Vascularization of the brains of the Atlantic and Pacific hagfishes, Myxine glutinosa and Eptatretus stouti: a scanning electron microscope study of vascular corrosion casts

The microvascularization of the brains of the hagfishes, Myxine glutinosa L. and Eptatretus stouti, were studied by scanning electron microscopy (SEM) of microvascular corrosion casts. Sections of these casts were used to determine the vascular territories of defined brain areas. Histological serial sections (10 microm) of the brains served for correlation of findings. Analysis of the microvascular casts of both species revealed that the blood supply to and from these brains arose ventrally and dorsally, respectively. Neither species possesses an arterial circle (Circulus Willisi) and both have similar microvascular patterns. The only difference between Myxine and Eptatretus was that the posterior cerebral artery in Myxine divides into mesencephalic and rhombencephalic branches, and in Eptatretus a third branch, termed telencephalic branch, arises from the posterior cerebral artery. 3D-morphometry revealed that luminal diameters of: 1) intracerebral arteries and arterioles range from 35.11 +/- 5.66 microm (mean +/- SEM) in the hypothalamus to 92.69 +/- 14.48 microm in the thalamus; 2) capillaries range from 17.8 +/- 0.44 microm in the olfactory bulb to 21.70 +/- 0.87 microm in the basal ganglia; and 3) intracerebral venules and veins range from 49.38 +/- 4.17 microm in the hypothalamus to 75.58 +/- 6.59 microm in the rhombencephalon. Interbranching distances of arteries and arterioles range from 179.19 +/- 11.32 microm in the optic tectum to 235.19 +/- 94.64 microm in the hypothalamus. Capillaries range from 91.07 +/- 6.22 microm in the hypothalamus to 116.15 +/- 9.45 microm in the thalamus, and venules and veins range from 137.30 +/- 18.11 microm in the hypothalamus to 189.83 +/- 17.47 microm in the optic tectum. Intervascular distances range from 70.58 +/- 3.58 microm in the olfactory bulb to 89.52 +/- 5.74 microm in the optic tectum. Branching angles of arteries and arterioles range from 38.39 +/- 10.9 degrees in the olfactory bulb to 100.73 +/- 9.4 degrees in the optic tectum, and the branching angles of capillaries range from 74.40 +/- 5.42 degrees in the optic tectum to 90.24 +/- 4.66 degrees in the olfactory bulb. Finally, the branching angles of the venules and veins range from 67.84 +/- 6.83 degrees in the tegmentum of the mesencephalon to 92.30 +/- 6.35 degrees in the optic tectum.     

Analysis of the structural parameters of the blood flow pathways in the microcirculatory system]

The reconstruction of the mesenterium microcirculatory bed was performed intravitally in albino rats and cats after biomicrophotograms. The number, length and caliber of arterioles, pericapillary arteriolec, capillaries, postcapillary venules and venules of the mesenterium were measured. According to these data summary indices of the cross section, surface and volume of the vessels of various functional subdivisions of the microcirculatory bed were calculated. The blood volume entering the microcirculatory system of the albino rat's mesenterium is distributed in the vessels as follows: 8,4% -- arterioles, 10,2% -- pericapillary arterioles, 41,9% -- capillaries, 22,1% -- postcapillary venules and 17,4% -- venules. Similar correlations were found in the cat. The working surface of capillaries is 60--70% of the working surface of all the vessels of the mesenterial microcirculatory system. The evidence of the functional variability of the microcirculatory bed geometry depending on the tissue needs in blood supply is presented.     

Oxygen tension in cerebral microvessels in acute anaemia in rats

Using polarographic oxygen microelectrodes, distribution of oxygen tension (pO2) in the rat cerebral arterioles (with a lumen diameter of 8-80 microm) and venules (with a lumen diameter of 8-120 microm) has been studied in acute reduction of haemoglobin concentration in the blood. Isovolumic haemodilution with 5 % albumin solution has been performed stepwise from 14 g/dl (control) to 10 g/dl (step 1), 7 g/dl (step 2) and to 4.6 g/dl (step 3). It was shown that step 1 of haemodilution led to no impairment of oxygen supply to the brain cortex. Step 2 resulted in moderate increase of pO2 in arterioles, whereas in venules oxygen tension fell down substantially (on the average, to 32 mm Hg). Step 3 resulted insignificant increase of pO2 in arterioles. A further fall of pO2 (to 27 mm Hg) in studied venules was recorded. The portion of venules with low pO2 grew to 31% (only 3 % in control). Microregions with a near-to-zero pO2 were recorded in some capillaries. This indicates presence of hypoxic zones in brain tissue. Hypoxic and anoxic microregions originate at this stage of anemia in locations with relatively low and/or impaired blood supply.     

TNF-alpha activation of arterioles and venules alters distribution and levels of ICAM-1 and affects leukocyte-endothelial cell interactions

The observation that leukocyte-endothelial cell (EC) interactions are localized to specific regions on the microvessel wall suggests that adhesion molecule distribution is not uniform. We investigated ICAM-1 distribution and leukocyte-EC interactions in blood-perfused microvessels (<80 mum) in cremaster muscle of anesthetized mice, using intravital confocal microscopy and immunofluorescent labeling. Variability of ICAM-1 expression directly determines leukocyte adhesion distribution within the venular microcirculation and contributes to leukocyte rolling in arterioles during inflammation. The number of rolling interactions increased with ICAM-1 intensity (r(2) = 0.69, P < 0.05), and rolling velocity was lower in regions of higher ICAM-1 intensity. In controls, venular ICAM-1 expression was approximately twofold higher than in arterioles. After TNF-alpha treatment, ICAM-1 expression was significantly increased, 2.8 +/- 0.2-fold in arterioles and 1.7 +/- 0.2-fold in venules (P < 0.05). ICAM-1 expression on activated arteriolar ECs only reached the level of control venular ICAM-1. Arteriolar but not venular ECs underwent redistribution of ICAM-1 among cells; some cells increased and some decreased ICAM-1 expression, magnifying the variability of ICAM-1. TNF-alpha treatment increased the length of bright fluorescent regions per unit vessel length (42%, control; 70%, TNF-alpha) along the arteriolar wall, whereas no significant change was observed in venules (60%, control; 63%, TNF-alpha). The spatial distribution and expression levels of adhesion molecules in the microcirculation determine the timing and placement of leukocyte interactions and hence significantly impact the inflammatory response. That arteriolar ECs respond to TNF-alpha by upregulation of ICAM-1, although in a different way compared with venules, suggests an explicit role for arterioles in inflammatory responses.     

Longitudinal oxygen gradients in cerebra micro vessels in acute anaemia in rats

Using a fine-tip oxygen microelectrodes the longitudinal gradients of oxygen tension (pO2) have been studied in small arterioles (with lumen diameter in control of 5 +/- 20 microm) and in capillaries of the rat brain cortex during stepwise decrease of the blood haemoglobin concentration [Hb] from control [Hb]--14.4 +/- 0.3 g/dl to 10.1 +/- 0.2 g/dl (step 1), 7.0 +/- 0.2 g/dl (step 2) and 3.7 +/- 0.2 g/dl (step 3). All data are presented as "mean +/- standard error". Oxygen tension was measured in arteriolar segments in two locations distanced deltaL = 265 +/- 34 microm, n = 30. Mean diameter of studied arterioles was 10.7 +/- 0.5 microm, n = 71. Length of studied capillary segments was about deltaL = 201 +/- 45 Mm, n = 18. The measured longitudinal pO2 gradient (deltapO2/deltaL) in arterioles amounted 0.03 +/- 0.01 mmHg/microm, n = 15 in control; 0.06 +/- 0.01 mmHg/microm, n = 16 (step 1); 0.07 +/- +/- 0.01 mmHg/microm, n = 14 (step 2); 0.1 +/- 0.01 mmHg/microm, n = 30 (step 3). In the capillaries, the deltapO2/deltaL amounted to: 0.07 +/- 0.01 mmHg/microm, n = 17 (control); 0.09 +/- 0.02 mmHg/microm, n = 16 (step 1); 0.08 +/- 0.01 mmHg/microm, n = 15 (step 2); 0.1 +/- 0.02 mmHg/microm, n = 18 (step 3). An over threefold decrease in the system blood oxygen capacity did not result in significant changes (p > 0.05) of the deltapO2/deltaL in capillaries that might result in relatively homogeneous oxygen flux from blood to tissue in acute anaemia. The longitudinal gradients of blood O2 saturation (deltaSO2/deltaL) in studied arterioles and capillaries were obtained using oxygen dissociation curve (ODC) of haemoglobin in the system blood. The gradients deltaSO2/deltaL in capillaries was shown to be threefold higher than the corresponding gradients in arterioles. The data show that anatomic capillaries are the main source of oxygen to brain tissue as in control and in hypoxic conditions. Sufficient oxygen delivery to brain tissue in acute anaemia is maintained by compensatory mechanisms of cardiovascular and respiratory systems. The data presented are the first measurements of the longitudinal pO, gradients in capillaries and minute cortical arterioles at acute anaemia.     

Sexual dimorphism in the permeability response of coronary microvessels to adenosine

Gender influences volume regulation via several mechanisms; whether these include microvascular exchange, especially in the heart, is not known. In response to adenosine (Ado), permeability (P(s)) to protein of coronary arterioles of female pigs decreases acutely. Whether Ado induces similar P(s) changes in arterioles from males or whether equivalent responses occur in coronary venules of either sex has not been determined. Hypotheses that 1) basal P(s) properties and 2) P(s) responses to vasoactive stimuli are sex independent were evaluated from measures of P(s) to two hydrophilic proteins, alpha-lactalbumin and porcine serum albumin (PSA), in arterioles and venules isolated from hearts of adult male and female pigs. Consistent with hypothesis 1, basal P(s) values of both microvessel types were independent of sex. Contrary to hypothesis 2, P(s) responses to Ado varied with sex, protein, and vessel type. Confirming earlier studies, Ado induced a approximately 20% decrease in P(s) to both proteins in coronary arterioles from females. In arterioles from males, Ado did not change P(s) for alpha-lactalbumin (P(s)(alpha-lactalb), 3 +/- 13%), whereas P(s) for PSA (P(s)(PSA)) decreased by 27 +/- 8% (P < 0.005). In venules from females, Ado elevated P(s)(PSA) by 44 +/- 20% (P < 0.05), whereas in those from males, Ado reduced P(s)(PSA) by 24 +/- 5% (P < 0.05). The variety of outcomes is consistent with transvascular protein and protein-carried solute flux being regulated by multiple sex-dependent mechanisms in the heart and provides evidence of differences in exchange homeostasis of males and females in health and, likely, disease.     

The cytoarchitecture of the wall and the innervation pattern of the microvessels in the rat mammary gland: a scanning electron microscopic observation

This report describes the morphology of the smooth muscle cells, pericytes, and the perivascular autonomic nerve plexus of blood vessels in the rat mammary gland as visualized by scanning electron microscopy after removal of connective-tissue components. From the differences in cellular morphology, eight vascular segments were identified: 1) terminal arterioles (10-30 microns in outer diameter), with a compact layer of spindle-shaped and circularly oriented smooth muscle cells; 2) precapillary arterioles (6-12 microns), with a less compact layer of branched smooth muscle cells having circular processes; 3) arterial capillaries (4-7 microns), with " spidery " pericytes having mostly circularly oriented processes; 4) true capillaries (3-5 microns), with widely scattered pericytes having longitudinal and several circular processes; 5) venous capillaries (5-8 microns), with spidery pericytes having ramifying processes; 6) postcapillary venules (10-40 microns), with clustered spidery pericytes; 7) collecting venules (30-60 microns), with a discontinuous layer of circularly oriented and elongated stellate or branched spindle-shaped cells which may represent primitive smooth muscle cells; and 8) muscular venules (over 60 microns), with a discontinuous layer of ribbon-like smooth muscle cells having a series of small lateral projections. No focal precapillary sphincters were found. The nerve plexus appears to innervate terminal arterioles densely and precapillary arterioles less densely. Fine nerve fibers are only occasionally associated with arterial capillaries. Venous microvessels in the rat mammary gland seemingly lack innervation.     

T4-induced cardiac hypertrophy and the perfused and total microvasculature of the heart

The purpose of the present investigation was to determine the effects of thyroxine (T4), which induces myocardial hypertrophy, on the number per square millimetre and volume per cubic millimetre of both the total and perfused portions of the arteriolar and capillary beds of the heart. Studies were conducted in the subendocardial and subepicardial regions of the left ventricle of anesthetized open-chest rabbits. Fluorescein isothiocyanate-dextran (i.v.) or radioactive microspheres (intra-atrial) were injected to label the perfused microvessels or to determine coronary flow in three groups of rabbits: controls, and rabbits given 0.5 mg/kg T4 for 3 days and for 16 days. Fluorescent photography was used to identify the perfused microvessels. An alkaline phosphatase stain was employed to locate the total microvascular bed. There were 2369 +/- 638 (SD) capillaries/mm2 and 4 +/- 3 arterioles/mm2 in control hearts. These decreased significantly to 1380 +/- 199/mm2 and 1 +/- 1/mm2, respectively, after 16 days of T4. In controls, 60 +/- 5% of the capillaries and 59 +/- 21% of the arterioles were perfused. This increased significantly to 90 +/- 5 and 86 +/- 18%, respectively, by 16 days of T4 treatment. Similar changes, although smaller, were observed after 3 days of T4. Coronary blood flow increased to 1.7 times control after 3 days and 2.9 times after 16 days of T4. No significant subepicardial versus subendocardial differences were observed in any condition or measurement. Thus, the physiological response to the increased work and increase in anatomic minimum diffusion distance is to increase flow and the proportion of the capillary bed perfused to at least maintain physiological diffusion distances.     

Impact of myocardial structure and function postinfarction on diastolic strain measurements: implications for assessment of myocardial viability

Venular control of arteriolar perfusion has been the focus of several investigations in recent years. This study investigated 1) whether endogenous adenosine helps control venule-dependent arteriolar dilation and 2) whether venular leukocyte adherence limits this response via an oxidant-dependent mechanism in which nitric oxide (NO) levels are decreased. Intravital microscopy was used to assess changes in arteriolar diameters and NO levels in rat mesentery. The average resting diameter of arterioles (27.5 +/- 1.0 microm) paired with venules with minimal leukocyte adherence (2.1 +/- 0.3 per 100-microm length) was significantly larger than that of unpaired arterioles (24.5 +/- 0.8 microm) and arterioles (23.3 +/- 1.3 microm) paired with venules with higher leukocyte adherence (9.0 +/- 0.5 per 100-microm length). Local superfusion of adenosine deaminase (ADA) induced significant decreases in diameter and perivascular NO concentration in arterioles closely paired to venules with minimal leukocyte adherence. However, ADA had little effect on arterioles closely paired to venules with high leukocyte adherence or on unpaired arterioles. To determine whether the attenuated response to ADA for the high-adherence group was oxidant dependent, the responses were also observed in arterioles treated with 10(-4) M Tempol. In the high-adherence group, Tempol fully restored NO levels to those of the low-adherence group; however, the ADA-induced constriction remained attenuated, suggesting a possible role for an oxidant-independent vasoconstrictor released from the inflamed venules. These findings suggest that adenosine- and venule-dependent dilation of paired arterioles may be mediated, in part, by NO and inhibited by venular leukocyte adherence.     

Differentiation of blood vessels in the adipose tissue of lean and obese fetal pigs, studied by differential enzyme histochemistry

Subcutaneous adipose tissue was obtained from fetuses removed from pregnant obese (Ossabaw) and lean (crossbred) sows at three stages of gestation (70, 90, and 110 days). Histochemical analysis for nucleo-side phosphatase (NPase), alkaline phosphatase (APase), and NADH tetrazoleum reductase (NADH-TR) was conducted on fresh-frozen cryostat sections. Age- associated changes in NPase and NADH-TR reactions in the arteriolar system were correlated with the morphological development of the medial layer of arterioles and arteries. For instance, a strong NPase reaction in small arterioles was associated temporally with the assumption of a normal smooth muscle cell morphology and arrangement in the medial layer. In the youngest fetuses, strong NADH-TR reactions were only evident in small and presumptive arterioles and venules (associated with fat cells). Little NADH-TR reactivity was evident in larger arterioles and venules in 70-day tissue. Arteries and large arterioles were distinguished from veins and venules (strong reactions vs. weak reactions) with NADH-TR and NPase reactions in the oldest fetuses. In the younger fetuses, the NPase distinction (arterioles vs. veinules) was obvious before NADH-TR distinction. Small adipocyte-associated vessels were APase positive in the youngest fetuses, but APase reactivity was limited to short segments of vessel between arterioles and capillaries in the oldest fetuses. With the following exceptions, all the above observations were independent of fetal strain. In obese fetuses (110 day) small venules and small arterioles were equally reactive for NPase activity. Capillaries in obese fetuses (110 day) were NADH-TR reactive, whereas no activity was evident in capillaries from lean fetuses (110 day).(ABSTRACT TRUNCATED AT 250 WORDS)     

Oxygen diffusion through the venule walls in the rat cerebral cortex during breathing with pure oxygen

Using oxygen microelectrodes, distribution of oxygen tension (pO2) has been studied in venules of the rat brain cortex at normobaric hyperoxia (spontaneous breathing with pure oxygen). It has been shown that inhalation of oxygen results in sharp increase of pO2 in majority of the venules under study. The pO2 distribution along the length of venous microvessels of 7-280 microns in diameter is best approximated by equation: pO2 = 76.44 e-0.0008D, n = 407. The pO2 distribution was characterised by extremely high pO2 values (180-240 mm Hg) in some minute venules. Heterogeneity of pO2 distribution in venous microvessels at hyperoxia was shown to be significantly increased. Profiles of pO2 between neighbouring arterioles and venules were for the first time measured. The data clearly evidenced that O2 diffusional shunting took place between cortical arterioles and venules, provided they were distanced from each other for not over 80-100 microns. Distribution of pO2 in venules has been shown to be dependent on the blood flow in the brain cortical microvessels.     

Peripheral vascularization of the dermal laminae of the equine hoof

The vascular architecture of the dermal laminae was studied by scanning electron microscopy of vascular corrosion casts. Ultrastructurally, the laminar vasculature consisted of arterioles, capillaries, venules and veins, arranged in a sheet-like network. Through the laminae, arterioles ran parallel to the solar surface and branched at two levels to form a continuous arteriolar arcade, parallel to the hoof wall. Capillaries originating from these arcades formed hairpin loops joining the marginal vein prior to forming an axially situated venous network. Additional capillaries were also given off by the arterioles, forming an abaxially arranged capillary plexus.     

Radial displacement of red blood cells during hemodilution and the effect on arteriolar oxygen profile

In this study, we assessed the magnitude of the erratic deviations in the radial position of red blood cells (RBCs) in the laminar flow regime of arterioles in a hamster window preparation and the intraluminal Po(2) profile to determine whether this variability affects the intraluminal distribution of oxygen in conditions of normal hematocrit and hemodilution. A gated image intensifier was used to visualize fluorescently labeled RBCs in tracer quantities and obtain multiple measurements of RBC radial and longitudinal positions at time intervals on the order of 5 ms within single arterioles (diameter range 40-95 microm). RBCs in the velocity range of 0.3-14 mm/s exhibit a mean coefficient of variation of velocity of 16.9 +/- 10.5% and a SD of the radial position of 1.98 +/- 0.98 microm. Both quantities were inversely related to hematocrit, and the former was significantly lowered by hemodilution. Our experimental results presented very similar values and shape compared with the intraluminal oxygen profile derived theoretically for normal hematocrit, suggesting that shear-augmented diffusion due to the measured radial displacement of RBCs did not significantly affect oxygen diffusion from blood into the arteriolar vessel wall. Po(2) profiles in the arterioles assumed an increasingly parabolic configuration with increasing levels of hemodilution.     

Prolonged tissue PO2 reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats

We tested the hypothesis that a deficit in oxygen extraction or an increase in oxygen demand after skeletal muscle contraction leads to delayed recovery of tissue oxygen tension (Po(2)) in the skeletal muscle of hypertensive rats compared with normotensive rats. Blood flow and Po(2) recovery at various sites in the spinotrapezius muscle of spontaneously hypertensive rats (SHRs) were evaluated after a 3-min period of muscle contraction and were compared with corresponding values in Wistar-Kyoto rats (WKYs). The recovery of tissue Po(2) [75 +/- 7 (SHRs) vs. 99 +/- 12% (WKYs) of resting values] and venular Po(2) [72 +/- 13 (SHRs) vs. 104 +/- 10% (WKYs) of resting values] were significantly depressed in the SHRs 30 s postcontraction. The delayed recovery persisted for 120 s postcontraction for both tissue [86 +/- 11 (SHRs) vs. 119 +/- 13% (WKYs) of resting values] and venular [74 +/- 2 (SHRs) vs. 100 +/- 9% (WKYs) of resting values] Po(2) levels. There was no significant difference in the recovery of arteriolar Po(2) between the two groups 30 s postcontraction [95 +/- 7 (SHRs) vs. 84 +/- 8% (WKYs) of resting values]. Values for resting diameter of arcade arterioles in the two groups were not different [52 +/- 3 (SHRs) vs. 51 +/- 3 microm (WKYs)], but the arteriolar diameter after the 3-min contraction period was greater in the SHRs (71 +/- 4 microm) than the WKYs (66 +/- 4). Likewise, red blood cell (RBC) velocity [5.8 +/- 0.3 (SHRs) vs. 4.7 +/- 0.2 mm/s (WKYs)] and blood flow [23.0 +/- 0.8 (SHRs) vs. 16.0 +/- 1.0 nl/s (WKYs)] measurements were significantly greater in the SHRs at 30 s postcontraction. The delayed recovery of tissue Po(2) in the SHRs compared with the WKYs can be explained by a decrease in oxygen diffusion from the rarefied microvascular network due to the increased RBC velocity and the shorter residence time in the microcirculation and the consequent disequilibrium for oxygen between plasma and RBCs. The delayed recovery of venular Po(2) in the SHRs is consistent with this explanation, as venular Po(2) is slowly restored to baseline by release of oxygen from the RBCs. This leaves the arterioles in the primary role as oxygen suppliers to restore Po(2) in the tissue after muscle contraction.     

Microfibril-microvessel connections in the uvea and optic nerve of the mammalian eye.

Light- and electron-microscopic examination of arterioles, venules and capillaries of the eyes of several mammalian species has shown that the microfibrils of ocular elastic tissue attach to microvascular basement membranes throughout the uvea (iris, ciliary body, choroid) and optic nerve. Although described sporadically in prior investigations, this report shows that the connections are a common feature of the mammalian eye. The connections appear most numerous at venules and capillaries and are sparse at arterioles. The connections may provide a mechanism by which perivascular elastic tissue influences microvascular function, e.g. the control of blood pressure in them or their response to changes in intraocular pressure.     

Effect of hemorrhage on regional morphometric indexes of cerebral capillarity

This study was performed to determine whether the brain can increase the number of perfused capillaries and arterioles supplying it regionally during hemorrhage. This was done using a technique to simultaneously determine total and perfused regional arteriolar and capillary morphology. Conscious Long-Evans rats served as unbled controls or were bled 65 mmHg or to 40-45 mmHg and stabilized for 30 min. Regional cerebral blood flow was determined using [14C]iodoantipyrine in half of these animals and fluorescein isothiocyanate-dextran was injected in the other half for determination of perfused cerebral microvascular morphometric indexes. The total microvasculature was labeled postmortem via an alkaline phosphatase stain. Regional cerebral blood flow was significantly increased in animals bled to 65 mmHg. During hemorrhage to 40-45 mmHg, cerebral blood flow was reduced 50% (from 59 +/- 28 to 26 +/- 11 ml X min-1 X 100 g-1, mean +/- SD) with no regional redistribution. For all treatments, total capillary density ranged from 400 to 500 capillaries/mm2, and in controls 47% were perfused. Animals bled to 65 mmHg did not mobilize their unperfused microvascular reserve even though they showed a slight tendency to do so. During hemorrhage to 40-45 mmHg, this percent increased significantly to 57% with the largest increase occurring in the pons. Approximately 51% of arterioles were perfused in controls and this was not different compared with the percent perfused during hemorrhage. Despite the overall lack of mobilization of unperfused arterioles, some regions within the brain significantly mobilized their reserves with severe hemorrhage, e.g., hippocampus (78%), hypothalamus (67%), and medulla (73%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Microcirculation in the pulmonary vessels during artificial ventilation of different frequencies and volumes

In acute experiments on cats with closed chest by means of biomicroscopic method it has been shown that artificial ventilation of increased frequency or volume causes the decrease of diameters of arterioles, venules, wide capillaries and also the decrease of the length of functional narrow capillaries. The constriction degree of arterioles and venules depends on their initial diameter. The length of the functional narrow capillaries is being changed to the great extent under frequency increase. Decrease of the volume of the artificial ventilation causes differently directed changes of these parameters in various regions of the lungs. It is supposed that other neuro-humoral factors take part in the realization of the determined changes except alveolar pressure.     

Local heat produces a shear-mediated biphasic response in the thermoregulatory microcirculation of the Pallid bat wing

Investigators report that local heat causes an increase in skin blood flow consisting of two phases. The first is solely sensory neural, and the second is nitric oxide mediated. We hypothesize that mechanisms behind these two phases are causally linked by shear stress. Because microvascular blood flow, endothelial shear stress, and vessel diameters cannot be measured in humans, bat wing arterioles (26.6 +/- 0.3, 42.0 +/- 0.4, and 58.7 +/- 2.2 microm) were visualized noninvasively on a transparent heat plate via intravital microscopy. Increasing plate temperature from 25 to 37 degrees C increased flow in all three arterial sizes (137.1 +/- 0.3, 251.9 +/- 0.5, and 184.3 +/- 0.6%) in a biphasic manner. With heat, diameter increased in large arterioles (n = 6) by 8.7 +/- 0.03% within 6 min, medium arterioles (n = 8) by 19.7 +/- 0.5% within 4 min, and small arterioles (n = 8) by 31.6 +/- 2.2% in the first minute. Lidocaine (0.2 ml, 2% wt/vol) and NG-nitro-L-arginine methyl ester (0.2 ml, 1% wt/vol) were applied topically to arterioles (approximately 40 microm) to block sensory nerves, modulate shear stress, and block nitric oxide generation. Local heat caused only a 10.4 +/- 5.5% increase in diameter with neural blockade (n = 8) and only a 7.5 +/- 4.1% increase in diameter when flow was reduced (n = 8), both significantly lower than control (P < 0.001). Diameter and flow increases were significantly reduced with NG-nitro-L-arginine methyl ester application (P < 0.05). Our novel thermoregulatory animal model illustrates 1) regulation of shear stress, 2) a nonneural component of the first phase, and 3) a shear-mediated second phase. The time course of dilation suggests that early dilation of small arterioles increases flow and enhances second-phase dilation of the large arterioles.     

Effect of acute hypoxia on microcirculatory and tissue oxygen levels in rat cremaster muscle.

Repeated exposure to brief periods of hypoxia leads to pathophysiological changes in experimental animals similar to those seen in sleep apnea. To determine the effects of such exposure on oxygen levels in vivo, we used an optical method to measure PO2 in microcirculatory vessels and tissue of the rat cremaster muscle during a 1-min step reduction of inspired oxygen fraction from 0.21 to 0.07. Under control conditions, PO2 was 98.1 +/- 1.9 Torr in arterial blood, 52.2 +/- 2.8 Torr in 29.0 +/- 2.7-microm arterioles, 26.8 +/- 1.7 Torr in the tissue interstitium near venous capillaries, and 35.1 +/- 2.6 Torr in 29.7 +/- 1.9-microm venules. The initial fall in PO2 during hypoxia was significantly greater in arterial blood, being 93% complete in the first 10 s, whereas it was 68% complete in arterioles, 47% at the tissue sites, and 38% in venules. In the 10- to 30-s period, the fall in normalized tissue and venular PO2 was significantly greater than in arterial PO2. At the end of hypoxic exposure, PO2 at all measurement sites had fallen very nearly in proportion to that in the inspired gas, but tissue oxygen levels did not reach critical PO2. Significant differences in oxyhemoglobin desaturation rate were also observed between arterial and microcirculatory vessels during hypoxia. In conclusion, the fall in microcirculatory and tissue oxygen levels in resting skeletal muscle is significantly slower than in arterial blood during a step reduction to an inspired oxygen fraction of 0.07, and tissue PO2 does not reach anaerobic levels.     

A comparison of the cutaneous microvascular properties of the Spontaneously Hypertensive rat and the Wistar-Kyoto rat

The Spontaneously Hypertensive rat (SHR) and its non-hypertensive companion strain, the Wistar-Kyoto (WKY) rat, provide an excellent comparative model to permit study of the differential properties of cutaneous microvascular beds. We explored the possibility that chronically elevated vascular pressures in the SHR rat might affect the microvascular constitution of the skin. We measured skin blood flow at the back and at the paw of a group of 20-week-old WKY rats and a contrast group of SHR rats. We then performed skin biopsies at these two locations and used the NIH Image program to count and measure the size of capillaries, arterioles, and venules. We also determined microvascular density as percentage of total tissue area. At basal temperature, skin blood flow was similar in the two rat strains at both the back and paw. Heat induced vasodilatation resulted in a 50% increase in blood flow at the back, reaching the same level in the two rat groups. However, at the paw site, thermal stimulation resulted in significantly greater flow (39.3 +/- 3.1 ml/100 gm tissue per min) in the SHR rats than the WKY rats (28.6 +/- 1.9 ml/100 gm tissue per min, P < 0.05). The ratio of systemic arterial pressure to skin blood flow was computed as an index of vascular resistance to flow. At basal temperature, this index was 50% greater for the SHR rats at both skin sites. At 44 degrees C, the resistance index decreased at both sites in both rat groups but was still approximately 50% higher at the back of the SHR than the WKY rats. In contrast, the resistance index at 44 degrees C at the paw site fell to the same level in both the SHR and WKY rats. There were twice as many capillaries at the back of the WKY rats than at the back of the SHR rats (9.2 +/- 2.0 per mm2 vs. 4.7 +/- 1.2 per mm2, P < 0.05). Expressed as a percentage of total tissue area, the capillary density at the back in the WKY rats was 0.064 +/- 0.010% as compared to 0.034 +/- 0.008% in the SHR rats (P < 0.05). There were five times more arterioles at the paw compared to the back in both rat groups with no significant difference between the groups. We measured the diameter of the lumen and the thickness of the wall of each arteriole and computed their ratio as an index of possible media hypertrophy. There were minimal differences seen in these parameters between the two rat groups at the back and paw sites. The venular density was significantly higher at the paw than at the back in both rat groups with no significant difference between them. Reduced capillary density at the back of the SHR rats may be a developmental adaptation to high blood pressure. Such a reduction in the pathways of blood flow may help account for increased flow resistance at that site, independent of arteriolar vasoconstriction.