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Biomedical subjects

H Henrich

Publications and source records attributed to H Henrich.

At least 37 records · Page 2Linked to original sources
PubMed1979

[Caries in supporting teeth with and without crowns].

On the basis of 1718 teeth in 212 patients fitted with removable partial dentures, it was established that the frequency of caries in uncontrolled noncrowned abutment teeth for partial dentures was twice as high and the number of extractions three times as high as in the control group. The special risk for abutment teeth was effectively reduced by using artificial crowns. The concept of crowning abutment teeth is discussed.

Crowns↗
PubMed1978

A video-angiometer for simultaneous and continuous measurement of inner and outer vessel diameters. Technical report.

A system is described for continuously measuring vessel diameters. It bases on the evaluation of video signal differences of a video camera which are induced by light intensity differences (grey levels) caused by the vascular wall structures. The system is electronically linear, automatically measuring and in addition eyeball controlled by the human sensor: the inaccuracy does not exceed the 5% level.

Blood Vessels↗
PubMed1978

Structural differences in the mesentery microcirculation between normotensive and spontaneously hypertensive rats.

The mesentery preparation of normotensive rats (NR) (Pcarotis97 +/- 4 mm Hg) and of spontaneously hypertensive rats (SHR) (161 +/- 2 mm Hg) of comparable age (20 +/- 3 weeks) was used to study morphological changes of the microvasculature in established hypertension. The arterioles, classified according to their branching order, had an increased inner diameter in SHR (by 20%). The smooth muscle hypertrophy decreased with smaller vessel size. Pre- and postcapillary vessels were shorter in SHR than in NR by 17 to 35%. The number of these vessels related to the number of the feeding terminal arterioles was found to be reduced by nearly 50% in SHR. The data suggest a lowered arteriolar flow resistance in individual vessels of the hypertensive group concomitant with a gradually disappearing smooth muscle hypertrophy towards the capillary bed. The elevation of the resistance to blood flow in the hypertensive rats is obviously caused by a reduced number of resistance vessels, as seen in the mesentery vascular bed. Similar results were obtained in the true capillaries, which showed greater inner diameters (SHR vs NR:7.2 micron vs 6.4 micron), shortened lengths (141 vs 170 micron) and a reduced number (50 vs 70). Red cell velocity in true capillaries did not differ (0.51 mm/s vs 0.49 mm/s). Arterio-venous shunt vessels were described with an average inner diameter of 11 micron. In SHR these vessels were shorter (424 vs 654 micron) and increased in number. The 'hydraulic hindrance' of AV-shunt vessels and true capillaries together was decreased in SHR; the surface area did not differ between SHR (55.7 . 10(3) micron2) and NR (50.1 . 10(3) micron2) suggesting no major variation in the exchange functions.

Animals↗
PubMed1978

Intravital measurement of arteriolar pressure and tangential wall stress in normotensive and spontaneously hypertensive rats (established hypertension).

Under intravital conditions, intravascular pressures of mesenteric resistance vessels were measured in normotensive (NR, mean blood pressure 92 mm Hg) and spontaneously hypertensive rats (SHR, 161 mm Hg) being elevated over all by about 75%; the tangential wall stress (sigma = p.r/h; p represents the intravascular pressure and r/h the ratio of internal radius to wall thickness) was found to be increased by 120-140% in SHR.

Animals↗
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

Effect of beta-sympatholytic agents on vascular responses to noradrenaline and potassium chloride.

Vasoconstrictory responses to noradrenaline (NA) or high potassium chloride (130 mM) usually show a biphasic behaviour: an initial peak is followed by a lower steady state level. The influence of three beta-sympatholytic agents (propranolol, pindolol, practolol) and a "Ca-antagonist" (verapamil) on this particular behaviour of KCl-induced vasoconstrictions was compared with responses to NA. Studies were performed on the intact vascular bed of an isolated intestinal preparation of the rat. 1. Increases in the concentration of propranolol and pindolol from 10(-10) to 10(-6) M attenuated the vascular responses to high KCl. Practolol, however, distinctly enhanced the KCl-responses. NA (1.3 microgram/ml)-elicited vasoconstriction was found to be influenced in a similar manner by the beta-receptor antagonists used, though lower concentrations of pindolol had an enhancing, higher concentrations a reducing effect on the constrictory responses to NA. 2. The extent to which the biphasic response adjusted to the steady state level was concentration-dependently increased KCl-responses and significantly decreased to a monophasic response to NA, in the presence of the beta-sympatholytic agents. 3. By using a quotient of deltaPs (steady-state phase) to deltaPi (initial vasoconstriction) and by comparing the effect of the three beta-sympatholytic agents with that of verapamil on this quotient showed a concentration-dependent decrease in presence of the beta-sympatholytic as well as of the Ca-antagonistic agents. These myotropic actions, i.e. negative influences on the mechanism of vascular smooth muscle activation ranged in the following sequence: Verapamil greater than propranolol greater than pindolol greater than practolol. 4. The mechanism underlying the biphasic responses to high potassium chloride are concluded to be basically different from the NA-responses because they are inversely affected by beta-sympatholytic agents. The steady-state response to KCl was found to be very sensitive to non-specific pharmacological actions of beta-sympatholytic substances. The myotropic action of the beta-receptor antagonists is compared with that of the Ca-antagonist verapamil and the role of calcium in the mechanism of activation of vascular smooth muscle is discussed.

Adrenergic beta-Antagonists↗
PubMed1976

Effect of occlusion duration on reactive hyperemia in sartorius muscle capillaries.

Reactive hyperemia was studied in cat sartorius muscle by measurement of venous outflow and capillary red cell velocity following occlusions of 5-120 s. The peak value for volume flow rose in a graded manner as occlusion duration increased, reaching a level of 280% above control following 120 s of occlusion. By contrast, peak values for capillary flow were 200% above control even after short (10-15 s) occlusions and increased moderately thereafter to 280% above control following 120-s occlusions.

Animals↗
PubMed1975

Oxygen supply and uptake in the liver and the intestine.

The oxygen supply to the liver was found to be dependent on the total blood flow only and not on the ratio of arterial to portal contribution. The mean value of O2-uptake in the liver, related to a blood flow of 110 ml/min - 100 g liver, amounted to 6.08 +/- 0.2 ml O2/min - 100 g liver (mean +/- S.E.M.). O2-uptake of the intestine was found to be 1.95 +/- 0.13 ml O2/min - 100 g tissue, related to a normal blood flow of 50 ml/min - 100 g tissue. With low oxygen supply O2 extraction in the liver reaches values of 97%, whereas the intestinal extraction does not surpass 75%. A rise in oxygen supply surmounting normal values does not increase the O2-consumption. Contrary to the intestinal circulation the liver showed no postocclusive vasodilatation. The oxygen debt was payed back by a greater extraction. The portal oxygen supply to the liver can markedly increase due to intestinal metabolic hyperemia. High O2-extraction capacity, rather than vasodilatation, is the main mechanism for matching hepatic oxygen supply with requirements. The hepatic venous blood may leave the liver with an extremely low O2-content.

Animals↗