of these variables during the rapid juvenile growth spurt from ages 4 to 6 and 10 to 12 weeks in Wistar-Kyoto rats. SEM revealed that smooth muscle cells of intestinal venules in weanling rats are very long (379 +/- 91 [SD] microns) and wide (6.0 +/- 1.3 microns) and very little further cell enlargement occurs during rapid juvenile growth. TEM studies indicated that passive inner vessel diameter and total muscle layer cross-sectional area of both the largest and intermediate diameter venules of young rats, as well as the percentage of the total wall area as muscle tissue in each venule type, did not significantly increase during body growth. These observations indicate that both the intestinal venules and their smooth muscle cells reach mature dimensions at a very early stage of life. Comparison of intestinal vascular smooth muscle cell dimensions indicates that venular smooth muscle cells are much larger in both cell length and volume than comparable arteriolar smooth muscle cells.

Aging↗
PubMed1991

Hepatic venular pressures of rats, dogs, and rabbits.

We tested the hypotheses that the hepatic venule pressures (Phv), just downstream from the hepatic sinusoids, are closely similar (less than 2 mmHg) either to the portal venous pressure (Ppv), indicating a high hepatic venous resistance, or to the inferior vena cava (Pivc) pressure, indicating a high portal-sinusoidal venous resistance, as reported by previous investigators. A micropipette servo-null pressure measurement technique was used with rats, dogs, and rabbits. Phv, referred to the anatomic level of the vena cava, averaged 5.1 +/- 1.0, 6.4 +/- 1.1, and 5.4 +/- 1.0 (SD) mmHg in the rats, puppies, and rabbits, respectively. Ppv averaged 8.0 +/- 1.4, 10.8 +/- 2.2, and 7.4 +/- 1.5 mmHg, respectively. Norepinephrine infusion into the portal vein (1-5 micrograms.min-1.kg-1) caused Ppv to increase and the portal venous flow to decrease but did not significantly affect Phv. The hepatic venous circuit contributed 44 +/- 17% (rats) and 31 +/- 26% (dogs) of the total liver venous vascular resistance under control conditions. We conclude that the portal and sinusoidal vasculatures are the dominant, but not exclusive, resistance sites of the liver venous vasculature both at rest and during norepinephrine-induced vasoconstriction.

Animals↗
PubMed1991

Mechanical characteristics and active tension generation in rat intestinal arterioles.

The contributions of active and passive wall tension to regulation of arteriolar diameters were determined for large (1A), intermediate (2A), and small (3A) arterioles in the small intestine of the anesthetized rat. Active tension (Ta) contributed greater than 85% of total wall force at rest in 2A and 3A and 75-80% of total force in 1A. Ta was approximately 90% of peak active tension (Ta,peak) for large through small arterioles, even though absolute Ta varied by fourfold. A linear relationship between microvascular pressure and Ta was observed for decreases in pressure in all arterioles. Ta remained nearly constant for pressure increases of 40% in 2A and 3A but was increased in 1A. Because of the plateau of the circumference-Ta relationship near Ta,peak, superfusion of progressively increasing concentrations of norepinephrine or adenosine resulted in maintenance of the close Ta-Ta,peak relationship unless the vessel diameter changed greater than 25%. These results indicate that, while arteriolar diameters vary substantially, near-peak Ta is generated for a variety of physiological conditions.

Adenosine↗
PubMed1991

Structural and functional origins of suppressed acetylcholine vasodilation in diabetic rat intestinal arterioles.

This study evaluated the possible impairments to endothelium-mediated vasodilation by structural and functional properties of the intestinal arterioles in adult (20-21-week-old) rats after 8-11 days or 7-8 weeks of streptozotocin-induced diabetes. Arteriolar intravascular pressures and luminal diameters were simultaneously measured during iontophoretic application of acetylcholine, bradykinin, and nitroprusside to the outer vessel wall, and passive diameter-pressure relations were obtained during maximal vasodilation. Microvascular pressures and circumference-passive wall tension relations were similar between all diabetic and normal rats and did not appear to significantly influence vasodilation. Both acute and chronic hyperglycemia were associated with near complete suppression of acetylcholine-induced vasodilation in large arterioles, and the threshold dose for vasodilation of intermediate arterioles was approximately 10-fold higher in diabetic rats. In both diabetic groups, dilatory responses to nitroprusside were normal, and in chronically diabetic rats, the relative vasodilation in response to various doses of bradykinin was equivalent to that found in normal rats. These observations indicate that a very specific deficit of acetylcholine-induced endothelium-derived relaxing factor action rapidly develops in intestinal arterioles of diabetic rats, but the arteriolar wall mechanical properties, cGMP-mediated muscle relaxation, and endothelial release of the bradykinin-stimulated relaxing factor are not compromised after 7-8 weeks of chronic hyperglycemia.

Acetylcholine↗
PubMed1990

Maturation of the rat intestinal microvasculature from juvenile to early adult life.

The same region of intestinal ileum was compared in the same rats at 10 and 20 wk of age to determine if reported differences in vessel density between these ages were the result of changes in vessel numbers. The number and branching pattern of arterioles observed remained remarkably constant during the 10 wk between observations, and minimal enlargement of bowel mass occurred. No significant change in average maximum diameter of arterioles was observed. Although the total number of small arterioles did not change, vessels were gained and lost at an equal rate (7%) between 10 and 20 wk. There was no significant changes in means or frequency distributions of intercapillary distances in the radial or longitudinal bowel muscle layers. The results indicate that the intestinal microvascular branching pattern changes very little from juvenile to adult life. However, a slow turnover of small arterioles does occur, indicating an ongoing remodeling of the terminal vasculature during juvenile life.

Aging↗
PubMed1990

EDRF from rat intestine and skeletal muscle venules causes dilation of arterioles.

Communication from venules to arterioles through the release of endothelial-derived relaxing factor (EDRF) was evaluated. To demonstrate that the rat intestinal and the spinotrapezius muscle arterioles can respond to EDRF, the vessels were dilated by iontophoretically applied acetylcholine (ACh), and this dilation was greatly attenuated by the inhibitors of EDRF actions, methylene blue (100 microM) and dithiothreitol (50 microM). The EDRF inhibitors did not suppress arteriolar dilation to typically applied adenosine (10(-4) M), an endothelium-independent dilator. Although ACh release onto the venular wall had minimal effects on the diameter of the venule, the paired arteriole would dilate 20-30% in the intestine and 50-60% in the spinotrapezius muscle. After EDRF inhibition, venular ACh exposure did not cause arteriolar dilation. ACh diffusion from venules to arterioles was not the cause of arteriolar dilation, because release of ACh into the tissue at the same distance as from the arteriole to the venular ACh release site caused minimal arteriolar dilation. Neither blockade of neural reflexes with tetrodotoxin (3 X 10(-6) M) nor suppression of prostaglandin formation with indomethacin (10(-5) M) prevented the arteriolar dilation during release of ACh onto the venular wall. The overall study indicated that communication from venules to arterioles through the release of EDRF from the venule did occur and caused substantial arteriolar vasodilation. Therefore circumstances within and around venules may influence regulation of nearby arterioles through an EDRF-mediated mechanism.

Acetylcholine↗
PubMed1990

Rat venular pressure-diameter relationships are regulated by sympathetic activity.

The hypothesis that the pressure-diameter relationship of intestinal venules in rats is primarily determined by sympathetic nervous system activity was tested. The pressure-diameter relationship of the smallest to largest diameter (20-100 microns) intestinal venules of the rat was measured at rest, during hemorrhage to increase sympathetic neural activity, and during saline volume expansion to decrease sympathetic activity. During hemorrhage, the diameter of all venules decreased approximately 10% at 10 mmHg venous pressure, and the slope of the pressure-diameter relationship increased approximately 50% above control. Blood volume expansion led to an approximately 10% increase in venule diameter at 10 mmHg and a 25% decrease in slope. Denervation of the vessels causes concomitant vasodilation, which was greater than the vasodilation caused by blood volume expansion. Hemorrhage after denervation caused no significant changes in the relationship when compared with denervated control. Nitroprusside caused an even greater vasodilation when compared with the pressure-diameter relationship after denervation. The results suggest that the slope and 10-mmHg intercept of the pressure-diameter relationship for the largest through smallest intestinal venules and, therefore, their vascular compliance and capacitance characteristics are primarily determined by sympathetic activity.

Animals↗
PubMed1989

Rat intestinal lymph osmolarity during glucose and oleic acid absorption.

The two major purposes of this study were to determine 1) how glucose and oleic acid absorption by the intestinal villi influenced the osmotic composition of lymph as it exited the villus base and 2) what if any changes in lymph osmolarity occurred as the lymph traversed through the bowel wall. The rat jejunum was used in all studies and lymph was collected from individual lymphatics at 0.5-1 nl/min during control states and luminal exposure to 35-550 mg% glucose solutions (isotonic in saline) and 5 and 20 mM oleic acidtaurocholate solutions. Lymph collected from the base of villi during vigorous motility had an osmolarity of 403 +/- 15 mosM at rest and was only increased 30-50 mosM more except during exposure to 550 mg% glucose, where osmolarity increased over 100 mosM. Under comparable conditions, the submucosal lymph osmolarity at rest was 302 +/- 3.5 mosM and increased to 330-350 mosM during exposure to all of the solutions tested. When intestinal motility was virtually stopped, the submucosal lymph osmolarity was isotonic for all solutions tested. These observations indicate that absorption of glucose and oleic acid increased the osmolarity of lymph, leaving the villus only 30-50 mosM unless a glucose concentration of 550 mg% was present. Furthermore, the increased flow of villus lymph during absorption raised the osmolarity of the submucosal lymph when bowel motility assisted the lymph propulsion. This movement of materials from the villus to the submucosa by venular blood and lymph flow provides an opportunity for the villus tissue to influence the composition of the submucosal interstitial environment.

Adsorption↗
PubMed1989

The microcirculation in hypertension.

Studies of the peripheral microcirculation in major organ systems during hypertension indicate that in anaesthetized spontaneously hypertensive rats (SHR) a combination of both vasoconstriction and temporary and permanent vessel closure occurs. The vasoconstriction is often limited to the largest and smallest arterioles and rarefaction is best expressed for arterioles with inner diameters less than 25 microns in the lower body musculature. Direct measurements of microvascular pressures in hypertensive rats indicate that while all arterioles in major organ systems are exposed to a pressure much higher than normal, the smallest arterioles dissipate a much higher than normal fraction of the mean arterial pressure. However, the transition vessels between the smallest arteries and the larger arterioles account for the largest fraction of total resistance (50-60%) and dominate the precapillary vascular resistance in the cerebral, intestinal and skeletal muscle vasculatures. In the established stages of hypertension, the relative influence of the transition resistance vessels is somewhat less than during the developmental phase of hypertension and also less than in adult normal animals. This latter observation has been made in a number of vasculatures and may indicate that resistance changes in the true microvessels and in the transition vessels do not occur simultaneously during the development of hypertension.

Animals↗
PubMed1988

Lymphatic pathways and role of valves in lymph propulsion from small intestine.

The pathways through which lymph is propelled from the mucosal, submucosal, and muscle layer lymphatics of the small intestine, the interconnections between these layers, and the location of lymphatic valves within these layers were studied. Injections of fluid into a single lacteal or submucosal lymphatic of rats, rabbits, dogs, and cats spread in all directions through the submucosal lymphatics and into laceteals but did not enter the lymphatics of the muscle layer. Injections into muscle layer lymphatics also spread in all directions but in no case entered the submucosal lymphatics. The submucosal and muscle layer lymphatics join within the bowel wall near the mesenteric border to form collecting lymphatics characterized by valves and spontaneous contractions. These data indicate that lymphatics of the mucosa and submucosa form a syncytium independent of the muscle layer lymphatics and that few if any valves exist within these lymphatic networks. Cycling lacteal pressures were measured when intestinal motility was present but not when motility was abolished, suggesting that intestinal motility might have a role in lymph propulsion.

Animals↗
PubMed1988

Arteriolar diameter and tissue oxygen tension during muscle contraction in hypertensive rats.

This study evaluated the possibility that in hypertension, mechanisms that maintain near normal arteriolar diameters at elevated arteriolar pressures limit the ability of skeletal muscle arterioles to dilate in response to an increase in tissue metabolism. The spinotrapezius muscles of 16- to 20-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were contracted at frequencies of 1, 2, 4, and 8 Hz. The inner diameters of first-order through third-order arterioles were measured at rest and following 3 minutes of contractions. Tissue oxygen tension (PO2) at the venous end of capillaries was monitored during 8-Hz contractions. At rest, following contractions, and after maximum dilation with adenosine, the inner diameters of arterioles of equivalent branch order were not significantly different in SHR and WKY. Opening of closed arterioles during muscle contraction and adenosine application occurred in less than 5% of the observations in both groups. The resting tissue PO2 was 25.5 +/- 1.3 mm Hg in normal rats and 26.1 +/- 2.1 mm Hg in SHR. At nearly maximum vasodilation during 8-Hz stimulation, tissue PO2 recovered to 81.9 +/- 12.7% of control in WKY but only to 41.2 +/- 13.0% of control in SHR. These observations indicate that the expression of local regulatory mechanisms related to tissue metabolism is virtually normal in the spinotrapezius muscle vasculature of SHR in the context of arteriolar dilation. However, at near maximum performance, factors other than absolute arteriolar diameter preclude the normal preservation of tissue PO2 in the spinotrapezius muscle of SHR.

Animals↗