SEARCH · PubMed Health

Results for “Microcirculation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,549 records · Page 86Linked to original sources

PubMed1992

In vivo effects of Escherichia coli endotoxemia on diaphragmatic microcirculation in rats.

We investigated the effects of Escherichia coli endotoxin administration on diaphragmatic microcirculation in rats by in vivo videomicroscopy. Rats were allocated into three groups: 1) intravenous inoculation of 10 mg/kg of E. col endotoxin (group E, n = 25), 2) intravenous inoculation of sterile 0.9% NaCl (group C, n = 20), and 3) induction of a controlled hemorrhage by reducing the vascular volume via an arterial catheter (group H, n = 15). Mean blood pressure (BP) and arteriolar diameters were measured at 15-min intervals and capillary perfusion pattern at 30-min intervals for 1 h. BP decreased similarly in groups E and H, whereas it was maintained in group C. Arterioles were classified as second (A2, n = 46), third (A3, n = 22), and fourth (A4, n = 21) order, according to their relative localization in the network. Basal diameters were the same in the three groups: 38.16, 17.33, and 6.80 microns in group C; 38.17, 17.41, and 7.04 microns in group E; and 37.82, 19.19, and 6.99 microns in group H for A2, A3, and A4, respectively. During the observation period, a significant and similar vasoconstriction of A2 arterioles was observed in groups E and H but not in group C. By contrast, in the three groups, no significant changes in diameter were found for the A3 and A4 arterioles. Capillary perfusion was markedly impaired in group E: at 60 min the percentage of non-perfused capillaries was 40.92 +/- 6.65% in group E compared with 21.17 +/- 5.45% in group C (P less than 0.05) and 18.18 +/- 8.11% in group H (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Diaphragmatic microcirculation during halothane and isoflurane exposure in pentobarbital-anesthetized rats.

We investigated the effects of halothane and isoflurane on diaphragmatic microcirculation in pentobarbital-anesthetized rats by in vivo video microscopy. After a baseline period, rats were randomly allocated into three groups according to administration of 0.5, 0.75, and 1 minimal alveolar concentration (MAC) of either halothane (group Hal, n = 16), isoflurane (group Iso, n = 14), or no halogenated agent (group C, n = 20) in three succeeding steps of 15 min. Mean arterial blood pressure (MAP), arteriolar diameters, and functional capillary density were analyzed in the last 3 min of each step. MAP remained unchanged in group C but decreased in a dose-dependent manner in both halogenated receiving groups. MAP was significantly lower in rats breathing Hal compared with those breathing Iso. Arterioles were classified in second (A2, n = 39), third (A3, n = 24), and fourth (A4, n = 30) order according to their relative location in the network. No changes in A2 and A3 diameters were noted in either group. A4 diameters remained unchanged in groups C and Iso, whereas a significant reduction was found in group Hal at 0.75 and 1 MAC exposure (P < 0.05 compared with baseline and with groups C and Iso, respectively). During Iso exposure, functional capillary density was not significantly different when compared with baseline and group C, whereas in group Hal it decreased significantly at 0.5, 0.75, and 1 MAC, amounting to 61.1 +/- 9, 30.7 +/- 10.3, and 22.8 +/- 6.3%, respectively, of baseline (P < 0.01 vs. baseline and P < 0.05 vs. groups Iso and C for 0.75 and 1 MAC).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1994

Leukocyte kinetics in pulmonary microcirculation: intravital fluorescence microscopic study.

To determine the site of sequestration of leukocytes in the lung, we investigated the kinetics of fluorescently labeled erythrocytes and leukocytes in pulmonary arterioles, venules, and alveolar capillaries in vivo by using fluorescence videomicroscopy. The subpleural pulmonary microcirculation of the ventilated rabbit lung was visualized via a transparent window implanted into the right thoracic wall. Fluorescein isothiocyanate-labeled erythrocytes were administered intravenously, whereas leukocytes were labeled in vivo by intravenous injection of rhodamine 6G. Rolling and adherence of leukocytes on the surface of the vessel walls were observed in arterioles as well as in venules. The median velocity of nonadherent leukocytes was significantly higher in arterioles than in venules (84 +/- 12 vs. 15 +/- 3% of erythrocyte velocity, respectively). In alveolar capillaries the majority of leukocytes were retained at distinct sites for periods of 0.1 to > 5 s (median 0.61 s). The relative velocity of leukocytes moving in capillaries was comparable to that determined in arterioles (80 +/- 9% of erythrocyte velocity). These measurements indicate that leukocyte sequestration in the lung is governed by the retention of leukocytes in capillaries and by the interaction of leukocytes with microvascular endothelium of arterioles and venules. We propose that the kinetics of these phenomena determine the equilibrium between circulating and sequestered leukocytes.

Animals↗

PubMed2003

Oxygen gradients in the microcirculation.

As arterialized blood transits from the central circulation to the periphery, oxygen exits through the vessel walls driven by radial oxygen gradients that extend from the red blood cell column, through the plasma, the vessel wall, and the parenchymal tissue. This exit determines a longitudinal gradient of blood oxygen saturation whose extent is inversely related to the level of metabolic activity of the tissue, being small for the brain and considerable for skeletal muscle at rest where hemoglobin is only half-saturated with oxygen when blood arrives to the capillaries. Data obtained by a variety of methods show that the oxygen loss is too great to be explained by diffusion alone, and oxygen gradients measured in the arteriolar wall provide evidence that this structure in vivo is a very large oxygen sink, and suggests a rate of oxygen consumption two orders of magnitude greater than seen in in vitro studies. Longitudinal gradients in the capillary network and radial gradients in surrounding tissue also show a dependence on the metabolic rate of the tissue, being more pronounced in brain than in resting skeletal muscle and mesentery. Mean PO2 values increase from the postcapillary venules to the distal vessels of this network while radial gradients indicate additional oxygen loss. This circumstance may be due to pathways with higher flow having higher oxygen content than low flow pathways as well as possible oxygen uptake from adjacent arterioles. Taken together, these newer findings on oxygen gradients in the microcirculation require a reexamination of existing concepts of oxygen delivery to tissue and the role of the capillaries in this process.

Animals↗

PubMed1996

Paracrine regulation of the renal microcirculation.

There has been an explosive growth of interest in the multiple interacting paracrine systems that influence renal microvascular function. This review first discusses the membrane activation mechanisms for renal vascular control. Evidence is provided that there are differential activating mechanisms regulating pre- and postglomerular arteriolar vascular smooth muscle cells. The next section deals with the critical role of the endothelium in the control of renal vascular function and covers the recent findings related to the role of nitric oxide and other endothelial-derived factors. This section is followed by an analysis of the roles of vasoactive paracrine systems that have their origin from adjoining tubular structures. The interplay of signals between the epithelial cells and the vascular network to provide feedback regulation of renal hemodynamics is developed. Because of their well-recognized contributions to the regulation of renal microvascular function, three major paracrine systems are discussed in separate sections. Recent findings related to the role of intrarenally formed angiotensin II and the prominence of the AT1 receptors are described. The possible contribution of purinergic compounds is then discussed. Recognition of the emerging role of extracellular ATP operating via P2 receptors as well as the more recognized functions of the P1 receptors provides fertile ground for further studies. In the next section, the family of vasoactive arachidonic acid metabolites is described. Possibilities for a myriad of interacting functions operating both directly on vascular smooth muscle cells and indirectly via influences on endothelial and epithelial cells are discussed. Particular attention is given to the more recent developments related to hemodynamic actions of the cytochrome P-450 metabolites. The final section discusses unique mechanisms that may be responsible for differential regulation of medullary blood flow by locally formed paracrine agents. Several sections provide perspectives on the complex interactions among the multiple mechanisms responsible for paracrine regulation of the renal microcirculation. This plurality of regulatory interactions highlights the need for experimental strategies that include integrative approaches that allow manifestation of indirect as well as direct influences of these paracrine systems on renal microvascular function.

Animals↗

PubMed1992

Experimental and clinical evaluation of capsular and parenchymal total liver perfusion. Liver microcirculation.

Liver blood flow measurements obtained from both the liver surface and deep within the parenchyma, were correlated in an effort to assess the usefulness of laser-Doppler flowmetry for non-invasive monitoring of total liver blood flow, the probe being positioned on either the surface or within the liver parenchyma. In 23 Wistar rats and 10 biliary surgery patients, anaesthetized prior to gallbladder removal, liver microcirculation was measured at 4 points on the capsular surface, and consequently at 4 points deep within the parenchyma, using probes connected to a laser-Doppler flowmeter. The findings revealed that laser-Doppler measurements on the liver surface and within the parenchyma were well correlated, as no statistically significant differences were found either in rats or humans. It is concluded that laser-Doppler flowmetry for monitoring of total liver perfusion can be applied either on the capsular surface or within the hepatic parenchyma.

Animals↗

PubMed1999

Effects of hypoxia and reoxygenation with 21% and 100%-oxygen on cerebral nitric oxide concentration and microcirculation in newborn piglets.

Bioelectric sensors for continuous registration of nitric oxide (NO) concentrations in tissues provide a new tool for invasive measurement of this gaseous molecule. This study sought to validate cerebral NO measurements using an amperiometric sensor. A series of experiments in 1- to 3-day-old piglets was carried out to study the response of NO and microcirculation during hypoxia (F(i)O(2) 0.06) and reoxygenation with 100% and 21% oxygen. Two-channel laser Doppler flowmetry was performed in the forebrain cortex. Significant decreases of NO levels were observed immediately after induction of hypoxemia (p < 0.05). During reoxygenation with 21 or 100% O(2) for 30 min, NO increased significantly compared to the values at the end of hypoxia (p < 0.05). The increase of NO levels in the 100% oxygen group was greater than the increase in the 21% oxygen group (p < 0. 05). There were no significant differences between the two groups during the following 3.5 h of observation. A significant increase in CBF was found in the first 2 min of hypoxia (p < 0.05), it then continued to fall to values significantly lower than baseline values at the end of hypoxemia (p < 0.05). During reoxygenation CBF normalised and there were consistent but no significant differences between the two reoxygenation groups. We conclude that NO concentration decreased during the course of hypoxia. Hypoxia-induced cerebral hyperaemia occurred in spite of significantly lower NO concentrations. Reoxygenation with 21 or 100% O(2) restored CBF in both groups similarly, although values were higher after reoxygenation with 100% O(2) compared to air. In fact, reoxygenation with 100% O(2) led to supranormal levels of NO by contrast to 21% O(2).

Animals↗

PubMedDate not supplied

Insulin-induced arteriolar dilation after tyrosine kinase and nitric oxide synthase inhibition in hamster cheek pouch microcirculation.

We investigated the effects of tyrosine kinase (TK) and nitric oxide synthase (NOS) inhibition on insulin-induced dilation of arterioles. We determined the arteriolar diameter, red blood cell velocity (VRBC) and blood flow changes in hamster cheek pouch microcirculation as affected by insulin in presence of TK and NOS inhibitors, genistein, piceatannol and NG-monomethyl-L-arginine (L-NMMA). Microvessels were visualized by a fluorescent microscopy technique. Arteriolar diameter and VRBC were measured after topical application of insulin and genistein or piceatannol or L-NMMA. Insulin (10 microU/ml) induced diameter and VRBC increase in A3 and A2 arterioles by 30 +/- 5 and 123 +/- 4%, 16 +/- 4 and 102 +/- 3%, as percent of baseline values, respectively. After genistein or piceatannol prior to insulin A3 and A2 arterioles dilated by 10 +/- 4, 5 +/- 2% and 9 +/- 4, 2 +/- 1%, respectively. After L-NMMA prior to insulin A2 and A3, arteriole diameters increased by 12 +/- 3 and 7 +/- 2%, respectively. VRBC increased significantly in all the cases. TK and NOS inhibitors applied together abolished insulin-induced dilation with a reduction in VRBC and blood flow. In conclusion, full insulin-induced dilation of hamster cheek pouch arterioles requires TK signaling pathways. Furthermore, activation of insulin receptors, as well as other TK receptors, appears to be required for vasomotor tone regulation.

Animals↗

PubMedDate not supplied

Life and death cell labeling in the microcirculation of the spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHRs) have elevated numbers of apoptotic cells. However, the extent and pattern of cell death at the microvascular level is unexplored. We developed a technique to determine early forms of cell death in vivo in the mesentery by use of the life/death indicator ethidium bromide (EB). The mesenteric microvasculature was superfused with 5 microM EB for a period of 3 min, rinsed and immediately viewed by digital fluorescence microscopy. EB-positive cell structures were observed both in the wall of microvessels as well as in the tissue parenchyma. The microvessels had about 2--4 EB-positive cell structures per 100 microm of vessel length. Larger arterioles (>25 microm) in the SHR had an increased EB-positive structure density. After normalization of the blood pressure in the SHR with adrenalectomy, no significant differences remained between Wistar-Kyoto (WKY) rats and SHRs. After dexamethasone treatment, the adrenalectomized SHRs had a higher EB-positive cell density in the smaller class of microvessels than the WKY rats. In addition, EB-positive cell fragments (0.5--2 microm) were observed in the mesentery microvessel wall, and with TUNEL labeling, they were demonstrated to represent DNA fragments. The percentage of microvessels with EB-positive fragments was higher in the SHR arterioles and capillaries. Capillaries and larger venules (>30 microm) in the SHR had higher levels of cell fragments per vessel length. After adrenalectomy, no significant differences remained between WKY rats and SHRs in any of the microvessel categories. When adrenalectomized rats were treated with dexamethasone, a higher number of EB-positive fragments was detected in the wall of SHR capillaries. These results indicate that the mesentery microcirculation in both strains is subject to an early and nonuniform pattern of cell death, as detected by EB, but is enhanced in selected individual microvascular segments of the SHR by a glucocorticoid-driven mechanism.

Adrenalectomy↗

PubMed2001

Effects of n-3 polyunsaturated fatty acids and vitamin E on colonic mucosal leukotriene generation, lipid peroxidation, and microcirculation in rats with experimental colitis.

AIMS: We investigated the effect of n-3 polyunsaturated fatty acids (PUFAs) on mucosal levels of leukotrienes (LTs) and lipid peroxide (LPO), and on mucosal microcirculation, in rats with experimental colitis induced by dextran sulfate sodium (DSS). METHODS: We fed Wistar rats a perilla oil-enriched diet containing alpha-linolenic acid (63.2% of total fatty acids) with various doses of vitamin E for 4 weeks, with 4% DSS added to the drinking water during the last week. Control rats were fed a diet produced from soybean oil containing alpha-linolenic acid (5.1% of total fatty acids). Colonic mucosal blood flow was measured with a laser Doppler flowmeter. RESULTS: The mucosal level of arachidonic acid was significantly lower and that of eicosapentaenoic acid was significantly higher in the experimental group. The mucosal level of LPO in the experimental group fed a trace or ordinary dose of vitamin E was significantly higher than that of the controls. The production of LTB(4) and LTC(4) from the colonic mucosa in the experimental group was significantly lower than that in controls. However, only the experimental group fed a vitamin E dose 4-fold higher than that given to the controls showed a significant increase in mucosal blood flow. CONCLUSION: These results suggest that n-3 PUFAs increase mucosal blood flow by inhibiting LT production when there is sufficient vitamin E to inhibit lipid peroxidation in rats with experimental colitis.

Administration, Oral↗

PubMed1999

Leukocyte adhesion after oxidant challenge in the hamster cheek pouch microcirculation.

Oral administration of S-5682 (Daflon 500 mg, 90% diosmin, 10% hesperidin) inhibits oxidant-induced increase in macromolecular permeability in the postcapillary venules of the hamster cheek pouch microcirculation. In this study, the effect of S-5682 on leukocyte-endothelium interaction was evaluated using the same experimental model. Hamsters kept on a standard diet were divided into 5 groups (n = 6) and treated orally, twice a day, with placebo (10% lactose solution), S-5682, 5, 20 or 80 mg/kg/day (suspended in 10% lactose solution) or alpha-tocopherol, 1 mg/kg/day, for 10 days prior to the oxidant challenge with tert-butylhydroperoxide (TBOOH). Topical application of TBOOH (10(-4) M for 5 min) to hamsters given acridine orange prior to TBOOH resulted in increases in the number of rolling and sticking (no movement for at least 30 s) leukocytes in postcapillary venules. No changes in the number of rolling leukocytes could be observed in the treated groups compared with the placebo group (p > 0.05). On the contrary, leukocyte adhesion was inhibited in groups treated with S-5682 (5, 20 and 80 mg/kg/day) or alpha-tocopherol: placebo 105 +/- 3/6 mm(2) (mean +/- SEM); S-5682, 5 mg/kg/day 68 +/- 3/6 mm(2) (p < 0.01), 20 mg/kg/day 55 +/- 3/6 mm(2) (p < 0.001) and 80 mg/ kg/day 39 +/- 2/6 mm(2) (p < 0.001) and alpha-tocopherol 36 +/- 1/6 mm(2) (p < 0.001). The inhibition of oxidant-induced leukocyte adhesion by S-5682 was similar to that seen for ischemia-reperfusion and the higher dose of S-5682 was as effective as alpha-tocopherol in inhibiting it.

Animals↗

PubMed2002

Videocapillaroscopic findings in the microcirculation of the psoriatic plaque.

BACKGROUND: Videocapillaroscopy (VCP) is a method to study the morphology and dynamics of microcirculation, but information about capillaroscopic features of the psoriatic plaque is limited. OBJECTIVE: To investigate the distribution, morphology and density of capillaries in lesional and perilesional skin of the psoriatic plaque. METHODS: VCP of a well-delimited plaque of the trunk, arms or legs in 15 consecutive patients with untreated, chronic plaque psoriasis was performed. RESULTS: In the lesional skin, capillaries were tortuous and dilated, homogeneously appearing as 'bushy'. In the perilesional skin, capillary loops seemed to be on a parallel course with respect to the skin surface, with their apex directed towards the marginal zone. The number of capillary loops per area unit was statistically increased in perilesional compared to lesional skin. CONCLUSION: According to the morphology, distribution and density of capillary loops, two different angiogenetic patterns were found in lesional and perilesional skin.

Adult↗

PubMed2005

Effect of nicotine on the renal microcirculation in anesthetized rats: a potential for medullary hypoxic injury?

BACKGROUND: Cigarette smoking has been associated with accelerated renal dysfunction among patients with chronic renal disease. Conceivably, repeated parenchymal hypoxic injury, induced by nicotine-related vasomotor changes, might contribute to the progression of renal failure in smokers. METHODS: Renal blood flow and selective cortical and outer medullary blood flows were determined in anesthetized rats. Changes in total renal, cortical and medullary vascular resistance were calculated. Nicotine was repeatedly infused at rising doses (50-200 microg/kg) to intact (CTR) animals and to rats chronically administered with nicotine in their drinking water (NIC). In a complementary study, nicotine-treated and control rats were subjected to medullary hypoxic stress, induced by radiocontrast and indomethacin. RESULTS: Chronic nicotine exposure led to lower baseline renal blood flow and creatinine clearance. Nicotine infusion induced a transient dose-dependent rise in blood pressure, renal blood flow and cortical flow, with a corresponding decline in renal vascular resistance and cortical resistance in both experimental groups. However, while medullary flow increased in CTR by up to 16 +/- 6%, it remained unchanged or even somewhat declined in the NIC group. Calculated medullary resistance reciprocally declined in CTR while it rose in the NIC group (p < 0.001). In animals subjected to radiocontrast and indomethacin, nicotine intensified renal dysfunction, associated with focal medullary hypoxic damage. CONCLUSIONS: Chronic exposure to nicotine selectively compromises the outer medullary microcirculation, blunting a local vasodilatory response to acute nicotine administration. Repeated acute-on-chronic exposure to nicotine may predispose to hypoxic medullary injury.

Acute Kidney Injury↗

PubMed1991

Finger microcirculation in classical migraine. A video-microscopic study of nailfold capillaries.

We assessed microcirculation in nailfold capillaries of 22 patients with classical migraine and 22 normal subjects matched for age and sex using video-microscopy. Blood flow measurements were performed under standardized room temperature, after a 3-min warm water bath and after local cooling. Under standardized conditions, skin temperature at the fingertip was significantly lower in patients with migraine. Morphological differences, however, could not be found between patients and controls. After cooling of the nailfold area, blood flow stop due to vasospasm occurred in 18 of the 22 migraine patients in contrast to 1 of the 22 control subjects only. Capillary blood cell velocity was significantly decreased in the migraine group under all test conditions. Drug treatment did not account for the different prevalences of vasospasm in migraine patients and normal controls. Our findings demonstrate that patients with migraine often have subclinical microcirculatory disorders of the upper limbs.

Adolescent↗

PubMed1991

In vivo fluorescence microscopy for quantitative analysis of the hepatic microcirculation in hamsters and rats.

Using intravital fluorescence microscopy and epi-illumination, the hepatic microcirculatory system of Syrian golden hamsters was analyzed, and the morphology and microhemodynamics were compared to those of rats. After contrast enhancement with 1 mumol/kg acridine orange i.v., the epi-illumination technique allows for visualization of capillary sinusoids and postsinusoidal venules, which are running in parallel with the liver surface, while afferent microvessels could be visualized in only few of the liver lobules investigated. In rat livers, the capillary sinusoids showed morphology similar to that of hamsters, however, postsinusoidal venules could frequently not be observed when applying epi-illumination, since these microvessels are piercing perpendicularly into the depth of the liver tissue. Microhemodynamic analysis, including the sinusoidal perfusion rate, sinusoidal red blood cell velocity and diameters, microvascular white blood cell (WBC) count and the phenomenon of WBC-endothelium interaction, as well as the hepatocellular uptake of the fluorescent compound acridine orange were found to be similar in hamsters as compared to rats. Although transillumination for in vivo microscopy may have the potential to visualize the complete hepatic microcirculatory system due to an increased focus depth, the epi-illumination technique has the advantage for quantitative assessment not only of the morphology of the hepatic microcirculatory system and microvascular blood perfusion, but also allows for evaluation of cellular phenomena within the hepatic microvessels, such as WBC accumulation, WBC-endothelium interaction, phagocytotic activity of Kupffer cells, and hepatocellular transport of fluorescent compounds. Hepatic microcircular disturbances, including accumulation of WBCs and WBC-endothelium interaction are causative in the development of organ failure in conditions such as hemorrhagic and septic shock, and, in particular, postischemic reperfusion injury following liver surgery and liver transplantation. Since accumulation of WBCs and their interaction with the microvascular endothelium are primarily found in postsinusoidal venules, in vivo microscopy of the hamster liver represents a favorable model for studies on cellular phenomena within the hepatic microcirculation.

Animals↗

PubMed1995

Ascorbate preserves gastric mucosal metabolism and microcirculation after hemorrhagic shock and retransfusion in rats.

The gastric mucosal microcirculation and purine nucleotide metabolism were studied in rats after hemorrhagic shock and retransfusion. The mucosal surface density of perfused vessels (SDPV) and the mucosal levels of ATP, ADP, AMP, IMP, hypoxanthine and uric acid were measured following 15 min of hemorrhagic shock and 10 and 30 min after retransfusion, and the effects of pretreatment with allopurinol or ascorbate were studied. During shock there was a dephosphorylation of nucleotides and a decline in the SDPV. Retransfusion led to an additional reduction in the SDPV, but a complete restoration of preshock nucleotide levels 30 min after retransfusion. Allopurinol accelerated early rephosphorylation of nucleotides without effects upon SDPV while ascorbate completely preserved the mucosal level of energy-rich nucleotides 15 min after hemorrhagic shock and increased SDPV during early reperfusion. The results showed that there was a renewal of energy stores in gastric mucosa after hemorrhagic shock and retransfusion although parts of the vascular bed were not reperfused. The mucosal energy depletion after 15 min of hemorrhagic shock and part of the mucosal vessel injury after retransfusion were prevented by pretreatment with ascorbate.

Allopurinol↗

PubMed1988

Microcirculation of the coronary band of the equine hoof.

Scanning-electron-microscopic examination of corrosion casts was used to investigate the microcirculation of the coronary border of the equine hoof. Numerous peg-shaped capillary plexuses derived from arterioles extended distally from the dorsal branches of the digital arteries parallel to the hoof wall. The plexuses varied in length and consisted of a fine network of interconnected capillaries that converged to join a centrally situated venule. These centrally situated venules within the papillary plexuses gave rise to a vast venous plexus deep to the coronary band.

Animals↗

PubMed1990

Portal-like microcirculation in rat sympathetic ganglia.

The fine structure of intraganglionic blood vessels of rat superior cervical sympathetic ganglia is studied with the light microscope and with both conventional and ultrastructural histochemical methods. Two sets of small capillaries together with larger sinusoidal ones are identified. One set of capillaries is associated with the clustered (type II) small catecholamine-containing (CC) cells and exhibits features suggestive of fluid transport function (multiple wide fenestrae and active pinocytosis). The second set of capillaries is in direct relation to the sympathetic neurons (SN) and shows characteristics suggestive of absorptive function (microvilli and pinocytotic vesicles). The larger sinusoidal capillaries are observed in the vicinity of type II CC cells, extend parallel to the long axes of the perikarya of the neurons and occasionally form loops around them. The latter are assumed to be larger blood spaces connecting the two capillary sets and serve to slow the circulation around the neurons. A pattern of portal-like intraganglionic microcirculation through which type II CC cells participate in modulating the SN is postulated. Type II CC cells secrete a catecholamine modulator which, driven by concentration gradient, gains access to the circulation through the fenestrated capillaries. The sinusoidal capillaries serve to perfuse the SN with a slow stream of blood rich in the catecholamine modulator. The latter can be filtered through the microvilli and pinocytotic vesicles of the second set of capillaries to induce slow inhibitory postsynaptic potential on the SN.

Animals↗