Ultrastructure of arterioles in the cat brain

A total of 110 arterioles were examined in the brains of cats; different sites were studied including the cortex, putamen, pons and crus cerebri. No internal elastic laminae were seen in the subendothelial space, although occasional fragments of elastic material were present in the larger arterioles. The media was composed of one, two or three layers of smooth muscle cells which interlocked in such a way that the vessel wall thickness was constant. Numerous tight junctions were seen between adjacent smooth muscle cells and between the endothelium and smooth muscle cells. Apart from the usual cell organelles, the smooth muscle cells of arterioles had numerous dense patches on the cell surface. The structure of the adventitia varied according to the diameter of the vessel and the site in the brain; it contained adventitial cells, bundles of collagen fibres and nerve fibres. Innervation of arterioles was more constant in the brain stem than in the cortex. Metarterioles had less specialised, atypical smooth muscle cells, a discontinuous media and numerous, extensive myoendothelial tight junctions; they were not innervated by nerve fibres. The diameter of metarterioles was less than 10 micronm whereas that of arterioles was 10-45 micronm. The possible functional aspects of arteriolar innervation are discussed.     

Growth of rabbit aortic smooth muscle cells in serum from patients with juvenile diabetes

The effect of human diabetic serum on the growth of rabbit arterial smooth muscle cell cultures was studied in the stationary phase of growth. The serum was obtained from young, male, non-obese, juvenile diabetics and non-diabetics. The experiments were carried out using dialysed as well as non-dialysed serum. The concentration of cholesterol and triglycerides were equal in normal and diabetic serum. Media supplemented with diabetic serum from both short term and long term diabetics stimulated the outgrowth of the smooth muscle cells significantly (2p less than 0.01). A statistically significantly stimulation of growth was also observed using dialysed human diabetic serum (2p less than 0.05). Autoradiographic studies showed that the number of 3H-thymidine labelled cells and of cells in mitosis increased appreciably after incubation in diabetic human serum (2p less than 0.005). The present data show that human serum from juvenile diabetics contains a factor or factors which promote an excessive growth of arterial medial cells. The factor(s) is not lipids as hyperlipemia was not present nor is it glucose, aminoacids, fructose or ketones, as the growth effect remained after dialysis.     

Changes in vessel ultrastructure during ischemia and reperfusion of rabbit hindlimb: implications for therapeutic intervention

Peripheral ischemia was induced in the rabbit by occlusion of the left iliac artery for 6 hr, followed by 24 hr of reperfusion. Biochemical and morphological investigations were performed to evaluate the extent of vascular and tissue injury. Blood samples for plasma enzyme determinations (creatine kinase (CK) and lactate dehydrogenase (LDH) activities) were obtained at times t = 0, t = 6, t = 30 hr. Plasma CK and LDH activities in ischemic animals were approximately twice as high as those in sham-operated animals at the end of reperfusion, although no difference was observed at the end of the period of ischemia. Morphological and morphometric analysis of extensor digitorum longus muscle from ischemic animals showed a reduction in the number of patent capillary vessels per muscle fiber (1.54 +/- 0.1 and 1.04 +/- 0.09, P < 0.05, in sham and ischemic groups, respectively; mean +/- SEM). In addition, the number of microvilli on endothelial surfaces were considerably increased in the ischemic group (0.14 +/- 0.02 and 0.41 +/- 0.01 microns -2, P < 0.001, in sham and ischemic groups, respectively). A great number of adhered leucocytes were found on the vessel surface with some leucocytes having migrated through the vessel wall. Microcirculatory damage was accompanied by the formation of microthrombi which sometimes occluded the entire vessel lumen. The infusion of 1 mg/kg/hr of cloricromene for 6 hr prevented ischemic injury in microvessels and also prevented swelling of muscle mitochondria. In the treated group the number of patent capillaries per muscle fiber was very similar to that found in sham-operated animals (1.49 +/- 0.08; P < 0.01 vs. ischemic control). In conclusion, several different cell types are involved in the pathophysiological changes which occur in microvessels during ischemia/reperfusion injury. Pharmacological interventions, which inhibit the interactions of blood cells with endothelium, may be of value in the treatment of peripheral ischemia/reperfusion injury.     

Melanoma cell adhesion to injured arterioles: mechanisms of stabilized tethering

An isolated perfused vessel model was used to examine the mechanisms underlying the adhesive interactions between circulating tumor cells and subendothelial matrix in denuded arterioles. Arterioles ranging from 70 to 100 microm in diameter were isolated from rat mesentery, transferred to an isolated vessel chamber, cannulated on both ends with glass micropipettes, and perfused with media containing 10(6) hamster melanoma (RPMI 1856) cells/ml. In a second group of arterioles, the endothelium was denuded by running 2 ml of air through the vessel lumen. Since the tumor cells did not adhere to the vessel wall when perfused at physiologically relevant shear rates, perfusate flow was stopped and the tumor cells were allowed to settle onto the vessel wall for 20 min. After counting the number of tumor cells that settled onto the arteriolar wall, perfusate flow was re-initiated and unattached cells were washed away. The number of cells remaining adherent were counted and the percentage of adherent cells (relative to the total number of cells that settled on to the vessel wall during the period of no-flow) were calculated and compared among different groups. We observed that tumor cells are much more adhesive to denuded arterioles than to intact arterioles. To determine the mechanisms responsible for the adhesive interactions that become established and stabilized during the period of flow reduction, denuded arterioles were treated with fibronectin antiserum or Arg-Gly-Asp (RGD) peptides. Both treatments significantly reduced tumor cell adhesion to denuded arterioles. In subsequent studies, melanoma cells were treated with a transglutaminase inhibitor, monodansylcadaverine (MDC), which reduced the ability of adherent tumor cells to withstand the anti-adhesive effects of a subsequent increase in perfusate flow rate after the period of no-flow. Our data suggest that tumor cells adhere to fibronectin in the subendothelial matrix in denuded arterioles by an RGD-dependent mechanism. Moreover, our observations are consistent with the concept that a transglutaminase-catalysed reaction acts to stabilize the adhesive interactions between subendothelial matrix components and melanoma cells during the period of flow stasis such that the cells are able to withstand subsequent substantial increases in wall shear rate and remain adherent.     

Oncocytes and oncocytic cell neoplasms

OBJECTIVE: To analyze the clinical results of a group of young and elderly diabetic patients on ambulatory peritoneal dialysis at a large comprehensive tertiary care community hospital in San Juan, Puerto Rico in relation to rehabilitation characteristics, compliance, complications and survival. DESIGN: The medical records of all patients with a diagnosis of diabetes mellitus trained between June 1985 and June 1992 were reviewed. This group of patients was subdivided according to age, in young (20-50 years) and elderly (50 or over). A comparable number of nondiabetics were selected at random for each of the two age groups. MAIN OUTCOME MEASURES: The patient were studied for age, sex, need of assistance from a partner during dialysis, causes of transfer and hospitalizations, peritonitis, rehabilitation, patients compliance and outcome including mortality. RESULTS: Young diabetics versus non-diabetics: There were 45 patients in the diabetic group (37.8% females) and 57 in the non-diabetic group (54.4% female) with a total observation time of 52.52 patient-months among the diabetics and 82.17 patient-months in the non-diabetic. Mean age of the diabetic patient was 39.9 +/- 8.8 and 36.7 +/- 8.7 for the non-diabetic. Assistance by a partner during the dialysis procedure was needed by 26.7% of the diabetics and by 3.7% of the non-diabetics (p < 0.01). Of the non-diabetics, 91.2% were classified as compliant versus 75.6% of the diabetics (p < 0.05). Peritonitis was the main cause of hospitalizations and of transfers in both groups. The two years patient survival for the diabetic was 81.7% and 100% for the non-diabetic and the two years technique survival was 32.5% for the diabetic and 43.5% for the non-diabetic. Elderly diabetics versus non-diabetics: There were 76 patients in the diabetic group (36.8% female) and 64 in the nondiabetic (43.8% female). The mean age of the diabetic group was 61.3 +/- 6.2 years and 59.3 +/- 7.3 years for the non-diabetic with a total observation time of 81.86 patients-months for the diabetic and 104.58 patient-months for the non-diabetic. Assistance by a partner during dialysis was needed in 63.5% of the diabetics and 19.45% of the non-diabetics (p < 0.01). No statistical difference was found in the rehabilitation or compliance evaluation. Peritonitis stands out again as the main cause of transfer out of the PD modality and main cause of hospitalization in both groups. The two year patient survival for the diabetic was 51.5% and 73.3% for the non-diabetic, while the two years technique survival was 49% for the diabetic and 52.9% for the non-diabetic. CONCLUSIONS: A shortened technique survival, problems of compliance, a high peritonitis rate plus dependency on a partner for dialysis are features of the diabetic group. These findings demonstrate that the diagnosis of diabetes mellitus provides for the development of complications and barriers to the PD modality in both the young and the elderly.     

Intramyocardial small-vessel disease in chronic alcoholism

A morphologic study of the small (50 to 200 micron) intramyocardial coronary arteries was performed. The cases chosen for study were selected from a relatively young group of patients without clinical evidence of alcoholic cardiomyopathy or pathologic evidence of large coronary artery disease, in order to evaluate alterations in the small vessels which could possibly be attributed to the chronic alcoholic state. Five basic vascular abnormalities were described. The most common alteration found in all nine cases was vascular wall edema (48 per cent), followed by perivascular fibrosis (42 per cent), vascular sclerosis (36 per cent), subendothelial humps (13 per cent), and vascular wall inflammation (11 per cent). The significance and pathogenesis of these changes were discussed. Primary endothelial cell damage was proposed as a common pathogenic mechanism for all five types of vascular abnormality. It was suggested that following endothelial damage, fluid and macromolecules penetrate into the vessel wall or into the perivascular space where, by incompletely understood processes, they induce vascular wall myocytes to produce collagen, elastin, and basement membrane-like substances. Evidence supporting this mechanism was derived from the common observation of vascular wall edema, from the occasional presence of erythrocytes and leukocytes within the vessel wall, and from experimental data in the literature. Several possible etiologic agents were implicated in the pathogenesis of endothelial and vessel wall injury. These included alcohol itself, acetaldehyde, biogenic amines, and magnesium deficiency. It is probable, however, that there are multiple etiologic factors which affect the small cardiac vessels of the chronic alcoholic. Finally, the proposal was advanced that the nonspecific pathology of the myocardium in chronic alcoholism may be a result of ischemia secondary to disease of the small intramyocardial coronary ateries.     

Alteration of vascular endothelium and endothelium smooth muscle interaction after carbogen gas perfusion of isolated rat and guinea pig heart

The aim of the study was to alter the vascular endothelium of the mammalian myocardium with respect to coronary flow regulation and vascular permeability. For this purpose, carbogen gas perfusion (GP) of Langendorff-type isolated rat and guinea pig heart was chosen. Perfusion of the hearts with carbogen gas was possible, as well as replacement of the GP by fluid perfusion. The energetic and mechanical state, the creatine kinase release, and the electron microscopic examination of the rat heart indicated only a moderate to minimal alteration of the cardiomyocytes after GP. As a result of GP a massive alteration of the vascular endothelium could be demonstrated in the rat heart, based on the release of the cytosolic endothelial marker enzyme, purine nucleoside phosphorylase, the partly altered vascular permeability and the morphologically detected endothelial damage to arterioles, capillaries and venules. Moreover, the reduced coronary flow response to short periods of anoxia (rat, guinea pig) and the inverted flow response to serotonin administration with maintained response to sodium nitroprusside (rat) in the post-gas perfusion period reflected an alteration of endothelial smooth muscular interaction in the rat and guinea pig heart. Furthermore, the distensibility of the coronary vasculature was increased in the rat and guinea pig heart in the post-gas perfusion period, where a relative autoregulatory behavior was maintained (rat) or partly maintained (guinea pig) in passively predilated vessels. In conclusion, carbogen gas perfusion of isolated hearts allows to induce preferred alteration of endothelium and endothelium-smooth muscle interaction.     

The influence of diabetes on neurological outcome and mortality in stroke patients

In a retrospective study of diabetic and non-diabetic patients with acute ischaemic stroke, mortality and neurological outcome were assessed. Mortality was determined 4 weeks after admission. The study population consisted of the consecutive patients (n = 609) admitted to the Department of Neurology with acute stroke between January 1994 and December 1995. There were 80 diabetic and 529 non-diabetic patients. The mortality rate was higher in diabetics (36.3%) than in non-diabetics (27%), but the difference was not significant (p = 0.08). The neurological status on admission, age, history of arterial hypertension, atrial fibrillation and coronary arterial disease were used to select groups of 41 diabetics and 84 non-diabetics with similar risk factors and similar onset of stroke. The neurological status on 10-th, 20-th and 28-th day of the hospital stay in both groups was compared. The study showed that insulin-dependent diabetics and older patients (above 65 years of age) with diabetes demonstrated a worse neurological outcome than non-diabetic patients, although the difference was not significant.     

Experimental model of pudendal nerve innervation of a skeletal muscle neosphincter for faecal incontinence

BACKGROUND: Faecal incontinence is difficult to treat. A variety of reconstructive procedures has been described, but none is entirely satisfactory. This study evaluated the feasibility of cross-innervating a skeletal muscle neosphincter with the pudendal nerve in a canine model. METHODS: Thirty dogs were rendered surgically incontinent (the pudendal nerve was cut and the external sphincter was partially excised). A neosphincter was then created using the semitendinosus muscle. In ten dogs pudendal nerve transposition (PNT) to the nerve to the semitendinosus muscle was performed. Ten dogs were given a dynamic neosphincter by inserting a pulse generator at 6 weeks. The remaining ten dogs served as controls with passive semitendinosus wraps. Anal manometry was performed before operation and monthly for 5 months. Muscle biopsies, performed at the initial operation and at 5 months, were stained for slow- and fast-twitch fibres, and were examined histologically. RESULTS: At 1 month, mean sphincter function was 32 per cent of the preoperative value in the control animals, 34 per cent in the PNT group and 27 per cent in the electrostimulation group; all dogs were incontinent. At 5 months the mean recovery of sphincter function was 42 per cent of the preoperative value in controls, 100 per cent in dogs with PNT (P < 0.001) and 63 per cent in dogs having electrostimulation (stimulator on) (P = 0.02). Six dogs with PNT had squeeze pressures equal to or greater than preoperative levels. At 5 months the ratio of slow to fast fibres was significantly greater in all dogs (control P = 0.01, PNT P < 0.005, electrostimulation P < 0.001). CONCLUSION: Use of the pudendal nerve to innervate a canine skeletal muscle anal wrap produced a functional anal sphincter that was superior to electrically stimulated and passive wraps.     

Effects of pregnancy on hemoglobin AIc in normal, gestational diabetic, and diabetic women

Hemoglobin AIc, a normal minor hemoglobin, has glucose linked by a Schiff base to the N-terminal end of the beta chain. The glucose interferes with the binding of 2,3 diphosphoglycerate, probably resulting in an increased affinity of that hemoglobin for oxygen. Hb AIc is increased to twice normal levels in juvenile-onset (insulin-dependent) diabetes. In the present studies, the Hb AIc, when expressed as per cent of total hemoglobin, was found to be elevated slightly in pregnany normal (m = 6.97 per cent), pregnant nondiabetic obese (m = 6.89 per cent), and gestationally diabetic subjects (m = 8.77 per cent) above that of normal females (m = 5.68 per cent). A remarkable difference was observed between the nonpregnant diabetics (m = 12.77 per cent) and the pregnant diabetics (m = 8.46 per cent). This decrease in the level of Hb AIc in diabetics who are pregnant more than 30 weeks may reflect either a better state of diabetic control and/or a compensatory mechanism to protect the fetus by facilitating oxygen exchange from mother to fetus.     

Insulin induces medial hypertrophy of myocardial arterioles in rats

To investigate the effect of hyperinsulinemia on arteriolar hypertrophy, myocardial hypertrophy, and blood pressure, we administered insulin intraperitoneally to SHR and WKY rats for 3 consecutive weeks. To prevent hypoglycemia, the drinking water contained 10% sugar, and to accentuate the blood pressure, their chow contained 8% table salt. Blood pressure was measured by the tail-cuff method. Heart weights were factored with body weights. Arterioles of approximately 100 microns in diameter were examined at the end of the experiment and the vascular wall thickness was factored with the lumen diameter. At the end of 3 weeks, blood pressure rose in the SHR but not in the WKY rats. The heart weights in the WKY normotensive rats did not increase, whereas in the SHR they did. Furthermore, there was a significant rise in vessel wall thickness in the rats that received insulin, whether there was a rise in blood pressure or not and whether they had an increase in heart weight or not. There was a similar rise in blood glucose in all the groups, with slightly more accentuated rise in the SHR that received insulin. Nevertheless the increase in vascular wall thickness occurred only in the groups which received insulin. This seems to preclude the importance of hyperglycemia per se as the causative agent for the increase in vascular wall thickness in this study. The increase was in the form of medial hypertrophy without any sign of atherosclerosis. It seems, therefore, that hyperinsulinemia is associated with hypertrophy of the media of arterioles regardless of the increase in heart weight or the rise in blood pressure.     

Diameter, wall tension, and flow in mesenteric arterioles during autoregulation

The effect of arterial pressure on vessel diameter, blood velocity, and intravascular pressure was examined in cat mesenteric arterioles in the arterial pressure range of 120--40 mmHg. Circumferential wall tension and volume flow in individual vessels were calculated. Twenty-nine arterioles with an average diameter of 25.1 micrometers were studied. Twenty-six reactive vessels dilated by an average of 6.5 micrometers with arterial pressure reduction, whereas three nonreactive arterioles narrowed by an average of 5.9 micrometers. When pressure was reduced, circumferential wall tension in reactive arterioles tended to be maintained, whereas in nonreactive vessels tension decreased more than pressure. Data from 25 of 26 reactive arterioles were consistent with the hypothesis that regulation of wall tension accounts for the autoregulatory response; however, in 18 of these vessels a flow-dependent mechanism could also account for the response. Thus the hypothesis that wall tension is a controlled variable responsible for autoregulation is supported, but an important role for flow regulation in local control is also supported.     

Heart transplantation in patients with diabetic end-organ damage before transplantation

Diabetes mellitus with preexisting end-organ damage (EOD) is considered a contraindication for heart transplantation. The outcome of such patients has not been well characterized. Among 138 patients transplanted between 12/88 and 7/94, 29 were diabetic (11 insulin-dependent); of these, 12 had preexisting EOD, defined as a creatinine clearance < or = 50 ml/min, a 24-hour urine protein concentration > or = 500 mg/L or typical symptoms of peripheral or autonomic polyneuropathy, and 17 had no EOD. We compared diabetics with and without EOD and non-diabetics (n = 109) for operative mortality, length of stay, serum creatinine, fasting glucose levels, and postoperative prednisone doses at 1,6, and 12 months. Actuarial survival and freedom from rejection and infection were analyzed. Both diabetic groups were significantly older than nondiabetics, Ischemic time, operative mortality, surgical technique, ICU- and total length of stay were similar. Actuarial survival and freedom from rejection were similar among the three groups. Infection rates including CMV did not differ. Serum creatinine levels increased in all groups compared to pretransplant levels (p = 0.001), but without significant differences among the groups. Post-transplant glucose levels at 6 and 12 months were higher for diabetic patients with EOD than for those without or for nondiabetics (183, 153, and 94 mg/dl at 6 months, p = 0.01; 202, 161, and 102 mg/dl at 12 months, p = 0.0001). Prednisone dosage was lower in diabetics with EOD at 6 months, but did not differ among the three groups at 12 months. The incidence of angiographically proven transplant vasculopathy did not differ at 1 and 2 years. Diabetics with preexisting EOD undergoing heart transplantation experience similar short- and intermediate-term results when compared to diabetics without EOD and nondiabetics. Metabolic control is more difficult to achieve, as indicated by higher fasting glucose levels. Larger and longer-term prospective studies have to confirm our findings, since the shortage of donor organs would increase if such patients were transplanted routinely.     

In-hospital and follow-up mortality of patients with acute myocardial infarction

Patients with definite acute MI who were admitted to Songkla University Hospital between 1982 and 1990 were studied. The 195 patients and 202 admissions were nearly equally distributed between these 65 and older versus those younger than 65. Three quarters were males. The in-hospital mortality was 19.5 per cent and 76.3 per cent of the deaths were from heart failure. Neither age nor gender determined the mortality once corrected for the Killip's staging. There was no difference in mortality when comparing Q versus non-Q MI, anterior versus inferior wall MI or males versus females. One hundred and thirty-eight patients could be followed for and average of 27.1 months. First year mortality was 11 per cent and the first 2 years was 14 per cent. The in-hospital mortality, representing the prethrombolytic era, appeared to be similar to values reported from the Thai and Western literature. The predominance of death from heart failure rather than from arrhythmia may be a consequence of delayed admission whence arrhythmic death had already occurred or patients will seek hospital advice only if highly symptomatic.     

Fucoidin reduces coronary microvascular leukocyte accumulation early in reperfusion

BACKGROUND: Leukocytes rapidly accumulate in the heart early in reperfusion after ischemia, contributing to reperfusion injury. The purpose of this study was to determine whether treatment with the selectin blocker fucoidin (FCN) would attenuate early leukocyte retention in coronary venules and capillaries during low flow reperfusion. METHODS: Isolated rat hearts subjected to 30 minutes of 37 degrees C, no-flow ischemia were initially reperfused with blood containing labeled leukocytes, followed by reperfusion with a Krebs red cell solution. The deposition of leukocytes in coronary capillaries and venules was observed using intravital microscopy. Three groups were studied: nonischemic control hearts, untreated postischemic hearts reperfused at low flow, and postischemic hearts reperfused at low flow, where both the hearts and the blood reperfusate were pretreated with FCN (0.36 mg/mL blood). RESULTS: In the ischemia-reperfusion group, we observed a rapid and significant increase in leukocyte accumulation in both capillaries and venules. Treatment with FCN significantly reduced the leukocyte accumulation in both capillaries and venules (p<0.05). In addition, FCN significantly reduced the persistence of leukostasis in both capillaries and venules, indicating that FCN affected a transient adhesion process. CONCLUSIONS: These results suggest that the selectin family of leukocyte-endothelial cell adhesion proteins mediates the initial retention of leukocytes in both coronary capillaries and venules during reperfusion. Selectin blockade may be effective in reducing the contribution of leukocytes to early reperfusion injury.     

Species differences in the expression of major histocompatibility complex class II antigens on coronary artery endothelium: implications for cell-mediated xenoreactivity

BACKGROUND: There is controversy in the literature as to whether swine coronary endothelium expresses major histocompatibility complex (MHC) class II antigens constitutively. METHODS: Because this issue has implications for cell-mediated human anti-swine xenogeneic responses, we stained tissue sections from human, pig, rat, and mouse hearts with the anti-class II monoclonal antibody ISCR3, which has a similar specificity and titer when binding to human, porcine, and rodent class II molecules. RESULTS: Immunoperoxidase staining of human and porcine hearts with ISCR3 resulted in a dense reaction on the coronary endothelium of epicardial arteries, intramuscular arterioles, and capillaries. In contrast, the coronary endothelium of rat and mouse hearts did not stain with ISCR3. When freshly harvested porcine aortic endothelial cells were placed in culture, class II MHC antigen expression was lost within three to four passages. CONCLUSIONS: Thus, using a single antibody with cross-species reactivities, we demonstrate that swine coronary endothelium, unlike rodent coronary arteries, expresses similar basal amounts of class II MHC antigens to human coronary vessels. The constitutive expression of class II MHC antigens on swine coronary artery endothelium may contribute to host T cell-mediated xenogeneic responses in clinical pig-to-human cardiac xenotransplantation and thus become a target for therapeutic intervention.     

Capillary supply of skeletal muscle fibers in untrained and endurance-trained men

Muscle fiber diameters and numbers of capillaries per fiber, per square millimeter, and around each fiber were determined in needle biopsies from the lateral part of the quadriceps muscle of 23 young men. Twelve subjects were untrained (UT) and eleven were endurance-trained (ET) athletes. Average values for maximal oxygen uptake were 51.3 (UT) and 72.0 ml/kg-min (ET). Mean fiber diameters were not significantly different in the two groups (48.8 and 49.1 micron). The capillaries per fiber ratios were 1.77+/-0.10 and 2.49+/-0.08 (mean+/-SE) in the UT and ET groups, respectively. The numbers of capillaries around each fiber were 4.43+/-0.19 (UT) and 5.87+/-0.18 (ET). The numbers of capillaries per mm2 were 585+/-40 (UT) and 821+/-28 (ET). Fiber diameters were 28% smaller in ultrathin than in fresh-frozen sections from the same biopsies. After correction for this difference, the numbers of capillaries per mm2 were 305 and 425 in the UT and ET, respectively. The capillaries per fiber ratio increased with increasing fiber diameter, but not sufficiently to maintain the number of capillaries per mm2. Fibers containing many mitochondria are surrounded by more capillaries than fibers with few mitochondria.     

Clinicopathological evaluation in the surgical treatment for ischemic heart disease

Discrepancy in coronary stenosis between angiogram and pathological specimen was moderately found. It is of a problem what is meaning by a significant narrowing. Coronary capacity per heart weight markedly reduced in multi-vessel disease and revealed an intimate relationship to sudded death and cardiac failure. Much of sclerosis in the arterial wall was relatively severe in spite of patency in lumen of the terminal artery. Intramuscular arterioles were intact even when severe extramuscular coronary atherosclerosis was seen. Well-developed collaterals were seen in much of multi-vessel disease. Muscle prevervation was relatively good even in the advanced sclerosis. It is reasonable to make an attempt on a newly construction of a vessel to introduce into preserved arteriola with well-developed collateral, and preserved myocardium.     

Microangioarchitectonics and microtopography of the blood vessels of the human stomach

The data of previous investigations on general principles of microarchitectonics of the human intraorganic gastric vessels have been checked. Peculiarities of branching and course of the stomach intraorganic vessels, arterio-venous anastomoses, twisted arterioles, sinusoid venules and veins confirm activity and variability of the organ's circulation at microcirculatory level. Certain slight differences in diameters and number of microvessels have been revealed in some anatomical parts of the serous membrane and submucous layer of the stomach. Maximal differences in vessel diameters of the microcirculatory bed and in number of capillaries per 1 mm2 have been revealed in the most active layers of the gastric wall--in muscular and mucous membranes. In the muscular membrane, large vessels and greater number of capillaries have been revealed in the area of the greater curvature and the pylorus. In the serous membrane in the pyloric area and in the area of the smaller curvature, microvessels have smaller diameters and the number of capillaries per square unit is less.     

Microvascular and tissue oxygen gradients in the rat mesentery

One of the most important functions of the blood circulation is O2 delivery to the tissue. This process occurs primarily in microvessels that also regulate blood flow and are the site of many metabolic processes that require O2. We measured the intraluminal and perivascular pO2 in rat mesenteric arterioles in vivo by using noninvasive phosphorescence quenching microscopy. From these measurements, we calculated the rate at which O2 diffuses out of microvessels from the blood. The rate of O2 efflux and the O2 gradients found in the immediate vicinity of arterioles indicate the presence of a large O2 sink at the interface between blood and tissue, a region that includes smooth muscle and endothelium. Mass balance analyses show that the loss of O2 from the arterioles in this vascular bed primarily is caused by O2 consumption in the microvascular wall. The high metabolic rate of the vessel wall relative to parenchymal tissue in the rat mesentery suggests that in addition to serving as a conduit for the delivery of O2 the microvasculature has other functions that require a significant amount of O2.