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P Weinbrecht

Publications and source records attributed to P Weinbrecht.

5 recordsLinked to original sources
PubMed1990

Histamine elicits competing endothelium-dependent constriction and endothelium-independent dilation in vivo in mouse cerebral arterioles.

We used television microscopy and an image-splitting technique to monitor the changes in diameter produced by histamine applied locally to mouse pial arterioles in vivo. A high dose (50 micrograms/ml, 3 X 10(-4) M) of histamine constricted the arterioles, whereas lower doses (20 and 10 micrograms/ml) relaxed them. Constriction was blocked and dilation occurred when selective injury of the endothelium was produced by light from a helium-neon laser in the presence of intravascular Evans blue. From this we conclude that the constriction was endothelium-dependent and was caused by the release of an endothelium-derived constricting factor. Constriction was also blocked by each of two antagonists of the H1 histamine receptor and by pretreatment of the arterioles with indomethacin. H1 blockade unmasked a dilating action of 1 micrograms/ml histamine, a dose too low to affect the diameter of arterioles not treated with the H1 blocker. An H2 blocker interfered with the relaxation by low-dose (10 micrograms/ml, 6 X 10(-5) M) histamine. These data indicate that for mouse pial arterioles, histamine can interact with H1 receptors on the endothelium to release an endothelium-derived constricting factor that causes constriction of the underlying muscle while simultaneously interacting with H2 receptors in the muscle that mediate relaxation of the vessel.

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PubMed1987

Cerebral microcirculatory changes during exposure to hypoxia.

Changes in the red blood cell content of the cat cerebral cortical vessels were monitored using reflecting light during a decrease in PIO2. The following observations were made: 1) the capillary bed red blood cell content increased during hypoxia prior to the arteriole response at an arterial oxygen tension of 52.0 mmHg; 2) at arterial oxygen tensions below 52 mmHg the red blood cell content increased in all vessels simultaneously; 3) as the PIO2 decreased, the increase in red blood cell content occurred earlier in all vessels. Capillaries, therefore, can respond to hypoxia independently of the arteriole in cat cerebral cortical tissue.

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PubMedDate not supplied

Endothelium dependence of a portion of the response to cGMP in brain microcirculation of mice.

The diameters of arterioles 30-40 microns on the surface of the mouse brain were monitored by TV microscopy with an image splitting technique. Endothelium was injured by light from a helium neon laser in the presence of intravascular Evans blue. This method was previously shown to selectively eliminate dilation by known endothelium dependent dilators which cause endothelial cells to release one or more relaxing factors (EDRFs). Dilation was produced by local application of 8 Br cGMP and dibutyryl cAMP, 10(-5) M. The response before endothelial damage was compared with the response after damage. Two separate studies were conducted. In one, 10 mice were treated with 8 Br cGMP and 10 with dibutyryl cAMP. In the second study 12 mice were treated with each nucleotide before endothelial injury and again after injury. In both studies only the response to 8 Br cGMP was impaired (p less than .01) by the endothelial injury. These data suggest that in these arterioles a portion of the response to GMP, but not to AMP, is controlled by endothelium and may reflect a role for guanylate cyclase/GMP in the synthesis/-release of an EDRF. This would provide a function for the guanylate cyclase in endothelial cells. The function of guanylate cyclase within these cells has not previously been defined.

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PubMedDate not supplied

Propagated constriction in mouse pial arterioles: possible role of endothelium in transmitting the propagated response.

Two lines of evidence are presented demonstrating propagated constriction in mouse pial arterioles. First, a 2 second microapplication from a 6 micron pipette tip of approximately 12 nanoliters of BaCl2 or uridine triphosphate produced constrictions which spread to points 300 microns or more upstream from the point of application. Second, constrictions were elicited between 2 points of endothelial injury, each made with a focused laser beam 18 microns wide. A helium-neon laser was used in the presence of intravascular Evans blue. The constrictions were produced when a very brief exposure at a downstream site was followed by a more prolonged exposure at an upstream site 300 to 1100 microns from the downstream injury. In approximately half the cases the upstream damage elicited a local platelet aggregate. Therefore, vasoconstrictors released by aggregating platelets may have played a role in initiating constriction. Constriction was limited to the segment between the two endothelial injuries. The necessity for 2 injuries, rather than one, suggests that local losses of endothelium derived vasodilators also played a role in initiating constriction and/or permitting its propagation. Abrupt cessation of constriction at the sites of endothelial damage suggests that endothelium plays a role in propagation of constriction. Propagated constriction may play a role in amplifying the spasmotic effects of local subarachnoid hemorrhage or in the spread of constriction beyond local areas of reduced metabolic demand.

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