PubMed Health⌕ Search

Biomedical subjects

H G Bohlen

Publications and source records attributed to H G Bohlen.

At least 73 records · Page 4Linked to original sources
PubMed1983

In vitro and in vivo measurement of red cell velocity with epi- and transillumination.

Measurement of red cell velocity with the dual-slit cross-correlation method in glass capillary tubes during transillumination indicates that the measured velocity must be divided by a correction factor of approximately 1.6 to equal the average velocity calculated from a known flow and inner diameter. Whether the same correction factor exists when red cell velocity is measured during epiillumination is questionable. Red cell velocity was measured with the dual-slit correlation method nearly simultaneously using epi- (EL) and transillumination (TL) while glass tubes (40-100 microns, i.d.) were pump perfused with whole human blood (hematocrit 39-42%). With TL, the measured velocity is 1.58 +/- 0.07 (SEM) times the calculated average velocity, whereas a factor of 2.04 +/- 0.04 (SEM) was obtained with epiillumination. When intestinal arterioles with approximately the same inner diameters and flow velocities as the glass tubes were used, the ratio of velocities measured with TL to EL was 1.21 +/- 0.02 (SEM) as compared to 1.31 +/- 0.09 (SEM) for glass tubes using TL and EL of the tube at the same pump flow. This similarity of TL to EL velocity ratios for glass tubes and microvessels may be fortuitous or indicate that comparable flow properties and measurement conditions exist for in vitro and in vivo situations. The major finding of the study is, however, that different velocity correction factors exist for EL and TL measurements when the dual-slit correlation method is used to estimate red cell velocities in tubes of an internal diameter of 40-100 microns at normal hematocrits.

Arterioles↗
PubMed1983

Early microvascular pathology during hyperglycemia in bats.

The microvascular changes in the wing of bats, Myoitis lucifugus, were observed during 3 weeks of normal life and 5 weeks of streptozotocin induced hyperglycemia (300-400 mg/dl, plasma). During normal life, week-to-week variations in diameter and blood flow in the same set of vessels were minor. After hyperglycemia was induced, the major initial response was dilation of all microvessels except the smallest arterioles which constricted. The dilation phase was followed by progressive constriction of all vessels. Blood flow was near normal during the dilation phase, but flow gradually decreased as hyperglycemia continued and vasoconstriction occurred. The ability to repeatedly observe the same set of microvessels on a week-to-week basis and the absence of anesthesia may make the diabetic bat a useful model in which to study the early phases of microvascular pathology during chronic hyperglycemia, which begins abruptly in adult life. In addition, the sequence of microvascular changes during chronic hyperglycemia in the bat are qualitatively similar to those in other diabetic mammals, including man.

Aging↗
PubMed1983

Tissue PO2 in the intestinal muscle layer of rats during chronic diabetes.

Chronic diabetes mellitus induced in rats by streptozotocin or of genetic origin in Db/Db mice is associated with a loss of capillaries, arteriolar constriction, and a decrease in resting and maximum blood flow. As a result of these vascular changes, as well as glycolysation of hemoglobin, it is possible that tissue Po2 is reduced at rest and cannot be substantially increased during dilatation. Tissue Po2 in the intestinal muscle layer was measured at rest and during maximal dilation. In addition, the spacing between capillaries with active flow and the velocity of red blood cell flow in capillaries were measured at rest and at maximum dilation. These measurements were made in normal and diabetic rats (streptozotocin) at age 26-30 weeks; the diabetic animals had been hyperglycemic (greater than 350 mg/100 ml) for 12-15 weeks. Tissue Po2 at a distance of about 15 microns from the arterial, mid-point, and venous end of capillaries in normal rats was 24.8 +/- 1.1 (SE), 23.1 +/- 1.2, and 22.4 +/- 0.9 mm Hg, respectively, compared with 25.8 +/- 0.9, 24.1 +/- 1.2, and 22.4 +/- 1.1 mm Hg, respectively, in diabetic rats. The maximum mid-capillary tissue Po2 during dilation was 27.7 +/- 1.3 mm Hg in normal rats and 29.7 +/- 1.5 mm Hg in diabetic rats. The average distance between capillaries was 37.6 +/- 2.0 microns in normal rats and 46.8 +/- 2.9 microns in diabetic animals; vasodilation did not change the capillary spacing in either group of animals. Capillary red cell velocity in normal rats increased from 0.98 +/- 0.11 mm/sec at rest to 2.1 +/- 0.4 mm/sec during dilatation. For comparable conditions in diabetic rats, the velocities were 0.41 +/- 0.07 and 1.06 +/- 0.19 mm/sec. The data presented indicate that the diabetic animals have tissue Po2 equivalent to those in normal rats, both at rest and during maximum vasodilation. The loss of capillaries and decreased resting and maximum capillary red cell velocity in diabetic rats would decrease the delivery of oxygen, but, apparently, a decrease in oxygen consumption occurred that allowed the intestinal tissue to have a normal Po2.

Animals↗
PubMed1982

A new morphological procedure for viewing microvessels: a scanning electron microscopic study of the vasculature of small intestine.

The present study details a new method for the exposure and viewing of individual microvessels located within the small intestine of rats. This procedure will selectively and consistently remove the outer muscle layers and underlying submucosa of the intestinal wall and thereby expose a variety of arterioles in their normal location within the tissue, with their normal relationship to each other undisturbed. The small intestine of the rat was initially fixed by vascular perfusion with 2.5% glutaraldehyde in 0.1 M cacodylate/HCL buffer, reinfused with heparinized whole blood, removed from the animal, and secured to a dissecting petri dish for further fixation. Subsequently, the external muscularis was dissected from the sample which exposed the submucosa. In order to remove the connective tissue elements from this layer and uncover the submucosal vasculature, the samples were first transferred to a solution of 30% potassium hydroxide for 2-5 minutes and then to a final digesting solution containing collagenase. Thereafter, the samples were routinely processed for light microscopy and for scanning (SEM) or transmission (TEM) electron microscopy. Examination of the samples revealed excellent preservation of the three-dimensional organization of the arteriolar wall with minimal membrane damage. This new technique now makes it possible to visualize the shape and position of individual smooth muscle cells along arterioles of differing size and branching order.

Animals↗
PubMed1982

Early arteriolar and capillary changes in streptozotocin-induced diabetic rats and intraperitoneal hyperglycaemic rats.

Comparison of intestinal arteriolar characteristics in vivo were made in normal rats, normal rats injected intraperitoneally twice daily with either 0.15 mmol/l saline or 16.6 mmol/l glucose in 0.15 mmol/l saline (total value 5% of body weight), and in streptozotocin treated rats (plasma glucose greater than 22.2 mmol/l). Each regimen was continued for 4-5 weeks before the study. Interperitoneal injection of glucose increased the plasma glucose concentration by 0.8-1.6 mmol/l for 2-2.5 h. The microvascular characteristics of normal and saline injected rats were identical. Results obtained in glucose-treated and diabetic animals were very similar and included: 1) resting arteriolar vasodilation, 2) subnormal dilation at removal of all vascular control with adenosine, 3) total arteriolar vessel wall, including smooth muscle, cross-sectional area and wall to lumen ratio one-third to one-half less than normal, and 4) capillary separation distances increased above normal by 40%-50%. The results indicate that the morphological and functional changes in intestinal arterioles and capillaries found in diabetic rats after 4-5 weeks can be reproduced in the intestinal tissues of a normal animal exposed to intermittent increases in intraperitoneal glucose concentration.

Animals↗
PubMed1982

Na+-induced intestinal interstitial hyperosmolality and vascular responses during absorptive hyperemia.

The coupled active transport of Na+ with sugars and amino acids could cause intestinal villus interstitial hyperosmolarity, which contributes to absorptive hyperemia. However, for the villus hyperosmolarity to cause a major vascular response, a mild-to-moderate hyperosmolarity must occur in the vicinity of the major resistance vessels of the submucosa. Interstitial Na+ activity was measured throughout the small intestinal wall of rats with monensin ion-selective electrodes during glucose absorption. In the upper half of villi, the resting [Na+] was 201 +/- 5 (SE) mM and increased to 267 +/- 6 mM during luminal exposure to 25-300 mg/100 ml glucose. The submucosal resting [Na+] was 144 +/- 1 mM and increased to 177 +/- 3 mM during luminal glucose exposure. The time courses of Na+ appearance and submucosal arterial dilation were almost identical. Calculations of tissue osmolarity indicate an increase in villus osmolarity of 150-200 mosM and 79-90 mosM in the submucosa during glucose absorption. The data are interpreted to indicate that villus hyperosmolarity during glucose absorption increased submucosal osmolarity and a naturally occurring osmotic dilatory component of absorptive hyperemia could exist.

Animals↗
PubMed1981

Exercise hyperemia in the absence of a tissue PO2 decrease.

The relationship between contraction-induced arteriolar vasodilation, estimated blood flow (BF), and tissue oxygen tension (PtO2) in skeletal muscle of young rats was investigated. Arteriolar diameters, BF, and PtO2 were measured during cremaster muscle stimulation at 2, 4, and 8 Hz. At a suffusate PO2 (PsO2) of 5-10 mm Hg, the caliber of second-order arterioles (2A, greater than 30 micrometer diameter) did not significantly increase after 8 Hz stimulation. In contrast, with the same PsO2, third-order arterioles (3A, less than 30 micrometer diameter) significantly dilated to 127 +/- 9 (SE), 135 +/- 12, and 160 +/- 13% of control, respectively at 2, 4, and 8 Hz stimulation. Third-order arteriolar BFs at the end of the stimulation periods were: 119 +/- 18, 176 +/- 14, and 258 +/- 43% of control, respectively. PtO2 remained essentially constant during and following 4 and 8 Hz stimulation if the systemic arterial blood pressure exceeded 80 mm Hg. When PsO2 was increased to 65-70 mm Hg, neither 3A diameters nor PtO2 during 8 Hz stimulation differed from paired comparisons of the response at low PsO2. These data indicate that dilation of small arterioles during increased muscle metabolic activity can occur without a mandatory change in PtO2. This circumstance is unaffected by a substantially increased supply of oxygen to the tissue.

Animals↗
PubMed1980

Intestinal tissue PO2 and microvascular responses during glucose exposure.

The microvessels responsible for the major decrease in intestinal vascular resistance during the presence of glucose were defined. In addition, the normal distribution of tissue PO2 in the various layers of the intestinal tissue was measured at rest and during glucose exposure to determine if part of the absorptive hyperemia mechanism is related to a decrease in tissue PO2. In the rat small intestine, exposure of the mucosa only to glucose concentrations of 25--500 mg/100 causes a 20--25% dilation of all submucosal vessels in series with the mucosal vessels and mucosal arterioles. Total intestinal blood flow increased to 200-210% of control at all glucose concentrations. The tissue and perivascular PO2 in the villus apex decreased from 14.8 +/- 1.2 (SE) mmHg at rest to 6--8 mmHg during glucose exposure; the PO2 in the muscle and submucosal layers tended to slightly increase above a normal of 26.4 +/- 1.6 mmHg during glucose exposure. The data indicate virtually all intestinal arterioles are equally involved in absorptive hyperemia. The dilation of mucosal vessels may be related to a decrease in tissue PO2, but submucosal vessels dilate even though PO2 is slightly increased.

Animals↗
PubMed1980

Intestinal mucosal oxygenation influences absorptive hyperemia.

Intestinal villus oxygen tension (PO2) is decreased from normal values of 14-17 to 4-7 mmHg, and blood flow is nearly doubled during glucose absorption. The current study evaluated The role of oxygen supply to the mucosa in the absorptive hyperemia mechanism. With a constant PO2 (40-45 mmHg) over the intestinal muscle layer, the mucosal tissue PO2 increased only 4-5 mmHg, and intestinal blood flow decreased from about 125 to 65% of control (PO2 = 4045) as the mucosal solution PO2 increased from 5 to 75 mmHg. When glucose was present (100 mg/100 mL), mucosal tissue PO2 was s-7 mmHg at mucosal suffusion PO2 of s-75 mmHg. When glucose was present (100 mg/100 mL), mucosal tissue PO2 was s-7 mmHg at mucosal suffusion PO2 of s-75 mmHg. Blood flow in the presence of glucose was 210 and 110% of control at a solution PO2 of 5-10 and 70-75 mmHg. Tissue PO2 in the vicinity of the submucosal series arterioles was only slightly affected by all of the manipulations described. At rest or during glucose exposure, elevation of mucosal solution PO2 caused constriction, and lowering the mucosal solution PO2 caused dilation even though tissue PO2 in the various regions of the bowel wall remained nearly constant. The data indicate that the supply of oxygen available for the tissue rather than the actual tissue PO2 is best correlated to oxygen's role in control of arterioles throughout the intestine during absorptive hyperemia.

Animals↗
PubMed1979

Arteriolar closure mediated by hyperresponsiveness to norepinephrine in hypertensive rats.

This study was designed to determine if a mechanism exists to cause abnormally large number of arterioles to be closed to blood flow in spontaneously hypertensive rats (SHR). The contributions to vessel closure by neural control and constrictor response to norepinephrine were investigated. Normal rats (WKY) and SHR were studied at age 18--20 wk. Their respective mean arterial blood pressures were 100 +/- 4 (SE) and 154 +/- 7 mmHg when anesthetized with 10% urethan and 2% alpha-chloralose (0.6 mg/100 g ip). The number of arterioles open to blood flow was counted in a large portion of the cremasteric muscle before and after denervation. The percent change in control diameter of denervated arterioles was measured during iontophoretic application (2 min) of norepinephrine at dose currents of 10--300 nA. Following denervation, a 22.2 +/- 6.3% (SE) and 61.8 +/- 12 increase in the number of third-order arterioles open to flow occurred in WKY and SHR. The diameters, wall thicknesses, and cross-sectional areas of vessel walls were not significantly (P less than 0.05) different for comparable types of denervated arterioles in WKY and SHR. The percent changes in diameters of arterioles in SHR were 3--5 times greater at all dose currents than for vessels of WKY. These data indicate arteriolar closure occurs with higher incidence in SHR than WKY and is mediated by hyperresponsiveness of arterioles to norepinephrine.

Animals↗
PubMed1979

Adult microvascular disturbances as a result of juvenile onset diabetes in Db/Db mice.

The arterioles in the cremaster muscle of 8 to 10-week-old Ob/Ob, Db/Db and stroptozotocin diabetic mice are characterized by a decreased number of arterioles, loss of vascular tone and a reduced cross-sectional area of the vessel walls. The present study was designed to determine if these abnormalities persist to adult life or if additional abnormalities develop to cause vascular dysfunction. The diameters, wall thickness to lumen ratios and vessel wall areas of comparable types of innervated arterioles in 24- to 28-week-old normal and Db/Db mice are equivalent, except that the smallest arterioles of Db/Db have thin vessel walls. However, blood flow at rest is only 3.0 +/- 0.9 ml/min/100 g of cremasteric muscle tissue in Db/Db mice as compared to 5.5 +/- 1.3 ml/min/100 g in normal mice. After all vascular control is abolished, the arterioles of Db/Db dilated, but significantly (p less than 0.05) less than in normal animals. The minimum distance between adjacent capillaries (wall to wall) during the passive state was 28 +/- 1.7 micron in Db/Db mice and 21.8 +/- 0.6 micron in normal mice; this indicates a major decrease of vascularity in the adult Db/Db mouse. The results obtained indicate that the reduction in numbers of arterioles and loss of vascular tone in juvenile diabetic mice persists to adult life but arteriolar wall characteristics become normal in adult life.

Age Factors↗
PubMed1978

Intestinal muscle and mucosal blood flow during direct sympathetic stimulation.

The effect of direct sympathetic stimulation on intestinal muscle and submucosal-mucosal vasculatures was studied in the anesthetized rat. Blood flow was calculated from direct measurements of vessel diameter and red cell velocity. Stimulation at 4 Hz caused a slight reduction (4%) in muscle flow, but had no measurable effect on submucosal-mucosal flow; stimulation at 8 and 16 Hz caused muscle flow to decrease to 58.3 +/- 8.7% (SE) and 31 +/- 5.1%, respectively, of control flow, and mucosal flow, to 73 +/- 3.4% and 54.1 +/- 1.2%, respectively, of control flow. Calculations of muscle and mucosal vascular resistances from flows and microvascular pressures indicate that muscle resistance increased proportionately more than mucosal resistance at 4 and 8 Hz. However, during stimulation at 16 Hz, the mucosal resistance is only 55% of control, and muscle resistance is not significantly (P less than 0.05) different from control. Therefore, reduction of muscle and mucosal flows during 16-Hz stimulation must be caused by the intestinal arterioles and venules in series with these vasculatures.

Animals↗
PubMed1978

In vivo study of microvascular wall characteristics and resting control in young and mature spontaneously hypertensive rats.

This study was designed to determine if vessel wall hypertrophy and increased expression of sympathetic activity occur in the microcirculation during the development of hypertension. The cremaster muscle microvasculature of normal Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats was observed at age 5--7 weeks and 16--18 weeks. For age-matched WKY and SHR rats, the diameters, wall thicknesses and vessel wall cross-sectional areas for the majority of comparable types of arterioles were not significantly (p greater than 0.05) different. After denervation of the cremasteric muscle, the large and intermediate diameter arterioles of young WKY rats dilated significantly (p less than 0.05) more than did comparable vessels of SHR rats. In contrast, the dilation of comparable types of arterioles in mature WKY and SHR rats following denervation was not significantly (p greater than 0.05) different. The results do not support either abnormal vessel wall hypertrophy, vasoconstriction or increased expression of sympathetic activity in SHR rats compared to WKY rats up to age 16--18 weeks.

Animals↗