Significant Decrease In Blood Flow Research Articles

Cardiovascular effects of centrally administered endothelin-1 and its relationship to changes in cerebral blood flow

Intracerebroventricular (i.c.v.) injection of endothelin-1 (ET-1; 100 ng, i.c.v.) produced an initial pressor (24%) (peak at 3 min following ET-1 administration) and a delayed depressor (−40%) (30 and 60 min following ET-1 administration) effects in urethane anesthetized rats. The pressor effect of ET-1 was due to an increase (21%) in cardiac output, while the depressor effect of ET-1 was associated with a marked decrease (−46%) in cardiac output. Stroke volume significantly decreased at 30 and 60 min after the administration of ET-1. No change in total peripheral vascular resistance and heart rate was observed following central administration of ET-1. The effects of ET-1 on blood pressure, cardiac output and stroke volume were not observed in BQ123 (10 μg, i.c.v.) treated rats. Blood flow to the cerebral hemispheres, cerebellum, midbrain and brain stem was not affected at 3 min, but a significant decrease in blood flow to all the regions of the brain was observed at 30 and 60 min following central administration of ET-1. BQ123 pretreatment completely blocked the central ET-1 induced decrease in blood flow to the brain regions. It is concluded that the pressor effect of centrally administered ET-1 is not accompanied by a severe decrease in brain blood flow, however, a subsequent decrease in blood pressure is associated with a decrease in blood flow to the brain. The cardiovascular effects of ET-1 including decrease in brain blood flow are mediated through central ET A receptors.

Redistribution of organ blood flow after hemorrhage and resuscitation in full-term piglets: J Pediatr Surg 1994; 29/8: 1097–1102

0 Newborn piglets (aged 1 to 2 days and 7 to 14 days) were used to study (1) the redistribution of organ blood flow after a 25% acute blood loss and (2) the response to resuscitation with shed blood (20 mL/ kg), crystalloid (normal saline [NS] or lactated Ringer’s [LR]; 60 mL/ kg), and colloid (Dextran-40, 20 mL/kg). Hemodynamic parameters showed little differences in the response to hemorrhage and resuscitation. The two age groups had no significant differences in parameters or blood flow (results combined). The animals maintained flow to the heart and central nervous system (CNS) and had significantly decreased flow to the kidneys and splanchnic organs. In the gastrointestinal tract, the small intestine was affected most severely, with a significant decrease in blood flow, especially to the mucosa. In all organ systems, Dextran 40 restored blood flow to levels significantly above the baseline. Shed blood and crystalloid restored flow to organs sustaining decreased flow, but crystalloid did not restore flow to the baseline level in the kidney and all segments of the gastrointestinal tract. Copyright Q 1994 by W.B. Saunders Company

The hemodynamic effect of GnRH agonist therapy on uterine leiomyoma vascularity: a prospective study using transvaginal color Doppler sonography.

The objective of this study was to correlate, during 12 weeks of therapy with gonadotropin releasing hormone agonist (GnRH-a), the chronological effect and the hemodynamic changes on the uterine artery and the leiomyometrial supplying vessels. Twenty-three premenopausal women with clinically diagnosed uterine leiomyomas received 3.75 mg of leuprolide acetate intramuscularly every 4 weeks for 12 weeks. Pretreatment values of serum estradiol, uterine and leiomyoma volumes and blood flow characteristics of the main uterine artery and leiomyoma supplying vessels-resistance index (RI), pulsatility index (PI) and peak-systolic velocity, obtained by transvaginal color Doppler sonography-were compared with treatment values at 4, 8 and 12 weeks of leuprolide acetate therapy. The first event in the chronological response to the GnRH-a therapy was a statistically significant increase in RI and PI values for major leiomyoma vessels, observed at the end of the 4th week (p < 0.05), which increased significantly after 8 and 12 weeks (p < 0.01 and p < 0.001, respectively). These findings were in direct correlation with a significant decrease of estradiol levels after 4, 8 and 12 weeks (p < 0.05, p < 0.001 and p < 0.001, respectively). The significant decrease of blood flow in the leiomyometrial vessels was followed by a significant decrease of the main uterine artery blood flow after 8 weeks and uterine and leiomyoma volumes by 42% and 55%, respectively, after 12 weeks of GnRH-a therapy. We concluded that a significant increase in leiomyometrial vessels RI and PI values, which was found 4 weeks after the first dose of GnRH-a, but without major leiomyoma volume decrease, emphasizes that the first significant effect of GnRH therapy in the process of uterine and leiomyoma volume shrinkage is the reduction of leiomyometrial rather than uterine blood flow. This effect is followed by a considerable reduction of uterine vascularity and a significant decrease of uterine and leiomyoma volumes. If a decrease of blood loss during myomectomy is the main aim of GnRH-a therapy, we believe that 8 weeks would be an appropriate therapy duration.

Blood flow changes in human somatosensory cortex during anticipated stimulation.

Positron emission tomography (PET) measurements of brain blood flow were used to monitor changes in the human primary and secondary somatosensory cortices during the period when somatosensory stimuli were expected. In anticipation of either focal or innocuous touching, or localized, painful shocks, blood flow decreased in parts of the primary somatosensory cortex map located outside the representation of the skin area that was the target of the expected stimulus. Specifically, attending to an impending stimulus to the fingers produced a significant decrease in blood flow in the somatosensory zones for the face, whereas attending to stimulation of the toe produced decreases in the zones for the fingers and face. Decreases were more prominent in the side ipsilateral to the location of the expected stimulus. No significant changes in blood flow occurred in the region of the cortex representing the skin locus of the awaited stimulation. These results are concurrent with a model of spatial attention in which potential signal enhancement may rely on generalized suppression of background activity.

The effects of nitric oxide inhibition on regional hemodynamics during hyperdynamic endotoxemia.

To determine the effect of the inhibition of nitric oxide (NO) on selective organ blood flow in endotoxin-induced sepsis. Nonrandomized, controlled experiment. Animal research facility in Brooklyn, NY. Eleven mongrel dogs. Eleven dogs were divided into one of two groups: a control group (n = 5) and an endotoxin-treated group (n = 6). The animals were anesthetized, and electromagnetic and ultrasonic flow probes were placed on the distal aorta, right internal carotid artery, superior mesenteric artery, and left renal artery. Sepsis was induced with a 60-mg/kg intravenous injection of Escherichia coli endotoxin. When the arterial blood pressure decreased to less than 60 mm Hg despite adequate fluid resuscitation, NO synthesis was inhibited with a 25-mg/kg intravenous administration of NG-monomethyl-L-arginine. After 15 minutes of inhibition, a 400-mg/kg intravenous administration of L-arginine, the substrate of NO synthase enzyme, was given. Physiologic measurements were continued for 15 minutes thereafter. Heart rate, blood pressure, central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac output, hematocrit, arterial and venous blood gas values, and blood flow measurements of right internal carotid artery, superior mesenteric artery, left renal artery, and distal aorta. Control animals did not demonstrate a significant (P > .05) decrease in blood flow in the internal carotid artery, superior mesenteric artery, and distal aorta after the administration of NG-monomethyl-L-arginine. The endotoxin-treated group showed a significant (P < .05) decrease in organ perfusion when treated with the NO synthase inhibitor, NG-monomethyl-L-arginine. Inhibition of NO production in the treatment of sepsis caused a significant decrease in blood flow to all vascular beds in vivo. The role, if any, of the inhibition of NO in the treatment of sepsis is questioned.

Effect of hemorrhagic hypotension on extracellular level of dopamine, cortical oxygen pressure and blood flow in brain of newborn piglets

The present study describes the relationships between extracellular striatal dopamine, cortical oxygen pressure and blood flow in brain of newborn piglets during hemorrhagic hypotension. Cerebral oxygen pressure was measured optically by the oxygen dependent quenching of phosphorescence; extracellular dopamine by in vivo microdialysis; striatal blood flow was monitored by a laser Doppler. Following a 2 h stabilization period after implanting the microdialysis and laser Doppler probes in the striatum, the mean arterial blood pressure (MABP) was decreased in stepwise manner from 87 ± 4 Torr (control) to 35 ± 5 Torr, during 63 min. The whole blood was then reinfused and measurements were continued for 45 min. Statistically significant decrease in blood flow, 10%, was observed when arterial blood pressure decreased to about 53 Torr. With further decrease blood pressure to 35 Torr, blood flow decreased to about 35% of control ( P < 0.01). Cortical oxygen pressure decreased almost proportional to decrease in blood pressure. The progressive decrease in MABP from 87 ± 4 Torr to 65 ± 6, 52 ± 7, and 35 ± 5 Torr resulted in cortical oxygen pressure decreasing from 45 ± 4 Torr to 33 ± 3 Torr ( P < 0.05), 24 ± 4 Torr ( P < 0.01) and 13 ± 3 Torr ( P < 0.01). The levels of extracellular dopamine in the striatum increased with decreasing cortical oxygen pressure. As cortical oxygen decreased, the extracellular dopamine increased to 230%, 420% and 3200% of control, respectively. Our results show that in mild hypotension total blood flow is well maintained but oxygen pressure in the microvasculature decreases, possibly due to heterogeneity in the regulatory mechanism. The decrease in cortical oxygen pressure in striatum is parallel to increase in striatal dopamine which then can be use as early indicator of brain hypoxia.

Redistribution of organ blood flow after hemorrhage and resuscitation in full-term piglets

Newborn piglets (aged 1 to 2 days and 7 to 14 days) were used to study (1) the redistribution of organ blood flow after a 25% acute blood loss and (2) the response to resuscitation with shed blood (20 mL/kg), crystalloid (normal saline [NS] or lactated Ringer's [LR]; 60 mL/kg), and colloid (dextran-40, 20 mL/kg). Hemodynamic parameters showed little differences in the response to hemorrhage and resuscitation. The two age groups had no significant differences in parameters or blood flow (results combined). The animals maintained flow to the heart and central nervous system (CNS) and had significantly decreased flow to the kidneys and splanchnic organs. In the gastrointestinal tract, the small intestine was affected most severely, with a significant decrease in blood flow, especially to the mucosa. In all organ systems, Dextran 40 restored blood flow to levels significantly above the baseline. Shed blood and crystalloid restored flow to organs sustaining decreased flow, but crystalloid did not restore flow to the baseline level in the kidney and all segments of the gastrointestinal tract.

Regional retinal blood flow reduction following half fundus photocoagulation treatment.

Regional changes in retinal blood flow following inferior and subsequent superior argon laser half fundus photocoagulation treatment were measured in six diabetic patients with advanced retinopathy. Centreline blood velocity, vessel diameter, and blood flow in major inferior and superior temporal retinal arteries were measured at baseline and following each treatment using the bidirectional laser Doppler technique and monochromatic fundus photography. Inferior fundus laser treatment produced a significant blood flow decrease in inferior temporal arteries ranging from 60% to 78%. Blood flow changes in superior temporal arteries were not significant, ranging from -7% to +14%. Subsequent superior fundus laser treatment produced a significant blood flow decrease in superior temporal arteries ranging from 50% to 66%. Subsequent blood flow changes in inferior temporal arteries were not significant, ranging from -19% to +21%. The results indicate that regional laser treatment produces a regional reduction in retinal blood flow, consistent with measurements of preretinal and intraretinal oxygen tension which have indicated increases in oxygen over photocoagulated regions.

Renal endothelin mechanism in altered thyroid states

Endothelin (ET) mechanisms were studied in hyper-and hypo-thyroid states in rats. Hyperthyroidism was induced by daily administration of thyroxine (0.1 mg/kg, i.p.) for 8 weeks, while hypothyroidism was induced by daily administration of methimazole (10 mg/kg, i.p.) for 8 weeks. The concentration of endogenous ET-1 was determined in the kidneys using radioimmunoassay. Systemic hemodynamics and renal blood circulation was measured using a radioactive microsphere technique. A significant increase in systolic and diastolic blood pressure, heart rate and cardiac output was observed in hyperthyroid rats as compared to eu- and hypo-thyroid rats. Total peripheral resistance was found to be similar in eu-, hyper- and hypo-thyroid rats. The endogenous concentration of ET-1 in the kidneys was significantly lower in hyper- as compared to eu- and hypo-thyroid rats. The blood flow to the kidneys was significantly increased in hyper- as compared to eu- and hypothyroid rats. Infusion of ET-1 (100 ng/kg/min i.v. for 45 min) produced a significant decrease in blood flow to the kidneys of eu-, hyper- and hypo-thyroid rats. The decrease in blood flow was similar in eu-, hyper- and hypo-thyroid rats, indicating that the response of renal blood vessels to exogenous ET-1 is not altered during thyroid dysfunction. Since endogenous ET-1 is involved in the regulation of vascular tone, it may be concluded that in hyper-thyroid rats decrease in concentration of the renal ET-1 could be contributing to an increase in blood flow to the kidney.

Hemodilution improves cerebral hemodynamics in internal carotid artery occlusion.

Hemodilution may be a useful form of therapy for patients with carotid occlusive disease and hemodynamic ischemia. Accordingly, we evaluated the effects of hemodilution on cerebral hemodynamics and oxygen metabolism in patients with carotid artery occlusion. Using positron emission tomography, we analyzed regional cerebral blood flow, oxygen extraction fraction, oxygen metabolic rate, and blood volume before and after isovolemic hemodilution in five patients with unilateral internal carotid artery occlusion and minor stroke. Hemodilution was accomplished by phlebotomy of 400 mL and infusion of 400 mL of hydroxyethyl starch. Before hemodilution, the patients had a significant decrease in blood flow and oxygen transport along with significantly elevated oxygen extraction fraction in the cerebral hemisphere with carotid artery occlusion compared with six control subjects. After hemodilution, the hematocrit and arterial oxygen content decreased from 41.2% and 18.6 mL/dL to 36.3% and 16.5 mL/dL, respectively. Both cerebral blood flow and oxygen transport were increased and oxygen extraction fraction was decreased without any change in oxygen consumption. The degree of increase in blood flow and oxygen transport was positively correlated with the ratio of oxygen extraction fraction to blood volume before hemodilution. These findings indicate that hemodilution improves oxygen transport as well as blood flow in patients with internal carotid occlusion and decreased perfusion and that this improvement may be more prominent in patients with a severely compromised hemodynamic state. Thus, hemodilution may be useful in patients with hemodynamic ischemia.

Indomethacin-induced blood flow distribution in premature and full-term piglets

Indomethacin (IND), widely used in premature infants to effect nonoperative closure of patent ductus arteriosus (PDA), has been implicated in gastrointestinal tract (GI) perforations and necrotizing enterocolitis (NEC). The vasoactive effects of IND could simultaneously affect regional blood flow distribution, specifically a decrease in intestinal blood flow. This study determined blood pressure (BP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR) and regional blood flows (mL/min/g) at baseline, 15, 60, and 120 minutes after intravenous infusion of IND (0.4 mg/kg) in three groups: preterm piglets delivered 7 to 10 days before term; 1- to 2-day-old piglets; and 7- to 14-day-old piglets. IND did not significantly affect hemodynamic parameters (BP, HR, CO, TPR) or regional blood flows to the heart, central nervous system, kidney or GI tract in the premature animals. In 1- to 2-day-old animals, a significant increase in BP and TPR occurred at 120 minutes, with significant decreases in blood flow to the GI tract in the esophagus, stomach, and rectosigmoid. In the 7- to 14-day group CO significantly decreased while TPR increased. Significant decreases in blood flow occurred throughout the GI tract, most pronounced in the small intestine and colon, essentially due to decreased mucosal blood flow. Our study indicates that indomethacin can cause selective GI tract mucosal ischemia, and that the effect is increased in the more developed animal. This effect on mucosal blood flow suggests the GI tract disturbances seen after IND administration are due to an ischemic injury to mucosa previously affected by ischemia-reperfusion injury from other stresses.

Effects of NG‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

1. The effects of 300 mg kg-1 of the nitric oxide (NO) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on the regional blood flow, on the flow response to 1 mg kg-1 of thyrotropin-releasing hormone (TRH) and on cerebral blood flow autoregulation were studied in urethane anesthetized rabbits subjected to unilateral sectioning of the cervical sympathetic claim. The blood flow measurements were performed by the tracer microspheres method. 2. The cerebral arteriovenous difference in oxygen saturation (CAVOD) was measured before and after the administration of L-NAME and TRH in order to ascertain whether the effects on cerebral blood flow that were observed were secondary to changes in cerebral metabolism. 3. L-NAME caused a significant decrease in blood flow in several cerebral regions; CBFtot decreased to 72 +/- 4% of control (P < 0.001). An increase in blood pressure and a concurrent decrease in heart rate and cardiac output were noted. 4. In the eye, L-NAME caused a reduction in uveal blood flow which was more pronounced on the sympathetically intact side; in the retina the blood flow decreased to 50% of control on both sides. 5. The administration of TRH in animals pretreated with L-NAME caused a significant increase in blood pressure and cerebral blood flow. 6. In L-NAME-treated animals the CBF was not affected when the mean arterial blood pressure was increased by ligation of the abdominal aorta. 7. The CAVOD increased from 56.0 +/- 5.2 to 73.6 +/- 3.5%, 20 min after the administration of L-NAME. In animals given 1 mg kg-1 TRH after L-NAME the CAVOD decreased to 54.6 +/- 4.6%, 5 min after the injection of TRH.8. The results of the present study indicate that endogenous NO is involved in the regulation of regional blood flow and blood pressure in the anaesthetized rabbit. The reduction in cerebral blood flow that was caused by L-NAME was not due to a reduction in cerebral metabolism. An interaction between the NO synthesis/release/effect and the sympathetic nervous system was found in the uvea. There was no evidence for a major involvement of NO in the cardiovascular responses to TRH and autoregulation of cerebral blood flow was not abolished by L-NAME.

Portal Hypertensive Colopathy —Endoscopic, Hernodynamic and Morphometric Study—

Abstract: Although it is widely accepted that congestive gastropathy is a well recognized manifestation of portal hypertension, the influence of the latter on the lower gastrointestinal tract has not been adequately studied. Therefore, we evaluated prospectively, by total colonoscopy, 30 consecutive cirrhotic patients after their varices were obliterated by endoscopic sclerotherapy. All of them had not had any bleeding episode for some time and all had varying degrees of congestive gastropathy identified by an UGI endoscopy at the time of the study. Additionally, colonic mucosal perfusion was assessed by means of laser‐Doppler flowmetry at 4 defined points on the transverse colon and two mucosal biopsy specimens were obtained from the same area for histology and morphometric analysis of mucosal capillaries. Seven non cirrhotic patients who had undergone colonoscopy for various reasons but had no findings, served as controls. Twenty‐eight patients [rate 93%] were found to have multiple vascular ectasis of differing degrees of severity. These vascular‐looking lesions were mainly located in the right colon and rectosigmoid. Less frequent lesions were non specific mucosal edema, sparse mucosal veins and rectal varices. The statistical evaluation of mucosal perfusion revealed a highly significant decrease of blood flow in the cirrhotic patients [p = 0.00001]. A morphometric analysis revealed a significantly higher mean number of capillaries [p = 0.0012] and a higher mean cross‐sectional vascular area per field in the cirrhotic patients than in the control subjects [p=0.0055]. We concluded that portal hypertension affects the lower gastrointestinal tract giving an endoscopic, microcirculatory and histopathologic pattern quite similar to that of the gastric mucosa.

Platelet-activating factor causes hypoketonaemia in starved rats.

1. The aim of this work was to examine whether platelet-activating factor could mimic the hypoketonaemia seen in septic and endotoxic experimental animals. Platelet-activating factor was administered either by the intraperitoneal (high dose) or intravenous (jugular vein, low dose) routes. 2. Intraperitoneal injection of platelet-activating factor (25 micrograms/kg body weight) decreased the blood ketone body concentration (acetoacetate plus 3-hydroxybutyrate) transiently (30 min after injection) in starved rats. Continuous intravenous infusion of platelet-activating factor (40 ng min-1 kg-1 for 5 h) caused comparable hypoketonaemia. 3. The hepatic acetoacetate concentration also decreased transiently after injection of platelet-activating factor and there was an increase in the 3-hydroxybutyrate/acetoacetate ratio. The hepatic ATP concentration decreased at 15 and 30 min after injection of platelet-activating factor. Infusion of platelet-activating factor caused a similar decrease in hepatic ketone body concentration, but no significant change in the 3-hydroxybutyrate/acetoacetate ratio or adenine nucleotide concentrations. 4. Platelet-activating factor administered by infusion, but not by injection, decreased the plasma non-esterified fatty acid concentration. The plasma glycerol concentration also decreased after infusion of platelet-activating factor, suggesting decreased lipolysis in adipose tissue. 5. Changes in plasma insulin concentration or white adipose tissue blood flow did not appear to contribute to the decrease in the plasma non-esterified fatty acid concentration after infusion of platelet-activating factor. However, there was a significant decrease in blood flow to interscapular brown adipose tissue in both the infused and injected groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Responses to endothelins in the rat cutaneous microvasculature: a modulatory role of locally-produced nitric oxide.

1. The response of the cutaneous microvasculature to intradermal injection of the endothelins (ET-1, ET-2 and ET-3) and the modulatory effect of endogenously produced nitric oxide (NO) have been determined in the rat. 2. Intradermal injection of endothelins (0.1- 10 pmol/site) induced dose-dependent local reductions in blood flow, measured by 133xenon clearance, with the following potency order; ET-1 = ET-2 greater than ET-3. 3. Laser Doppler blood flowmetry established that ET-1 (10 pmol/site) significantly (P less than 0.05) reduced microvascular blood flow for 3 h after injection. Over a wide dose-range, the response to the endothelins did not include any vasodilatation or visible flare. 4. A possible modulatory role of locally-produced NO was investigated by the intradermal injection of the potent inhibitor of NO generation NG-nitro-L-arginine methyl ester (L-NAME). L-NAME (100 nmol/site) injected alone induced a significant decrease in blood flow. The vasoconstriction induced by L-NAME was partially reversed by L-arginine (P less than 0.05) but not observed with NG-nitro-D-arginine methyl ester (D-NAME). 5. L-NAME significantly (P less than 0.05) enhanced the decrease in blood flow induced by submaximal doses of ET-1, ET-2 and ET-3 and vasopressin, although the results do not suggest that any of the vasoconstrictors stimulate NO release. The response to L-NAME was still observed 3.5 h after inducing a prolonged constriction with ET-1 (10 pmol/site).6. These results indicate that locally produced NO maintains a dilator tone in the cutaneous microvasculature of the rat and acts to modulate the effect of vasoconstrictors such as endothelins. Hence, it is suggested that in conditions where endogenous NO release is reduced, vasoconstrictor agents such as the endothelins could induce a dangerous decrease in blood flow possibly leading to ischaemia and tissue necrosis.

The circulation in the nipple-areola complex following subcutaneous mastectomy in breast cancer.

To evaluate the decrease in circulation in the nipple-areola complex after subcutaneous mastectomy and immediate implantation of a submuscular prosthesis, the blood flow was studied by both fluorescein flowmetry and laser Doppler flowmetry in 24 patients with invasive breast cancer. In 14 patients a lazy-S-shaped horizontal lateral incision was used, and 10 underwent a subcutaneous reduction mammaplasty. After subcutaneous mastectomy with a lazy-S incision there was no significant decrease in blood flow in the nipple-areola complex compared with that in the untreated contralateral breast. In the breasts in which reduction mammaplasty had been done, the blood flow was reduced by 74% as measured by fluorescein (p less than 0.01), and 70% by laser Doppler flowmetry (p less than 0.05), compared with the contralateral breast. Five patients had partial or complete epidermal, and one patient had total dermal, necrosis of the complex, but there was no deep necrosis. No fluorescence was seen within the areas in which necrosis later developed in any of these six cases. The laser Doppler signal in the corresponding areas, however, was not reduced. The results show that the circulation in the nipple-areola complex is reduced more after subcutaneous reduction mammaplasty than after subcutaneous mastectomy with a lazy-S incision.

Bleeding Peptic Ulcer After Abdominal Aortic Aneurysm Surgery

A retrospective study of 112 patients with abdominal aortic aneurysm (AAA) and 232 with arteriosclerosis obliterans (ASO) demonstrated that 16.7% of those with AAA and 1.6% of those with ASO had a history of gastroduodenal ulcer; 83% of these lesions with AAA were gastric ulcers. Ulcer bleeding after vascular reconstruction developed in seven patients with AAA and one with ASO. Serum fibrinogen levels and platelet counts were significantly lower in patients with AAA than in those with ASO or controls. A prospective study showed that 25 (52.1%) of 48 patients with AAA and six (20.0%) of 30 patients with ASO had endoscopically proved gastroduodenal lesions before vascular reconstruction. None of them developed postoperative bleeding after treatment of both their gastroduodenal lesions and coagulopathy. Furthermore, the significant decrease in blood flow and prostaglandin content of gastric mucosa was demonstrated in patients with AAA.

Chronic pain: a PET study of the central effects of percutaneous high cervical cordotomy

We have studied 5 patients with unilateral, severe chronic pain due to cancer before and after percutaneous, ventrolateral cervical cordotomy to investigate the central effects of the procedure. The aim was to identify the functional anatomical correlates of abolishing unilateral nociceptive input to the brain. Patients were investigated by positron emission tomography using C 15O 2 to evaluate cerebral blood flow. Comparisons were made between the patients with unilateral pain before cordotomy and normal volunteers. These demonstrated significantly less blood flow in 3 out of 4 of the individual quadrants of the hemithalamus contralateral to the side of pain ( P < 0.01–0.05). These differences were abolished by cordotomy. Comparison of the patients before and after cordotomy showed a significant decrease in blood flow in the dorsal anterior quadrant of the thalamus contralateral to the side of pain ( P < 0.05) which was normalised after cordotomy. There were no significant changes in the prefrontal or primary somatosensory cortex. We conclude that chronic pain results in a decrease of synaptic activity at thalamic level either from decreased activity in neurones projecting to that region and/or attenuated local neuronal firing. We have demonstrated no secondary remote effects in cortex, indicating the importance of subcortical mechanisms in central responses to chronic pain.

Altered sensitivity of digital blood flow to acute vibration in patients with vasospastic disease

Fifteen patients with primary Raynaud's, 18 patients with vibration induced white finger (VWF) and 15 controls were exposed to sine wave vibration, with an amplitude of 0.15 mm and frequencies of 40, 80 and 120 Hz. Baseline digital blood flow was measured using venous occlusion strain gauge plethysmography. A digit was vibrated for 1 min and subsequent blood flow measurements were taken from both vibrated and non-vibrated digits. Vibration at 40 Hz causes a significant decrease in flow in the vibrated digits of the control group only ( P < 0.05, Wilcoxon test). Vibration at 80 Hz shows a significant decrease in blood flow in the vibrated digits of both the control and the VWF groups ( P < 0.005) and also in the non-vibrated digits of the VWF group ( P < 0.05). Vibration at 120 Hz significantly decreases blood flow in the vibrated digits of control, VWF and Raynauds groups ( P < 0.001). The Raynaud's non-vibrated digits also had decreased flow ( P < 0.005). These results imply that patients with established vasospastic disease are less sensitive to the direct effects of acute vibration than controls. The results also imply that vibration at 40, 80 and 120 Hz affect digital blood flow in controls through local mechanism. Vibration at certain frequencies, appears to modulate blood flow in patients with vasospastic disease by acting through central mechanisms.

Effects of venous hypertension on rabbit free flap survival

A two-stage project was developed to study the effect of increased venous pressure on blood flow and survival in microvascular free tissue transfers. A rabbit epigastric fasciocutaneous free flap model was used. The blood flow in the rabbit epigastric free flap is 1.07 +/- 0.06 ml/min. The average venous pressure is 8.6 +/- 1.7 cm water. A logarithmic relationship between blood flow and venous pressure was demonstrated, with a statistically significant decrease in blood flow to 20-35% of the control values when the venous pressure rose above 28-30 cm water. This study stands in support of the tolerance by free tissue transfers of pressures below this range. The results further show a positive correlation between increasing venous pressure and free flap failure.