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H H Dietrich

Publications and source records attributed to H H Dietrich.

At least 19 recordsLinked to original sources
PubMed1996

Local and conducted vasomotor responses in isolated rat cerebral arterioles.

We tested the hypothesis that conduction of vasomotor responses occurs in cannulated and isolated rat cerebral penetrating arterioles. Both at the site of stimulation (local) and 500-650 microns distant from it, we observed the diameter responses and time courses thereof to pressure-ejected vasoactive stimuli. ATP locally caused an initial constriction (response onset at 0.3 s, average diameter 85% of control at 450-ms pulse with a maximum at 1.6 s after stimulation) followed by a secondary dilation (111% at 7 s). Conducted vasodilation of 111% was observed over a distance of 520 microns. Prostaglandin F2 alpha (PGF2 alpha) constricted the vessels locally (80%) and caused conducted vasodilation (110%). For both ATP and PGF2 alpha the local constriction occurred simultaneously to the conducted vasodilation. Adenosine dilated the vessels (123%) but produced only inconsistent conducted vasodilation. Hydrogen ions initially constricted the vessels (88%) and then dilated them to 113%. Thus, although ATP and PGF2 alpha are strong promoters of conduction, adenosine and hydrogen ions are not. Paradoxically, ATP and PGF2 alpha caused conducted vasodilation even though the initial local response was a vasoconstriction, indicating that in cerebral arterioles conduction may be mediated through endothelial cell mechanisms rather than through smooth muscle cell communication.

Acids↗
PubMed1996

Effects of oxyhemoglobin on local and propagated vasodilatory responses induced by adenosine, adenosine diphosphate, and adenosine triphosphate in rat cerebral arterioles.

After subarachnoid hemorrhage (SAH), cerebral arteries display impaired vasomotor control, resulting in decreased regional cerebral blood flow. Recently, propagation of vasomotor responses has been recognized as an important regulatory mechanism in microcirculation. In this study, the authors tested the hypothesis that oxyhemoglobin (OxyHb) inhibits the vasodilatory effect of chemical mediators such as adenosine and adenine nucleotides at a local and/or propagated site. Penetrating intracerebral arterioles were surgically isolated from the middle cerebral arteries of rat brains, cannulated, and observed videomicroscopically in an organ bath under an inverted microscope. The effects of 10(-5) M OxyHb on vasoactive responses to adenosine, adenosine diphosphate (ADP), and adenosine triphosphate (ATP) were examined. The drugs were extraluminally applied either to the bath (10(-10)-10(-3) M) or, using pressure microejection (pipette concentration 10(-2) M), locally. The ATP and ADP initially constricted and then significantly dilated the vessels after both extraluminal application and microapplication. Furthermore, local microstimulation by these drugs produced conducted vasodilation. Adenosine elicited significant vasodilation after both extraluminal and local stimulation. Again, conducted vasodilation was observed. The vasomotor responses that were induced by a maximum local stimulation corresponded in magnitude to those observed at bath concentrations of 10(-5) to 10(-4) M of the same drug. Pretreatment with OxyHb constricted arterioles to an average of 87% of control and blunted extraluminally induced dilation at low concentrations (10(-10)-10(-8)) of ATP and ADP, but did not affect vasodilation induced by 10(-4) M or greater concentrations of ATP, ADP, or adenosine. Although the local response to local microstimulation was unaltered, propagated vasodilation as a response to ATP, ADP, and adenosine was significantly attenuated by OxyHb. These findings indicate that vasodilatory propagation plays an important role in the regulation of brain microcirculation and that its impairment by OxyHb could, in part, explain the cerebral hypoperfusion that is observed after SAH.

Adenosine↗
PubMed1995

The erythrocyte as a regulator of vascular tone.

Local regulation of microvascular blood flow is a complex process in which the needs of the tissue must be communicated to the vasculature, enabling the appropriate matching of O2 supply to demand. We hypothesize that the red blood cell is not only the major O2 carrier but also serves as an O2 sensor and affecter of changes in O2 delivery via its release of ATP, which subsequently binds to P2y receptors on the vascular endothelium, altering vessel caliber. Using the hamster as a model, we determined that the efflux of ATP from red blood cells after exposure to low-PO2 (PO2 = 17 +/- 6 mmHg) and low-pH (pH = 7.06 +/- 0.07) solutions was significantly (P < 0.01) greater than that after exposure to normoxic, normal pH (PO2 = 87 +/- 4; pH = 7.38 +/- 0.04) solutions, indicating that two factors that are associated with an impaired O2 supply relative to demand increase the release of ATP from the red blood cell. To ascertain whether ATP alters vascular caliber, we applied 10(-6) M ATP intraluminally to arterioles of the retractor muscle, using a micropressure system. Vessel diameter increased 8 and 10%, 140 +/- 60 microns upstream of the site of infusion after 50- and 500-ms pulses, respectively. Application of ATP to arteriolar and venular capillaries induced a 31 and 81% increase in red blood cell supply rate, respectively. These results support our hypothesis that the red blood cell is more than just an O2 carrier and has a direct role in the regulation of vascular tone.

Adenosine Triphosphate↗
PubMed1994

N omega-nitro-L-arginine constricts cerebral arterioles without increasing intracellular calcium levels.

The coupling between intracellular Ca2+ concentration ([Ca2+]i) and smooth muscle cell (SMC) contractility is well known, but recent reports suggest that SMCs can contract without an increase in [Ca2+]i. Penetrating arterioles were isolated from rat cortex, cannulated, and loaded extraluminally with fura 2. We used ratio imaging of corresponding vessel wall areas to estimate and correlate [Ca2+]i to the vessel diameter during various extraluminal treatments. Control diameter was 45.6 +/- 3.9 (SE) microns with an estimated [Ca2+]i of 181 +/- 18 nM. Extraluminal papaverine or pH of 6.8 dilated the vessels to 61.0 +/- 6.6 and 57.8 +/- 5.8 microns and decreased [Ca2+]i to 108 +/- 33 and 155 +/- 8 nM, respectively. Alkaline pH of 7.65 or the Ca2+ ionophore ionomycin constricted the arterioles to 34.8 +/- 3.9 and 30.0 +/- 5.8 microns and increased [Ca2+]i to 273 +/- 47 and 853 +/- 155 nM, respectively. These results show an inverse relationship between vessel diameter and [Ca2+]i. Blocking the production of endothelium-derived nitric oxide (EDNO) with N omega-nitro-L-arginine constricted the vessels to 34.4 +/- 3.5 microns without raising but lowering [Ca2+]i to 157 +/- 44 nM. The dissociation of vessel tone and estimated [Ca2+]i after EDNO blocking has not been reported before in cerebral arterioles and may indicate that EDNO regulates vascular tone in a Ca(2+)-independent manner.

Animals↗
PubMed1994

Nitric oxide regulates cerebral arteriolar tone in rats.

BACKGROUND AND PURPOSE: Although cerebral penetrating arterioles are main regulators of the brain microcirculation, little is known about the effect of endothelium-derived relaxation factor on these vessels. This study examined the effects of nitric oxide synthase inhibitors on the spontaneous tone of isolated rat cerebral arterioles. METHODS: Intraparenchymal penetrating arterioles (53 to 102 microns in passive diameter) isolated from Sprague-Dawley rats were cannulated with glass pipettes and subjected to 60 mm Hg of intraluminal pressure. The diameter response to intraluminal and extraluminal treatments was observed with an inverted microscope. RESULTS: Extraluminal application of Nw-nitro-L-arginine (10(-5) mol/L) contracted the arterioles to 63.9 +/- 2.8% (P < .05) of the control diameter. This contracting effect was stereospecific and easily reversed by L-arginine dose dependently (10(-3), 10(-2) mol/L) but not by D-arginine. Intraluminally applied Nw-nitro-L-arginine also induced a similar degree of contraction. Another nitric oxide synthase inhibitor, NG-monomethyl L-arginine (10(-5), 10(-4) mol/L), applied extraluminally induced a dose-dependent contraction to 77.5 +/- 6.6% and 68.6 +/- 5.4% of the control (P < .05), which was also reversed by L-arginine. L-Arginine alone did not significantly affect vessel diameter, however. Treatment with indomethacin, a cyclooxygenase inhibitor, dilated the vessel to 115.2 +/- 7% (P < .05) but did not change the constricting effect of Nw-nitro-L-arginine. CONCLUSIONS: Nw-Nitro-L-arginine and NG-monomethyl L-arginine produce substantial contraction in isolated brain arterioles, suggesting that nitric oxide of brain arterioles is continuously produced within the vessel wall. The dilatory effect of indomethacin appears to be independent of the vasoconstriction induced by nitric oxide synthase inhibitor. In these vessels, the effect of nitric oxide synthase inhibitors is not mediated by an indomethacin-sensitive mechanism. A balance probably exists between factors tending to constrict these arterioles and the elaboration of nitric oxide from endothelial cells, which tends to dilate them. The production of nitric oxide from isolated vessels indicates that parenchymal and vessel wall sources of nitric oxide are probably important in brain microcirculatory regulation.

Animals↗
PubMed1994

Effects of extravascular acidification and extravascular alkalinization on constriction and depolarization in rat cerebral arterioles in vitro.

The relationship between cell membrane potential, vessel diameter, and pH in small cerebral arterioles is not completely understood. This study involved direct, simultaneous measurement of cell membrane potential and vessel diameter at various extracellular pH levels. Arterioles ranging from 44 to 91 microns in diameter were isolated, transferred to a temperature-controlled microscope chamber, which was used as an organ bath, and observed through an inverted videomicroscope. Two vessel cannulation procedures were used: a single-sided cannulation with the other side occluded, and a double-sided and perfused cannulation. After cannulation, the vessels were pressurized to 60 mm Hg intraluminally and the bath temperature was raised to 37 degrees C. Cell membrane potentials of vessel wall cells were obtained after the bath temperature reached 37 degrees C with the vessels partly constricted and again after spontaneous tone (constriction) of the healthy vessels had developed. The effect of extraluminal pH on cell membrane potentials was studied by changing the bath pH from 7.3 to either 7.65 or 6.8 in the single-sided cannulation. The average cell membrane potential for vessels at 37 degrees C, with 60 mm Hg of intraluminal pressure and pH 7.3, was -37.5 mV. The cell membrane potential depolarized to -30.9 mV at pH 7.65 and hyperpolarized to -58.4 mV at pH 6.8, with a slope of 25.8 mV/pH unit. The effect of depolarizing extracellular potassium ions on the cell membrane potential was examined by perfusing two vessels with modified Ringer's solution containing 70 mM KCl. This perfusion method decreased the vessel diameter by 48% and depolarized the observed cell membrane potential from -41.9 to -19.8 mV, with a slope of -0.42 mV per percentage diameter change. These data provide the first measurements of membrane potentials of isolated penetrating arteriole wall cells in vitro. The results indicate that the cell membrane potential relates linearly to the vessel diameter. This new technique opens the possibility for studying vessel response to stimuli under controlled conditions and regulatory mechanisms such as the propagation of vasomotor responses.

Animals↗
PubMed1993

Measurement of hydraulic conductivity in isolated arterioles of rat brain cortex.

We have developed a new method for quantification of arteriolar hydraulic conductivity (Lp) from isolated rat brain vessels. The volume flux of water per unit surface area across the arteriole wall (Jv/S) was assessed from measurements of silicon oil drop movement within an occluded vessel at two to three pressures (between 20 and 70 mmHg); the Lp was derived from the slope of the relationship between Jv/S and applied pressure. Lp was measured in isolated cerebral arterioles 1) at room temperature (22 degrees C) without spontaneous vessel tone (control Lp; n = 11), 2) at room temperature with 10(-4) M adenosine (n = 5), and 3) at 37 degrees C with vessels dilated submaximally with 10(-4) M adenosine (n = 6). Lp at 22 degrees C without adenosine was 13.2 +/- 4.2 x 10(-9) (+/- SE) cm.s-1.cmH2O-1 for all vessels studied. Lp values ranged from 1.2 to 44.1 x 10(-9) cm.s-1.cmH2O-1 with a median value that was 5.9 x 10(-9) cm.s-1.cmH2O-1. Lp increased significantly (on average, 2.6-fold) with adenosine at 37 degrees C but not with adenosine at 22 degrees C. Control Lp bore no relationship to either the development of spontaneous tone or the diameter response to pH change, two recognized indicators of vessel viability.

Adenosine↗
PubMed1993

Ischemia-reperfusion induced microvascular dysfunction in skeletal muscle: application of intravital video microscopy.

Video microscopy of red cell flow in capillaries at the surface of skeletal muscle provided the opportunity to quantitate ischemia-reperfusion (I-R) induced microcirculatory changes, in vivo. Extensor Digitorum Longus (EDL) muscles of 22 male Wistar rats (300-400 g), anesthetized with sodium pentobarbital (Somnotol, 65 mg kg,-1 IP), were used to measure the number of perfused capillaries (CDper: mm-1) crossing lines drawn perpendicular to the muscle axis, and red blood cell velocity (VRBC: mm/s) within individual capillaries from controls (n = 6), and after 2 hr (n = 4), 3 hr (n = 4), and 4 hr (n = 5) of no-flow ischemia with the muscle temperature maintained at its normal value of 32 degrees C. Ischemia was induced by tightening a tourniquet placed around the limb above the EDL muscle. Measurements were made after 30, 60, and 90 min of reperfusion. To test the usefulness of this skeletal muscle model for evaluating proposed interventions in I-R, the effect of hypothermia (24 degrees C) on the microcirculation following 4 hr ischemia (n = 3) was measured. Edema formation was estimated from the wet/dry weight ratio of the ischemic and contralateral control EDL muscles. Capillary perfusion at the surface of the control muscles was remarkably stable over the 5 hr period studied, while significant changes occurred following the ischemic periods. Significantly lower CDper was measured 30 min following all periods of normothermic ischemia. However, unlike the 2 and 4 hr ischemic periods 3 hr normothermic ischemia resulted in a progressive decline in CDper throughout the reperfusion period. VRBC showed evidence of a hyperemic response following 2 hr normothermic ischemia (control: 0.12 mm/s +/- 0.19 compared to 0.26 mm/s +/- 0.03 following 90 min reperfusion; mean +/- sem). However, no such hyperemia was measured following either 3 or 4 hr normothermic ischemia (i.e., 3 hr control: 0.24 mm/s +/- 0.01 compared to 0.07 mm s +/- 0.003 following 90 min reperfusion). In fact, VRBC was essentially zero 90 min following 4 hr normothermic ischemia (0.01 mm/s +/- 0.01). However, when the muscle was allowed to cool to 24 degrees C during 4 hr ischemia no significant change in either VRBC or CDper was measured compared to pre-ischemic controls. Evidence of edema was found after 3 and 4 hr normothermic ischemia. This study establishes a skeletal muscle model of I-R, which may be useful in testing hypotheses regarding mechanisms of I-R injury, and effectiveness of proposed treatments of I-R.

Animals↗
PubMed1992

Microvascular flow response to localized application of norepinephrine on capillaries in rat and frog skeletal muscle.

Recently, Dietrich (1989, Microvasc. Res. 38, 125-135) demonstrated that a local application of a minute amount of norepinephrine (NE, 5.5 mM, 0.01-88 pmole) on a capillary in rat mesentery can elicit constriction of the feeding arteriole 0.5-1.0 mm away. This constriction can reduce or even stop blood flow in capillaries supplied by the arteriole. The main objective here was to show that the phenomenon of reduced flow occurs not only in the rat mesentery but also in other tissues and species. We chose to study the rat tibialis anterior and frog sartorius muscles. Using the same intravital video-microscopic approach as in the mesentery, strong NE stimuli (3 mM) were applied iontophoretically 48 times to 19 capillaries in 10 rats anesthetized with pentobarbital. They resulted in significant reductions (average: 80%) of the red blood cell velocity (VRBC) in capillaries. The onset of these reductions (i.e., 10% decrease from control) occurred within 3-52 sec (average: 20.9 sec) from the time of NE application. Reductions lasted 6.0 min. The same stimuli were applied 42 times to 15 capillaries in 6 frogs anesthetized with urethane. The average VRBC reduction was 86%. The onset occurred within 30.6 sec while the reduction lasted 6.6 min. Under the same conditions, arteriolar diameters in the sartorius muscle decreased significantly from 28.5 to 22.5 microns (n = 8). We also used local microinjection of small droplets of NE (30 mM) to 13 capillaries in 7 frogs. This resulted in a significant VRBC reduction of 64% with an onset time of 44.2 sec and a reduction duration of 17.2 min. Weak NE stimuli (3 microM) applied iontophoretically to 10 capillaries in 5 frogs resulted in marginal, but significant, VRBC reductions (9%). The present study demonstrates that the phenomenon of reduced flow after local application of NE may be a general phenomenon as it occurs also in skeletal muscle in both rat and frog. Our accompanying paper addresses the hypothesis that the phenomenon reflects communication of a NE-induced signal along the capillary.

Animals↗
PubMed1992

Capillary as a communicating medium in the microvasculature.

The preceding study (Dietrich and Tyml, 1992. Microvasc. Res. 43) demonstrated that a local application of norepinephrine (NE) on a capillary in a skeletal muscle produces a temporary reduction in blood flow within this capillary. The reduction is mediated via constriction of the supplying arteriole. The objective of the present study was to address the mechanism by which the local NE stimulus is propagated from the capillary to the arteriole. Using intravital video microscopy we measured red blood cell velocity in capillaries, and diameter of supplying arterioles, in the sartorius muscle in anesthetized frogs. Velocity responses were measured following iontophoretic application of NE (3 mM in the pipette) on the capillary, with or without pretreatment with 0.9 mM tetrodotoxin (nerve-specific sodium channel blocker), 30 mM lidocaine (nonspecific sodium channel blocker), and 30 mM yohimbine (alpha 2-receptor blocker). Diameter responses were measured before and after capillary damage introduced by microcautery. Tetrodotoxin did not block the NE-induced velocity reduction (i.e., from 0.2 to 0.07 mm/sec), while lidocaine attenuated it. Yohimbine blocked it only when applied on the same site as NE. Capillary damage abolished the NE-induced arteriolar constriction (i.e., from 27.8 to 21.5 microns). We conclude that the observed responses were not due to (1) direct diffusion of NE from the capillary to the arteriole, (2) conduction along adrenergic nerves, or (3) venous-arteriolar diffusional cross-talk. We interpret our data to indicate that the capillary itself could function as a communicating medium.

Animals↗
PubMed1989

Effect of locally applied epinephrine and norepinephrine on blood flow and diameter in capillaries of rat mesentery.

Epinephrine (5.5 mM; quantity: 0.01-87 pmole) and norepinephrine (5.9 mM; quantity: 0.01-88 pmole) were applied to 144 and 26 mesenteric capillaries, respectively, in 39 rats. Neither of these agents had a significant effect on the mean capillary diameter (control diameter before epinephrine application: 9.6 +/- 3.6 microns SD; before norepinephrine application: 11.4 +/- 6.6 microns SD). Unexpectedly, in 36% of the epinephrine applications and 49% of the norepinephrine applications, capillary blood flow was either reduced (epinephrine: within 6-61 sec; norepinephrine: within 3-36 sec) or stopped completely (epinephrine: within 8-124 sec; norepinephrine: 11-124 sec). These reductions (duration: 12 sec-32 min for epinephrine; 21 sec-12 min for norepinephrine) were associated with flow reductions in all neighboring capillaries fed by a common supplying arteriole. In order to check the possible direct effect of drug diffusion norepinephrine was applied at increasing distances up to 400 microns from the arteriole. For all such distances arterioles constricted much quicker than predicted by diffusion. Fluorescent staining using glyoxylic acid showed the presence of adrenergic nerves around arterioles, along capillaries as well as in the avascular tissue. It is concluded that conduction along nerves, or possibly via endothelial cell-to-cell communication, could explain the intriguing retrograde effect of locally applied drugs on the supplying arteriole.

Animals↗
PubMed1989

[Ophthalmologists on postage stamps. A contribution to the history of medicine].

An attempt should be made to summarize the history of ophthalmology in a small series of postage stamps. Eighteen stamps could be dedicated to themes recalling the achievements of famous ophthalmologists. In this way it would be possible to acquaint the public with some medical history while at the same time encouraging an interesting leisure pastime.

Europe↗
PubMed1985

In vivo micro application of adrenaline to capillaries in frog mesentery.

In-vivo studies were carried out on frog mesentery in order to determine the precise and specific actions of micropipette application of adrenaline on arterioles, precapillary sphincters and capillaries. A technique was employed, using liquid paraffin and micropipettes to deliver droplets to a particular microvessel; the droplets varied between 10-20 microns in diameter. All vessel types, including segments of capillaries, demonstrated constrictor responses to the local application of adrenaline. The time course of these constrictor events varied with the vessel type, with the sphincter being the most rapid in response.

Animals↗