Monoamine oxidase activity in the cardiovascular system of young and aged rats.
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Thirty-two patients with liver cirrhosis underwent cerebral magnetic resonance imaging (MRI) to evaluate clinical and subclinical portal-systemic encephalopathy (PSE). Symmetrically hyperintense globus pallidi were observed on T1-weighted images in all 11 patients with PSE and in 15 of the 21 patients with PSE. This abnormality was classified as grade I (bilateral globus pallidi with mild to moderate hyperintensity relative to white matter), and grade II (marked hyperintensity bilaterally in the globus pallidi with mildly increased signal intensities in the surrounding structures). Portal-systemic collateral vessels were demonstrated in 23 of 24 patients who underwent abdominal angiography. In 18 of the 19 patients with abnormal MRI, collateral vessels were supplied by the superior mesenteric vein with or without the splenic vein, including four patients with collaterals which were less than 10 mm in diameter. We concluded that hyperintense globus pallidi on T1-weighted images are significant manifestations of clinical PSE. When portal-systemic collaterals supplied by the superior mesenteric vein are observed, even if they are of small diameter, cerebral MRI should be performed to evaluate for subclinical PSE.
OBJECTIVES: Estrogen exerts cardiac protection via multiple cellular mechanisms. Estrogen modifies vasodilatation induced by certain relaxants such as beta-adrenoceptor agonists. However, little is known whether low concentrations of beta-adrenoceptor agonists would reciprocally influence the acute relaxant response to estrogen. The present study was designed to investigate the synergistic interaction between isoproterenol and 17 beta-estradiol, and the role of endothelium and cyclic AMP-dependent pathway in this interaction. METHODS: Changes in vessel tone of the isolated rat mesenteric artery rings were measured using a force-displacement Grass transducer. RESULTS: In 9,11-dideoxy-11 alpha, 9 alpha-epoxy-methanoprostaglandin F(2 alpha)-preconstricted endothelium-intact rings, 17 beta-estradiol induced relaxations with pD(2) of 5.06 +/- 0.06. Pretreatment of endothelium-intact rings with isoproterenol (1-3 x 10(-9) M, 1 h incubation time) significantly enhanced 17 beta-estradiol-induced relaxation. This effect was inhibited by Rp-cGMPS triethylamine (3 x 10(-6) M), and abolished in the presence of 3 x 10(-5) M N(G)-nitro-L-arginine methyl ester or in endothelium-denuded rings. The effect of isoproterenol was antagonized by propranolol (3 x 10(-6) M), ICI 118,551 (3 x 10(-6) M), but not by atenolol (10(-5) M). Rp-cAMPS triethylamine (3 x 10(-6) M) abolished the effect of isoproterenol. Besides, exposure to 3 x 10(-9) M forskolin for 1 h also potentiated the relaxant response to 17 beta-estradiol. CONCLUSION: In endothelium-intact rat mesenteric arteries pretreatment with low concentrations of isoproterenol enhanced the acute relaxant response to 17 beta-estradiol. This enhancement was dependent on the presence of endothelium and abolished by L-NAME via a beta(2)-adrenoceptor-mediated cyclic AMP-dependent mechanism.
The administration of digitalis glycosides causes a variety of extracardiac effects. In both normal human subjects and in other species, digitalis increases smooth muscle tone of resistance and capacitance vessels. The vasoconstriction is mediated, in part, by a direct action of these glycosides on smooth muscle and, in part, by an increase in alpha-adrenergic tone. Constriction of coronary and splanchnic vessels may lead to myocardial or mesenteric ischemia. In contrast to normal subjects, patients with congestive heart failure demonstrate arteriolar and venodilation in response to these glycosides, possibly because the myocardial effect, to increase cardiac output and peripheral blood flow, overcomes the vasoconstrictor properties of these drugs. Other important actions of digitalis glycosides occur in the central and peripheral nervous systems. Their effects on the area postrema of the medulla oblongata are largely responsible for the alpha-adrenergic-mediated peripheral vasoconstriction, as well as the nausea and vomiting that frequently accompany digitalis intoxication. Actions of glycosides on the cerebral cortex are responsible for the wide range of neurotoxic effects that range from visual disturbances and headaches to seizures and coma. Finally, peripheral neurologic effects of digitalis glycosides on baroreceptor and cardiac afferent fibers may: improve the depressed function of these receptors in the situation of heart failure, and reflexly lower peripheral vascular resistance, thereby partially preventing the vascular constrictor action of these glycosides.
The case is reported of a 26-year-old man who had several episodes of subileus which responded to spasmolytics. Mesenteric angiography revealed a paraduodenal hernia, with displacement of several jejunal arteries towards the mesenteric root and compression of intestinal vessels at about the level of Treitz' ligament. The angiographic findings were confirmed at operation, which consisted of repositioning the jejunal loop and closing the hernial orifice. The patient has since been free of complaints.
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PURPOSE: To evaluate the safety of superselective arterial embolization therapy in the lower gastrointestinal tract. The sequelae on normal enteric tissue in lower gastrointestinal arterial embolization were retrospectively reviewed. MATERIAL AND METHODS: To control hemorrhage and tumor blood supply, 14 patients were treated by superselective transcatheter embolization at different levels of the colonic and small intestine vessels via the superior and inferior mesenteric arteries using microcoils and/or gelatin sponge. Normal enteric tissues in the embolized areas were analyzed for the occurrence of ischemic changes by clinical follow-up, colonoscopy, and surgery. RESULTS: Normal bowel function was preserved in 13 patients. In 1 patient treated with numerous gelatin sponge particles delivered from the proximal arcade of the superior mesenteric artery, significant muscular fibrosis occurred. CONCLUSION: Superselective arterial embolization for lower gastrointestinal hemorrhage can be safely performed by minimizing the amount of embolic materials and delivering them as distally as possible.
The organization of actin and myosin in vascular endothelial cells in situ was studied by immunofluorescence microscopy. Examination of perfusion-fixed, whole mounts of normal mouse and rat descending thoracic aorta revealed the presence of axially oriented stress fibers containing both actin and myosin within the endothelial cells. In both species, the proportion of cells containing stress fibers varied from region to region within the same vessel. Some endothelial cells in mouse mesenteric vein and in rat inferior vena cava also contained stress fibers. Quantitative studies of the proportion of endothelial cells containing stress fibers in the descending thoracic aorta of age-matched normotensive and spontaneously hypertensive rats revealed significant differences. When animals of the same sex of the two strains were compared, the proportion was approximately two times greater in the spontaneously hypertensive rats. The proportion of endothelial cells containing stress fibers was about two times greater in males than in females of both strains. These observations suggest that multiple factors, including anatomical, sex, and hemodynamic differences, influence the organization of the endothelial cell cytoskeleton in situ.
This study investigated the effects of diltiazem (a Ca2(+)-entry blocker) on neuromuscular junctions of blood vessels in hypertension. In isolated perfused mesenteric vasculatures prepared from spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY), the effects of diltiazem on norepinephrine release from vascular adrenergic neurons and pressor responses were examined. The influences of extracellular Ca2(+)-reduction on these responses were also studied. Stimulation evoked pressor responses and norepinephrine release were significantly greater in the mesenteric vasculatures of SHR than in those of WKY. Diltiazem inhibited both pressor responses and norepinephrine release during electrical nerve stimulation in a dose-dependent manner. The suppression of these responses was more pronounced in SHR than in WKY. Reduction of extracellular Ca2(+)-concentration also decreased the responses in SHR and WKY, and the inhibitory degree was significantly greater in SHR than in WKY. These results demonstrate that diltiazem affected the presynaptic site of the mesenteric vasculatures and decreased the stimulation-evoked norepinephrine release from vascular adrenergic neurons with a concomitant reduction of pressor responses of the preparation. Furthermore, the marked inhibition of pressor responses and norepinephrine release by diltiazem or Ca2(+)-depletion in SHR may suggest the increased Ca2(+)-dependency in vascular neurotransmission in this model of hypertension.
In a patient with pancreatic cancer, an arterial anomaly was observed that apparently consisted of the congenital absence of the celiac axis and the replacement of the pancreaticoduodenal arcade by an anomalous vessel. The complete or near-complete arterial flow to the liver and spleen depended upon this anomalous prepancreatic vessel that arose from the superior mesenteric artery. The anomaly was demonstrated preoperatively by arteriography. At laparotomy, the anomalous artery was prominent, lying across the surface of the head of the pancreas. Unrecognized, its operative interruption might have threatened the life of the patient. Resection of the head of the pancreas would have required restoration of the arterial flow, preferably by vascular grafting. The anomaly appears to be different from those previously described.
An aberrant right hepatic artery was visualized between the portal vein and inferior vena cava in 20 of 100 patients examined by computed tomography. The origin of this aberrant vessel from the celiac or superior mesenteric artery was visualized in five cases. It is important to recognize this as a normal variant, especially if surgery in the area of the hepatoduodenal ligament is planned, so as to avoid necrosis of the right lobe of the liver.
Computed tomography (CT) plays an important role in diagnosis of acute intestinal obstruction and planning of surgical treatment. Although internal hernias are uncommon, they may be included in the differential diagnosis in cases of intestinal obstruction, especially in the absence of a history of abdominal surgery or trauma. CT findings of internal hernias include evidence of small bowel obstruction (SBO); the most common manifestation of internal hernias is strangulating SBO, which occurs after closed-loop obstruction. Therefore, in patients suspected to have internal hernias, early surgical intervention may be indicated to reduce the high morbidity and mortality rates. In a study of 13 cases of internal hernias, nine different types of internal hernias were found and the surgical and radiologic findings were correlated. The following factors may be helpful in preoperative diagnosis of internal hernias with CT: (a) knowledge of the normal anatomy of the peritoneal cavity and the characteristic anatomic location of each type of internal hernia; (b) observation of a saclike mass or cluster of dilated small bowel loops at an abnormal anatomic location in the presence of SBO; and (c) observation of an engorged, stretched, and displaced mesenteric vascular pedicle and of converging vessels at the hernial orifice.
The effects of sustained mesenteric nerve stimulation on intestinal oxygenation were determined in 3- and 35-day-old swine. Studies were conducted in pentobarbital-anesthetized animals during free-flow or constant-flow perfusion. Square-wave stimuli sufficient to induce maximal resistance vessel constriction were applied to postganglionic periarterial mesenteric nerves and each stimulation was sustained until measured variables reached steady state. When vascular resistance data were analyzed without data transformation, autoregulatory escape of intestinal vascular resistance was more complete in 3- than in 35-day-old animals when the escape process was complete; however, expression of these data as escape indexes revealed a similar degree of escape in both age groups. In 35-day-old animals, (a-v)O2 increased during sustained nerve stimulation under free-flow conditions; under constant-flow conditions, (a-v)O2, 86Rb extraction, and capillary permeability-surface area product were lower at completion of the escape process compared with baseline. In 3-day-old swine, these variables remained unchanged from baseline. Intestinal O2 uptake was compromised by sustained nerve stimulation, and this effect was similar in both age groups. We conclude that sustained nerve stimulation reduces intestinal oxygenation to a similar degree in 3- and 35-day-old swine. It is important to note, however, that the response of 3-day-old swine may be dissimilar from that which occurs during immediate postnatal life; indeed, the intestinal hemodynamic response of swine less than or equal to 1 day old should not be extrapolated from the response of 3-day-old animals.
The distances between fibroblasts and adrenergic varicosities were measured in four distinct blood vessels of the dog, concomitantly with the measurement of corresponding distances between smooth muscle cells and adrenergic varicosities. The results showed a closer anatomical relationship between fibroblasts and adrenergic varicosities as compared to that of adrenergic varicosities and smooth muscle cells. These morphological results indicate that sympathetic neurotransmitter(s) may attain at the fibroblast membrane concentrations similar to those occurring at the smooth muscle cell membrane.
Subthreshold concentrations of angiotensin II (Ang II) potentiate agonist-induced tone in a variety of blood vessels. We measured in vivo the mesenteric artery diameter and blood flow in 12-week-old normotensive Wistar-Kyoto (WKY) rats (n = 20) and spontaneously hypertensive rats (SHR, n = 20); systemic blood pressure was monitored continuously. Phenylephrine (10 mumol/L) superfused on the exteriorized mesentery reduced arterial diameter from 480 +/- 40 to 256 +/- 18 microns (P < .05) in WKY rats and from 562 +/- 26 to 273 +/- 7 microns (P < .05) in SHR, whereas blood flow was lowered by 77% in WKY rats and 76% in SHR (P < .05 in both strains). Topical superfusion of an angiotensin-converting enzyme inhibitor (perindoprilat, 10 and 100 mumol/L) attenuated the phenylephrine-induced decrease in diameter and blood flow in both strains (P < .05). The Ang II type 1 receptor blocker losartan (10 mumol/L) attenuated the phenylephrine-induced decrease in diameter and blood flow in both strains (P < .05). The relaxing effect of losartan was significantly accentuated by the addition of perindoprilat (10 mumol/L) to the superfusate (P < .05 in both strains). Systemic blood pressure was unaffected by the topical application of phenylephrine (10 mumol/L), perindoprilat (10 or 100 mumol/L), or losartan (10 mumol/L). We conclude that phenylephrine-induced tone impairment by angiotensin-converting enzyme inhibition and Ang II type 1 receptor blockade in vivo probably reflects the role of endogenous Ang II in the potentiation of the adrenergic response during the control of vascular tone. This role is identical in both normotensive and hypertensive rats.
In 6 of 15 postmortem-treated cadaveric specimens, we found macroscopically thick lymphatic collecting vessels that originated from not only the nodes along the common hepatic artery (No. 8 nodes) but also from the pancreaticoduodenal region, and which drained directly into the para-aortic nodes immediately below the left renal vein (No. 16b1-inter or -latero nodes). The collecting vessels, if they originated from the ventral (dorsal) visceral side, passed to the left (right) of the superior mesenteric and celiac arteries. Moreover, the right-side vessels (5 specimens) were classified into superficial and deep courses to the celiac plexus, whereas they were superficial in the left side (2 specimens). One of the deep (right) courses continued to the thoracic duct without any intercalated nodes. In addition, another deep route drained into the para-aortic node immediately above the left renal vein (No. 16a2-inter node). We consider that these collecting vessels form "direct descending pathways" from the relatively peripheral lymphatics in the upper abdomen toward the thoracic duct origin. The pathway seems to be a collateral, or even major drainage route, and it appears responsible for skipped metastasis of primary cancer. Since the classical, limited entity of the intestinal lymph trunk does not coincide with our pathway, it should be reconsidered. The proposed entity of the direct, long descending pathway will influence the selection and modification of lymphadenectomy methods in cancer surgery in the pancreaticoduodenal region.
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A 54-year-old man who had been administered chlormadinone acetate 3 months after prostatectomy for prostate cancer, acutely developed disorientation and memory disturbance. Six days later, he experienced high grade fever and epigastralgia. He was suspected to have hepatic encephalopathy, because the Fischer ratio was low although serum ammonia level remained normal. Further examinations including abdominal echography and CT scan disclosed a thrombus extending from the portal vein to the superior mesenteric vein together with abnormal collateral vessels originating from the portal vein. He was successfully treated with warfarin potassium, urokinase and heparin sodium. It was suggested that the patient developed hepatic encephalopathy due to portal-systemic circulation shunting secondary to portal vein thrombosis.