The interrelationship between compact tissue defect and bone shaft cavity circulation

The intraosseous pressure of tissue fluid, the electrical resistance between electrodes and the parameters of hemodynamics in tibial shaft cavity were measured experimentally. It was established that the occurrence and increase of compact defects led to the enhancement of fluid filtration from capillaries and tissue blood filling, whereas the reduction of compact defects led to hemodynamics parameter decrease. The shunting influence of newly formed regenerate bone capillaries cause an arterial wall elasticity increase and volumetric circulation rate limitation. The filtration-and-resorption balance of bone shaft cavity restored and circulation enhanced after compact defect healing.     

Effect of bradykinin on blood circulation in the human celiac artery bed]

Selective angiography and direct measurements of the arterial pressure in the celiac artery was used to study the influence of bradykinin on the blood circulation in healthy organs in the celiac region in 24 patients. A high sensitivity of the vessels to the action of bradykinin (0.1--10 mkg) was revealed: it decreased the blood pressure, increased the rate of blood flow, increased the diameter of arterial and venous vessels, arterio-venous anastomosis, increased the number of functioning capillaries. No differences were found in the reaction of the vessels of the liver, spleen pancreas, duodenum and the stomach to bradykinin.     

Histological study of brain in the rats exposed to 93-days' tail-suspension

Antiorthostatic position of rats during 93-days' tail suspension induced in the brain strongly pronounced edema of nervous tissue, alteration of structure in horoid plexus, pointing out the decrease in liquor secretion by exocytosis and increase in itraventricular pressure, morphological changes in veins and capillaries, reflecting the development of plethora in veins and tendency to thrombogenesis, and also the appearance of structural signs of prolonged arterial vasoconstriction and narrowing of arterial lumen in surface arteries which be considered as an adaptive process lying the obstacles to excessive blood inflow to brain and dumping the pulse wave during prolonged antiorthostatic state.     

Tissue blood flow and the sympathomimetic amines

In the arteries, blood flow and blood pressure are pulsatile in nature (Roston, 1962a; Roston 1962b). The patterns of blood movement and mural distension in the arteries are important because they may be associated with life-threatening degenerative changes in the arterial walls. As the vascular channels narrow, the pulsation decreases. At the level of the capillaries, almost no pulsation exists (Best and Taylor, 1961). The tissues are affected by the direct flow in the capillaries and not by the pulsation in the arteries. Thus, such quantities as pulse pressure, systolic pressure, and diastolic pressure which characterize blood movement in the arteries are not important as far as the tissues are concerned. Rather, the average pressure and flow in the capillaries are the quantities significant for tissue blood flow. The present study analyzes the local blood circulation in a typical tissue. Logical extension of this analysis results in insights into the physiological behavior of the circulation which integrate a considerable body of experimental data.     

Site of recruitment in the pulmonary microcirculation

Increasing the total surface area of the pulmonary blood-gas interface by capillary recruitment is an important factor in maintaining adequate oxygenation when metabolic demands increase. Capillaries are known to be recruited during conditions that raise pulmonary blood flow and pressure. To determine whether pulmonary arterioles and venules are part of the recruitment process, we made in vivo microscopic observations of the subpleural microcirculation (all vessels less than 100 microns) in the upper lung where blood flow is low (zone 2). To evoke recruitment, pulmonary arterial pressure was elevated either by an intravascular fluid load or by airway hypoxia. Of 209 arteriolar segments compared during low and high pulmonary arterial pressures, none recruited or derecruited. Elevated arterial pressure, however, did increase the number of perfused capillary segments by 96% with hypoxia and 165% with fluid load. Recruitment was essentially absent in venules (4 cases of recruitment in 289 segments as pressure was raised). These data support the concept that recruitment in the pulmonary circulation is exclusively a capillary event.     

Metabolic and myogenic factors in local regulation of the microcirculation.

Patterns of flow were recorded from individual capillaries of mesentery and muscle during autoregulation and reactive hyperemia. In cat mesentery at normal arterial pressure capillary blood flow was often periodic in nature. When arterial pressure was reduced periodicity was abolished and in certain cases mean flow increased. Elevation of venous pressure at this time caused restoration of flow periodicity and simultaneously a large fall in mean flow. Vasomotion and autoregulation in mesentery appear to be dependent on intravascular pressure per se. In cat sartorius muscle substantial increase in flow was seen in most capillaries during reactive hyperemia. In certain capillaries the pattern resembled the gross flow pattern while others showed a brief hyperemia and then a period of flow arrest that is presumably due to a strong precapillary vasoconstriction. The latter response is suggestive of a myogenic control while the former may be due to accumulation of metabolites. In frog pectoralis muscle reactive hyperemia was very prolonged in comparison to cat sartorius muscle. The general pattern of flow was consistent with the notion of a strong metabolic control mechanism. The three tissues studied provide examples of strong myogenic, strong metabolic, and combined metabolic and myogenic control of the microcirculation.     

The influence of adrenal vein occlusion on whole-kidney hemodynamics in the spontaneously hypertensive rats.

It has been shown that occlusion of the adrenal vein causes an increase in renal vascular resistance in the ipsilateral kidney in Wistar Kyoto rats (WKY). The most probable mechanism of this phenomenon is the direct inflow of adrenal catecholamines to the kidney by the adrenal renal portal circulation (ARPC). As the number of vessels of the ARPC is bigger and the tonic sympathetic activity is higher in spontaneously hypertensive rats (SHR), the aim of the current study was to compare the effect of adrenal vein occlusion on renal vascular resistance between SHR and WKY. Mean arterial blood pressure and renal blood flow (RBF) were measured and renal vascular resistance (RVR) was calculated before and after closure of the adrenal vein. Occlusion of the adrenal vein significantly reduced RBF and increased RVR in both strains of rats. The rise of the RVR was significantly higher in SHR than in WKY. Therefore we assume that the hemodynamic responsiveness of the kidney due to increase in blood flow through ARPC is greater in SHR and may contribute to the development of arterial hypertension in this strain of rat.     

Capillary filtration coefficient is independent of number of perfused capillaries in cat skeletal muscle

The capillary filtration coefficient (CFC) is assumed to reflect both microvascular hydraulic conductivity and the number of perfused capillaries at a given moment (precapillary sphincter activity). Estimation of hydraulic conductivity in vivo with the CFC method has therefore been performed under conditions of unchanged vascular tone and metabolic influence. There are studies, however, that did not show any change in CFC after changes in vascular tone and metabolic influence, and these studies indicate that CFC may not be influenced by alteration in the number of perfused capillaries. The present study reexamined to what extent CFC in a pressure-controlled preparation depends on the vascular tone and number of perfused capillaries by analyzing how CFC is influenced by 1) vasoconstriction, 2) increase in metabolic influence by decrease in arterial blood pressure, and 3) occlusion of precapillary microvessels by arterial infusion of microspheres. CFC was calculated from the filtration rate induced by a fixed decrease in tissue pressure. Vascular tone was increased in two steps by norepinephrine (n = 7) or angiotensin II (n = 6), causing a blood flow reduction from 7.2 +/- 0.8 to at most 2.7 +/- 0.2 ml x min(-1) x 100 g(-1) (P < 0.05). The decrease in arterial pressure reduced blood flow from 4.8 +/- 0.4 to 1.40 +/- 0.1 ml x min(-1) x 100 g(-1) (n = 6). Vascular resistance increased to 990 +/- 260% of control after the infusion of microspheres (n = 6). CFC was not significantly altered from control after any of the experimental interventions. We conclude that CFC under these conditions is independent of the vascular tone and number of perfused capillaries and that variation in CFC reflects variation in microvascular hydraulic conductivity.     

Effect of portacaval surgical anastomosis on systemic and splanchnic hemodynamics in portal hypertensive, cirrhotic rats

The effect of surgical end-to-side portacaval anastomosis (PCSA) on systemic and splanchnic circulation has been studied in cirrhotic rats with portal hypertension (CCl4-phenobarbital method) and in control animals. Hemodynamics have been measured using the microsphere technique, with a reference sample for the systemic hemodynamic measurements, and intrasplenic injection for portal systemic shunting rate measurements. Compared with controls, sham-operated (SO) cirrhotic rats showed a hyperdynamic circulation with increased cardiac output (CO) and decreased mean arterial pressure and peripheral resistances. PCSA in control rats induced only a small change in systemic hemodynamics, with parallel decreases in arterial pressure and peripheral resistances, and a small, nonsignificant increase in CO. In cirrhotic rats, PCSA induced a decrease of CO to values similar to those of control rats, with an increase in total peripheral resistances. PCSA induced an increase in hepatic arterial blood flow in control and in cirrhotic rats, portal pressure becoming in this latter group not different from that of control rats. Blood flow to splanchnic organs was higher in SO cirrhotic than in SO control animals. Thus portal venous inflow was also increased in SO cirrhotic rats. PCSA induced an increase in portal venous inflow in control rats, which was only significant in cirrhotic rats when expressed as a percentage of CO. In SO control animals, a significant correlation was observed between total peripheral resistances and splanchnic arteriolar resistances and between CO and splanchnic blood flow. These correlations were not observed in cirrhotic rats. These results do not support the hypothesis that hyperdynamic circulation shown by cirrhotic rats is based on increases in splanchnic blood flow and (or) massive portal systemic shunting.     

Effects of stenosis on non-newtonian flow of the blood in an artery

It has been shown that the resistance of flow and the wall shear increase with the size of the stenosis but these increases are comparatively small due to non-Newtonian behaviour of the blood indicating the usefulness of its rheological character in the functioning of the diseased arterial circulation.     

Changes in cerebral oxygenation and blood flow during LBNP in spinal cord-injured individuals.

Spinal cord-injured (SCI) individuals, having a sympathetic nervous system lesion, experience hypotension during sitting and standing. Surprisingly, they experience few syncopal events. This suggests adaptations in cerebrovascular regulation. Therefore, changes in systemic circulation, cerebral blood flow, and oxygenation in eight SCI individuals were compared with eight able-bodied (AB) individuals. Systemic circulation was manipulated by lower body negative pressure at several levels down to -60 mmHg. At each level, we measured steady-state blood pressure, changes in cerebral blood velocity with transcranial Doppler, and cerebral oxygenation using near-infrared spectroscopy. We found that mean arterial pressure decreased significantly in SCI but not in AB individuals, in accordance with the sympathetic impairment in the SCI group. Cerebral blood flow velocity decreased during orthostatic stress in both groups, but this decrease was significantly greater in SCI individuals. Cerebral oxygenation decreased in both groups, with a tendency to a greater decrease in SCI individuals. Thus present data do not support an advantageous mechanism during orthostatic stress in the cerebrovascular regulation of SCI individuals.     

Experimental study on mechanism of absorption of cryonecrotized tumor antigens

On Day 7 of subcutaneous MRMT-1 tumor inoculation in the thigh of Sprague-Dawley rats, the tumor was treated cryosurgically by contact method. Postoperative changes in local blood circulation were observed by colloidal carbon perfusion and hydrogen-clearance methods, and the pathway and time course of tumor antigen absorption were observed by measuring uptake in serum and lymph nodes of [3H]thymidine injected intratumorally. Results were: At 0.5 to 1 hr after cryosurgery, vascular stasis, dilatation, and tortuosity were observed. There was no inflow of carbon and almost no uptake of [3H]thymidine. At 6 hr, vascular stasis and sludging become more marked. There was no inflow of carbon, while uptake of [3H]thymidine markedly increased. At 24 hr, some carbon inflow in fin vessels and partial recovery of blood circulation in the peritumoral region were observed. Rate of [3H]thymidine uptake was further increased. At 72 hr, carbon inflow and blood circulation increased further, while the cryonecrotized tumor showed hyaline degeneration. At 168 hr, increase of newly formed vessels and recovery of blood circulation were remarkable, but uptake of [3H]thymidine was decreased in parallel with increased demarcation of the cryonecrotized tumor. From these results, it was suggested that the absorption of cryonecrotized tumor antigens started through lymphatic channels in the early period and then took place also through newly formed capillaries surrounding the tumor at 24 hr after cryosurgery and continued until 72 hr after cryosurgery.     

Blood vessels of the periodontium of incisors and molars of the lower jaw of the white rat

By means of injective and noninjective methods, the structural organization of the incisor and molar blood bed has been studied in the white rat mandible. For the periodontal blood bed, distinguishing by a pronounced organo-specificity, distribution of arterial and venous vessels between collagenous fiber bundles and a reticular arrangement of the capillaries is peculiar. A definite connection is clearly seen between angioarchitectonics of different segments of the periodontium, its structure and function. Unequal density of the capillary networks in the area of the epithelial dental organ and difference of the periodontal angioarchitectonics with the lingual and labial surfaces of the incisors are noted. The area of the epithelial dental organ, having a peculiar functional importance, is characterized by multiple pathways of blood inflow and outflow, by concentration of structural-functional adaptations which increase expansiveness, capacity and diffusive surface of metabolic microvessels, by a small critical thickness of the tissue layer between neighbouring capillaries.     

Dynamic viscous flow in distensible vessels of skeletal muscle microcirculation: application to pressure and flow transients

Blood flow in the microcirculation of the rat skeletal muscle during transient changes of arterial pressure is analyzed theoretically. Although flow in such small vessels is quasi-steady and has a very low Reynolds number, time-dependent nonuniform flows along the length of the blood vessels can be observed due to vessel distensibility. The governing equations for a single microvessel are derived using previously measured microvessel elasticity, and several solutions to different inflow and outflow pressures and flow conditions are investigated. The results indicate that when such distensible microvessels are subjected to a step increase of arterial pressure, the arterial flow shows a rapid overshoot followed by a progressive decay to steady-state. An arterial step flow induces a different response which takes the form of a monotonically increasing pressure. Pressure and flows are nonuniform along the vessel length during such transients. In-vitro whole organ pressure-flow data are presented in the dilated rat gracilis muscle which qualitatively agree with the theoretical predictions.     

Hemodynamic indices versus gastric tonometric measurements for prognosis of hemorrhagic shock: a porcine model

The aim of the study reported here was to assess the prognostic value of gastric tonometry and its implications in the initial phases of hemorrhagic shock. Hemorrhagic shock was induced by use of femoral arterial bleeding in 12 hybrid swine under general anesthesia. Approximately 30% of the circulating blood volume was removed, until mean arterial pressure of 45 mmHg was reached. The shock conditions were observed over a limited period (90 min) by comparing traditional hemodynamic parameters with gastric tonometric measurements and tissue oxygenation. After a shock period of 90 min without pharmacologic treatment, blood was collected in acid-citrate dextrose-treated bags and was reinfused via the right femoral vein. At the end of the experiment, seven animals had good hemodynamic recovery on reinfusion (group A), whereas values in five animals deceased in the same phase (group B). Hemodynamic and gastric tonometric results were compared between survivors and nonsurvivors. Intravascular volume restoration and reduction of systemic vascular resistance (SVR) enabled the animals of group A to maintain standard ventricular kinetics and recover in terms of splanchnic regional flow. In addition, increase in intramucosal gastric pH (pHi), decrease in the pH-gap (pHa-Hi), and progressive restoration in gastric wall tissue oxygenation (PtO2) also were observed. These results suggest that useful diagnostic and therapeutic indications can be obtained by acquisition of simple hemodynamic measurements at the beginning of the shock period. On the basis of results of statistical analysis, only mean arterial pressure and SVR were good indicators of shock development, whereas pHi was not a significant factor in this experimental model.     

Syncope, cerebral perfusion, and oxygenation.

During standing, both the position of the cerebral circulation and the reductions in mean arterial pressure (MAP) and cardiac output challenge cerebral autoregulatory (CA) mechanisms. Syncope is most often associated with the upright position and can be provoked by any condition that jeopardizes cerebral blood flow (CBF) and regional cerebral tissue oxygenation (cO(2)Hb). Reflex (vasovagal) responses, cardiac arrhythmias, and autonomic failure are common causes. An important defense against a critical reduction in the central blood volume is that of muscle activity ("the muscle pump"), and if it is not applied even normal humans faint. Continuous tracking of CBF by transcranial Doppler-determined cerebral blood velocity (V(mean)) and near-infrared spectroscopy-determined cO(2)Hb contribute to understanding the cerebrovascular adjustments to postural stress; e.g., MAP does not necessarily reflect the cerebrovascular phenomena associated with (pre)syncope. CA may be interpreted as a frequency-dependent phenomenon with attenuated transfer of oscillations in MAP to V(mean) at low frequencies. The clinical implication is that CA does not respond to rapid changes in MAP; e.g., there is a transient fall in V(mean) on standing up and therefore a feeling of lightheadedness that even healthy humans sometimes experience. In subjects with recurrent vasovagal syncope, dynamic CA seems not different from that of healthy controls even during the last minutes before the syncope. Redistribution of cardiac output may affect cerebral perfusion by increased cerebral vascular resistance, supporting the view that cerebral perfusion depends on arterial inflow pressure provided that there is a sufficient cardiac output.     

Sympathetic innervation of the splanchnic region mediates the beneficial hemodynamic effects of 8-OH-DPAT in hemorrhagic shock

Administration of the 5-HT(1A) receptor agonist, 8-OH-DPAT, improves cardiovascular hemodynamics and tissue oxygenation in conscious rats subjected to hypovolemic shock. This effect is mediated by sympathetic-dependent increases in venous tone. To determine the role of splanchnic nerves in this response, effects of 8-OH-DPAT (30 nmol/kg iv) were measured following fixed-arterial blood pressure hemorrhagic shock (i.e., maintenance of 50 mmHg arterial pressure for 25 min) in rats subjected to bilateral splanchnic nerve denervation (SD). Splanchnic denervation decreased baseline venous tone as measured by mean circulatory filling pressure (MCFP) and accelerated the onset of hypotension during blood loss. Splanchnic denervation did not affect the immediate pressor effect of 8-OH-DPAT but did reverse the drug's lasting pressor effect, as well as its ability to increase MCFP and improve metabolic acidosis. Like SD, adrenal demedullation (ADMX) lowered baseline MCFP and accelerated the hypotensive response to blood withdrawal but also reduced the volume of blood withdrawal required to maintain arterial blood pressure at 50 mmHg. 8-OH-DPAT raised MCFP early after administration in ADMX rats, but the response did not persist throughout the posthemorrhage period. In a fixed-volume hemorrhage model, 8-OH-DPAT continued to raise blood pressure in ADMX rats. However, it produced only a transient and variable rise in MCFP compared with sham-operated animals. The data indicate that 8-OH-DPAT increases venoconstriction and improves acid-base balance in hypovolemic rats through activation of splanchnic nerves. This effect is due, in part, to activation of the adrenal medulla.     

Understanding Guyton's venous return curves

Based on observations that as cardiac output (as determined by an artificial pump) was experimentally increased the right atrial pressure decreased, Arthur Guyton and coworkers proposed an interpretation that right atrial pressure represents a back pressure restricting venous return (equal to cardiac output in steady state). The idea that right atrial pressure is a back pressure limiting cardiac output and the associated idea that "venous recoil" does work to produce flow have confused physiologists and clinicians for decades because Guyton's interpretation interchanges independent and dependent variables. Here Guyton's model and data are reanalyzed to clarify the role of arterial and right atrial pressures and cardiac output and to clearly delineate that cardiac output is the independent (causal) variable in the experiments. Guyton's original mathematical model is used with his data to show that a simultaneous increase in arterial pressure and decrease in right atrial pressure with increasing cardiac output is due to a blood volume shift into the systemic arterial circulation from the systemic venous circulation. This is because Guyton's model assumes a constant blood volume in the systemic circulation. The increase in right atrial pressure observed when cardiac output decreases in a closed circulation with constant resistance and capacitance is due to the redistribution of blood volume and not because right atrial pressure limits venous return. Because Guyton's venous return curves have generated much confusion and little clarity, we suggest that the concept and previous interpretations of venous return be removed from educational materials.     

Microvascular pressure and functional capillary density in extreme hemodilution with low- and high-viscosity dextran and a low-viscosity Hb-based O2 carrier

Blood losses are usually corrected initially by the restitution of volume with plasma expanders and subsequently by the restoration of oxygen-carrying capacity using either a blood transfusion or possibly, in the near future, oxygen-carrying plasma expanders. The present study was carried out to test the hypothesis that high-plasma viscosity hemodilution maintains perfused functional capillary density (FCD) by preserving capillary pressure. Microvascular pressure responses to extreme hemodilution with low- (LV) and high-viscosity (HV) plasma expanders and an exchange transfusion with a polymerized bovine cell-free Hb (PBH) solution were analyzed in the awake hamster window chamber model (n = 26). Systemic hematocrit was reduced from 50% to 11%. PBH produced a greater mean arterial blood pressure than the nonoxygen carriers. FCD was higher after a HV plasma expander (70 +/- 15%) vs. PBH (47 +/- 12%). Microvascular pressure spanning the capillary network was higher after a HV plasma expander (16-19 mmHg) compared with PBH (12-16 mmHg) and a LV plasma expander (11-14 mmHg) but lower than control (22-26 mmHg). FCD was found to be directly proportional to capillary pressure. The use of a HV plasma expander in extreme hemodilution maintained the number of perfused capillaries and tissue perfusion by comparison with a LV plasma expander due to increased mean arterial blood pressure and capillary pressure. The use of PBH increased mean arterial pressure but reduced capillary pressure due to vasoconstriction and did not maintain FCD.