PubMed Health⌕ Search

Biomedical subjects

H G Bohlen

Publications and source records attributed to H G Bohlen.

At least 55 records · Page 3Linked to original sources

Intestinal microvascular growth during maturation in diabetic juvenile rats.

To determine if intestinal microvascular growth is impaired in diabetic juvenile animals, a segment of the terminal ileum was marked and the microvasculature of this segment observed at the age of 5 weeks and again at the age of 10-11 weeks in normal and diabetic Sprague Dawley rats. Diabetes was induced by streptozotocin after the first observation period and the plasma glucose concentration exceeded 500 mg% by the age of 10-11 weeks. Microvascular growth was quantitated by measurements of the number, length, and maximally dilated inner diameters of specific arterioles and by intercapillary distances in the marked intestinal region at both ages. Although intestinal enlargement was much greater in diabetics, there was no change in the number of arterioles during maturation and intercapillary distances were equivalent in diabetic and normal rats. In normal and diabetic animals, the arteriolar length increased to match bowel elongation, however, increases in bowel and arteriolar lengths in diabetic animals were about twice that of normal rats. During juvenile maturation, the maximally dilated inner diameters of the small arterioles in diabetic animals were increased compared with their normal counterparts. Thus, arteriolar growth during maturation is characterized by changes in the length but not in the number of vessels in intestine of both normal and diabetic rats. The perfusion of about 90% more tissue by mass for each arteriole in diabetic rats is facilitated by arteriolar dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Determinants of resting and passive intestinal vascular pressures in rat and rabbit.

Microvascular pressures in the intestinal arteries, submucosal arterioles, and mucosal venules were measured in rats and rabbits at rest and during maximum dilation. From these data and Doppler velocimetry measurements of relative changes in whole organ blood flow on maximum dilation, it was possible to determine to what extent microvascular pressures at rest depend on the active control and passive hemodynamic characteristics of specific vascular segments. New Zealand White rabbits (2-3 kg body wt) had a mean arterial pressure of 70-75 mmHg. However, pressures in arterioles of both species became equivalent at the second order of arteriolar branching within the bowel wall, and pressures in the smallest mucosal venules were 13.7 +/- 0.6 (SE) mmHg in rabbits and 14.9 +/- 0.3 mmHg in rats. Maximum vasodilation to approximately 300% of the control blood flow increased mucosal venule pressures approximately 10 mmHg in rats compared with approximately 4 mmHg in rabbits. The increased mucosal venule pressure during vasodilation was primarily due to increased pressures within the submucosal small arterioles, which immediately precede the villus vasculature in both species. The increased blood flow during vasodilation was due primarily to a decreased resistance of the small arteries and large arterioles, even though pressures in these larger vessels changed only approximately 10%. This situation allows a major decrease in intestinal vascular resistance to substantially increase blood flow with a minimal increase in mucosal microvascular pressures.

Adenosine↗

Perivascular and tissue PO2 in contracting rat spinotrapezius muscle.

This study evaluated the possibility that during skeletal muscle contractions tissue O2 tension (Po2) around arterioles and venules decreases substantially more than in the middle of the capillary bed and thereby influences functional hyperemia. Periarteriolar [H+] and [K+] were also measured because most large arterioles are in close proximity to venules such that the biochemical status of the periarteriolar tissue could be influenced by a large decrease in O2 availability in the annulet of tissue surrounding the venules. Stimulation frequencies in the range of 2-12 Hz were used to activate the rat spinotrapezius muscle. Periarteriolar and capillary bed Po2, [H+], and [K+] changed during the first few minutes of stimulation but were restored to near resting concentrations as the functional hyperemia developed. However, perivenular Po2 decreased rapidly to approximately 50-60% of the resting gas tension as contractions began, and only minor recovery occurred. Elevation of tissue and periarteriolar Po2 with an O2-enriched superfusion solution did not prevent dilation during contractions to the same diameter as during the response at very low superfusion Po2. Therefore, the extent to which O2 influences arteriolar dilation and exercise hyperemia in the spinotrapezius muscle of the rat may depend less on periarteriolar and capillary bed Po2 than on the release of vasoactive materials from the nearby perivenular tissues as the availability of O2 decreases.

Animals↗

Cell and wall morphology of intestinal arterioles from 4- to 6- and 17- to 19-week-old Wistar-Kyoto and spontaneously hypertensive rats.

To determine whether vascular smooth muscle cells around intestinal arterioles of various sizes undergo comparable changes in spontaneously hypertensive rats, 4- to 6-week-old (n = 10) and 17- to 19-week-old (n = 10) rats from the Wistar-Kyoto and the spontaneously hypertensive strains were used to study the external morphology of vascular smooth muscle cells by scanning electron microscopy and the vessel wall cross-sectional characteristics by light microscopy. At the time of fixation all vascular tone had been abolished. Scanning electron microscopy analysis revealed that all Wistar-Kyoto and spontaneously hypertensive rats at a given age have spindle-shaped vascular smooth muscle cells of comparable length and longitudinal width for a given branching order of arterioles. However, normal maturation is associated with elongation and widening of the vascular smooth muscle cells. Light and scanning electron microscopy indicated that a monolayer of vascular smooth muscle cells, wrapped at almost 0 degree to the vessel's radial axis, is maintained in adult spontaneously hypertensive rats. The radial thickness of this vascular smooth muscle cell monolayer was significantly (p less than 0.025) increased for only the largest arterioles of young and adult spontaneously hypertensive rats. This radial thickening of individual vascular smooth muscle cells increased the muscular component of the wall area for the largest arterioles by about 50% in adult spontaneously hypertensive rats. Other smaller submucosal arterioles of young and adult spontaneously hypertensive rats had normal vessel wall and vascular smooth muscle cell characteristics. These data indicate that hypertrophy in the smooth muscle cell's radial dimension is the primary morphological change in intestinal arterioles of spontaneously hypertensive rats. However, the vascular smooth muscle cell hypertrophy is confined to the largest arterioles such that the remaining smaller arteriolar vessels in the spontaneously hypertensive rat retain a normal smooth muscle cell and overall wall morphology.

Aging↗

Enhanced cerebral vascular regulation occurs by age 4 to 5 weeks in spontaneously hypertensive rats.

Although the primary emphasis of research on spontaneously hypertensive rats (SHR) tends to be on adult animals, the young SHR can have a mean arterial pressure that is elevated above normal almost proportionately as much as in adult SHR. This study attempted to determine whether the cerebral vasculature of 4- to 5-week-old SHR used existing normal mechanisms to tolerate hypertension or had microvascular characteristics uniquely suited for hypertensive life. At mean arterial pressures above about 60 mm Hg, the arterioles of SHR were constricted compared with similar branch order vessels of normal Wistar-Kyoto rats (WKY). At arterial pressures below 60 mm Hg, however, the inner diameters of arterioles in normal and hypertensive rats can be similar. At arterial pressures of 40 to 120 mm Hg, normal WKY maintained blood flow within +/- 10 of that at the resting arterial pressure of 90 mm Hg; SHR with a mean arterial pressure of 120 mm Hg regulated blood flow over a pressure range of 60 to 160 mm Hg. Normal WKY had petechial hemorrhages from venules and sustained loss of arteriolar tone at arterial pressures above 120 mm Hg, which is the resting arterial pressure of 4- to 5-week-old SHR. Microvascular pressure measurements indicated that the resistance of cerebral arteries was increased, because they dissipated about 50% of the arterial pressure in SHR compared with about 40% in WKY.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Myogenic vasoregulation overrides local metabolic control in resting rat skeletal muscle.

Microvascular reactions to increases in intravascular pressure were studied in the cremaster muscle of the anesthetized rat by enclosing the animal in an airtight box with the muscle exteriorized for observation of the microcirculation. Since the cremaster was exposed to atmospheric pressure, increasing pressure within the box produced equal increases in arterial and venous pressures. Thus, intravascular pressure was altered without affecting the pressure gradient for blood flow. Raising box pressure had no effect on respiration or heart rate and did not change the systemic activity of the sympathetic system, angiotensin II, or vasopressin. Diameters and flows were measured for first (107 +/- 3 micron, mean +/- SEM), second (87 +/- 5), third (29 +/- 2), and fourth (15 +/- 2) order arterioles during increases in intravascular pressure of +10, +20, and +30 mm Hg. No significant changes in the diameters of first or second order arterioles were elicited when pressure was increased. However, when box pressure was increased to +10, +20, or +30 mm Hg, a sustained constriction occurred in third (29%, 45%, and 63%, respectively) and fourth (5%, 38%, and 57%, respectively) order arterioles. Blood flow was significantly reduced in all arterioles, and perivascular PO2 was decreased adjacent to third and fourth order arterioles. Furthermore, the third order arteriole constrictor response was not abolished by local alpha-receptor blockade (phentolamine), indicating that it was not mediated by a local sympathetic axon reflex. Collectively, these data indicate that a potent, non-neural, pressure-dependent mechanism for vasoregulation is present in small arterioles of the cremaster. The sustained constriction in the presence of reduced blood flow and reduced periarteriolar oxygen tension indicates that the vascular response is independent of and capable of overriding flow-dependent (i.e., metabolic) control in resting skeletal muscle. The observations are compatible with the operation of a powerful myogenic mechanism in small arterioles.

Animals↗

Quantification of intestinal microvascular growth during maturation: techniques and observations.

This study was undertaken to determine what changes occur in the intestinal microvasculature during the rapid growth associated with juvenile maturation. A technique was developed that permitted the comparison of the same microvessels in exactly the same intestinal region at two time periods of an animal's life. A region of the terminal ileum of 5-week-old rats was exposed and marked, and photographs and video recordings were made of the microvessels. Four weeks later, the marked intestinal region was located, and photography and videography of the microvessels were repeated. Comparison of indexes for body, intestinal, and microvascular growth for the treated rats and age- and colony-matched controls revealed no significant differences. The number and branching pattern of arterioles observed in the marked region remained remarkably constant during the 4 weeks between observation periods, even though body and bowel mass of the treated animals increased approximately 2.5 times. The lengths of the arterioles were increased (18%) by almost the same proportion as the axis of bowel (22%) in which they were oriented. The average distance between capillaries in the radial intestinal muscle layer was also increased by about the same percentage (24%) as that of tissue elongation (22%). The overall data are consistent with the hypothesis that during the growth spurt of juvenile life, the arterioles present at the weanling stage are elongated and new branches do not develop. The net effect of tissue growth with a minimal change in numbers of arterioles is a decreased ratio of number of arterioles to tissue mass as a normal consequence of maturation.

Animals↗

Exposure of vascular smooth muscle cells for analysis with the scanning electron microscope.

There has been interest in using the scanning electron microscope (SEM) to study the structure of tissues obscured by other cellular or non-cellular elements almost since the SEM was first used to examine biological tissues. Such interest includes the vessel wall and, in particular, the vascular smooth muscle cells. This paper presents a review of the three basic methodologies that have been employed to allow examination of the vascular smooth muscle, 1) blunt dissection, 2) digestion and 3) microdissection. Discussion of other perivascular elements was not a focus of this review. Also presented is the application of these different methodologies to different pathophysiologic conditions.

Animals↗

Morphological evaluation of vascular smooth muscle cell: length and width from a single scanning electron micrograph of microvessels.

Accurate three-dimensional data on the structure of vascular smooth muscle cells is essential for understanding the microvascular system in both normal or disease conditions. The laborious serial reconstruction methods have limited the amount of data collected on the structure of individual vascular smooth muscle (VSM) cells. The circumferential viewing of whole vessel segments via scanning electron microscopy provides an alternative approach, but even this technique is highly specialized and tedious. This study presents a simplified method to determine the average cell length and width of individual VSM cells by using only one view of a microvessel (single view). The vessels do not have to be isolated for circumferential viewing and can be left in their host tissue if desired. Values for the average VSM cell length and width were obtained by both circumferential- and single-view approach on the same vessels. The average cell length and width obtained from the single-view method (using one-third circumference) duplicated the mean length and width measurements obtained by circumferential viewing.

Animals↗

Hypertrophy of arteriolar smooth muscle cells in the rat small intestine during maturation.

The purpose of this study was to define structural characteristics for vascular smooth muscle (VSM) cells from the submucosal arteriolar system of the rat small intestine during maturation. Arterioles from 6- to 8-week-old and 10- to 12-week-old male WKY animals were selected from tissue prepared for scanning electron microscopy and mounted on end so that the entire circumference of each vessel could be observed by serial photography using scanning electron microscopy. From each vessel segment, the following measurements were made: outer vessel diameter, number of VSM cells occupying a length of vessel, the number of resolutions each VSM cell makes around the vessel, length of individual VSM cells, and width of lateral processes along their length. At a given age, the length and width of the VSM cell was statistically similar for all types of arterioles. However, the VSM cell increased substantially in length and width from the 6-8- to 10-12-week time periods. The outer diameter for a particular arteriolar type also increased with age. These data suggest that the intestinal vasculature as a common population of smooth muscle cells at a given age in terms of their length, size, and process morphology for the various types of arterioles. Furthermore, maturation of the microvessels is associated with a uniform hypertrophy of the VSM cells from the majority of arterioles such that cells of young adult rats and those of juvenile animals represent distinctly different populations.

Aging↗

Vasoactive agents and the mesenteric microcirculation.

Vasoactive agents are known to have a variety of effects on the dynamics of the mesenteric microcirculation. We compare and contrast the effects of both vasodilators and vasoconstrictors on capillary filtration coefficient, vascular permeability, tissue oxygen tension, and microvascular pressure. The various methodologies used to determine the above quantities are discussed, as well as the limitations and advantages of each approach. Discrepancies between the results obtained with particular classes of vasoactive agents are discussed relative to both dosage and route of administration. In addition, data obtained for each parameter using both whole-organ and in vivo microscopic techniques are reconciled relative to the characteristics of each approach. Experimental designs are proposed that may help minimize future inconsistencies in the data, as well as maximize the relative advantages of available techniques.

Animals↗

Intestinal vasoregulation in spontaneously hypertensive rats.

The intestinal vascular responses to graded reductions in arterial pressure and elevations in venous pressure were measured in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Blood flow and capillary pressure were measured in denervated, autoperfused segments of small intestine. Blood flow, capillary pressure, and total vascular resistance were significantly higher in SHR than WKY at the resting mean arterial pressures. Decrements in arterial pressure led to significant reductions in total vascular resistance in WKY but not in SHR. There was a significant tendency for capillary pressure autoregulation in WKY but not in SHR. Increments in venous pressure did not alter vascular resistance in WKY, yet significantly increased total vascular resistance in SHR. The latter effect was due entirely to a rise in precapillary resistance and is consistent with an enhanced sensitivity of the vasculature to myogenic factors. Intestinal blood flow, measured using 15-micro microspheres, was not significantly different between WKY and SHR in innervated preparations. However, in denervated preparations intestinal blood flow was significantly higher in SHR than WKY, indicating that there is a significant neural component to the increased intestinal vascular resistance in SHR.

Animals↗

Cerebral vascular autoregulation of blood flow and tissue PO2 in diabetic rats.

The effect of chronic, severe diabetes mellitus on the morphology, blood flow regulation, and tissue PO2 of the cerebral cortex was evaluated in adult rats. The arterioles of the diabetic animals were enlarged in terms of both lumen diameter and vessel wall area. Although resting blood flow in the diabetic rats was greater than in the normal rats, the autoregulation of cerebral blood flow was very good within an arterial pressure range of 40-150 mmHg, just as in normal rats. The resting tissue PO2 in diabetic rats was 14.9 +/- 0.5 (SEM) compared with 12.7 +/- 0.6 mmHg in normal animals and in both groups remained at or near the resting PO2 at arterial pressures from 40 to 150 mmHg. There was no apparent loss of arterioles on the cortex surface or change in length of individual arterioles in diabetic animals but there was a 20-30% decrease in the number of venules and no change in the length of individual venules. These data indicate that although the arteriolar morphology and number of venules change in the brain during diabetes, physiological function in terms of tissue PO2 and blood flow regulation is maintained within normal limits.

Adenosine↗

Cellular and vessel wall morphology of cerebral cortical arterioles after short-term diabetes in adult rats.

Microvascular pathology is one of the major problems associated with prolonged diabetes mellitus. The purpose of the present study was to determine if anatomical cellular pathology of the cerebral cortical microvessels could be detected very early after the onset of a streptozotocin-induced model of diabetes. Male rats at age 14-16 weeks were hyperglycemic (greater than 250 mg/dl) for 4 weeks prior to scanning and transmission electron microscopic analysis of the external and internal cell and vessel wall morphology of the arterioles. Scanning electron microscopic studies indicated that many processes of vascular smooth muscle cells changed their normal spindle shape to a branched or stellate configuration. The internal cellular changes included swollen mitochondria and cisternae of the endoplasmic reticulum and reduced cytoplasmic staining. Necrosis of arteriolar endothelial cells was evident in virtually every vessel section studied. These data indicate that vascular smooth muscle and endothelial cellular degeneration of cerebral cortical arterioles begins in the very early stages of the streptozotocin model of diabetes.

Animals↗

Arterial and microvascular contributions to cerebral cortical autoregulation in rats.

The responsiveness of the microvasculature and arteries during cerebral cortical autoregulation in rats was determined from measurements of microvascular pressures and blood flow as the systemic arterial pressure was altered. At systemic arterial pressures from 65 to 155 mmHg, cortical blood flow was essentially constant. Arterioles with a resting internal diameter of 20-70 microns responded by nearly equal proportional changes in diameter over this pressure range, but microvascular pressures were a linear function of arterial pressure. The percent of control changes in arterial and microvascular resistances at systemic pressures from 80 to 180 mmHg were nearly identical. Therefore, the microvasculature and arterial vasculature were approximately equally responsive to changes in arterial pressure over most of the autoregulatory pressure range. In addition, the arterial vasculature controlled 45-50% of the total vascular resistance at systemic arterial pressures from 40 to 180 mmHg. These data indicate that the cerebral vascular autoregulation in the rat depended substantially on the approximately equal responsiveness of the arterial vasculature and microvasculature. Similar results have been reported in cats and may indicate a common form of cerebral vascular control, which involves both the microvasculature and brain arteries among different species.

Animals↗

Evidence of myogenic vascular control in the rat cerebral cortex.

The potential presence of myogenic regulation in the cerebral microvasculature of the rat was investigated using a method which alters intravascular pressure without appreciably changing cerebral perfusion pressure (arterial minus venous pressure). The entire rat was placed in a sealed box, with the cranial cavity open to the atmosphere and prepared for in vivo microscopy. By increasing the ambient pressure in the box, both systemic arterial and venous pressure could be changed by nearly equal amounts (+/- 20 mm Hg). Heart and respiratory rates were not influenced by changing ambient pressure by +/- 20 mm Hg. At elevated ambient pressures, cortical arterioles constricted in linear proportion to the ambient pressure, whereas subatmospheric ambient pressures caused vasodilation whose magnitude was about equal at ambient pressures of -6 to -18 mm Hg. The calculated vessel wall tension typically remained within about +/- 10-15% of control during changes of transmural pressure of +/- 20-40%. In all cases, arteriolar responses to changes in ambient and intravascular pressure reached a new steady state within 10-15 seconds and were sustained for up to 30 minutes. These data are interpreted to indicate the presence of a myogenic vascular response in the brain vasculature of the rat.

Animals↗