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PubMed2002

Preoperative chemoradiation in the management of adenocarcinoma of the body of the pancreas.

Adenocarcinoma of the body of the pancreas has been traditionally associated with low resectability and poor prognosis. We reviewed 30 consecutive cases of pancreatic body adenocarcinoma presenting between 1988 and 2001. Twenty-six (87%) patients received preoperative chemotherapy (either 5-fluorouracil with or without mitomycin C or gemcitabine) plus radiation therapy (50.4 Gy), and four patients received chemoradiation postoperatively. During or shortly after chemoradiation 16 (53%) patients developed distant metastasis (n = 12), tumor progression (n = 2), or fatal septic complications (n = 2). Fourteen patients underwent surgical resection with curative intent. Resections performed included distal subtotal pancreatectomies (n = 6), extended pancreaticoduodenectomies (n = 6), and total pancreatectomies (n = 2). Ten patients (71%) required vascular reconstruction as a result of involvement of the portal vein or the superior mesenteric, hepatic arterial, or celiac vessels. Median overall survival was 34 months (range 8-152) for the resected group as compared with 8 months (range 1-14) in the unresected group (P = 0.005). Five-year actuarial overall survival is projected at 45 per cent for the resected group. In this poor-prognostic subset of patients with pancreatic cancer preoperative chemoradiation followed by an aggressive surgical approach was associated with resectability and long-term survival of a significant minority of patients.

Adenocarcinoma↗

PubMed1989

Antihypertensive mechanism of alacepril. Effects of its metabolites on the peripheral sympathetic nervous system.

To elucidate the antihypertensive mechanisms of alacepril (DU-1219), the drug itself and its metabolites, desacetylalacepril (DU-1227) and captopril, were examined both in vitro and in vivo for their effects on the sympathetic nerve which innervates the peripheral vessels. 1. In isolated perfused mesenteric preparations from spontaneously hypertensive rats (SHR, DU-1227 (10(-6)-10(-5) mol/l) attenuated dose-dependently the increases in perfusion pressure and in norepinephrine (NE) overflow which were induced by electrical stimulation of periarterial sympathetic nerves (15 Hz). Captopril (10(-6)-10(-5) mol/l) caused a similar attenuation, though to a lesser degree, of the perfusion pressure but did not inhibit the increase in NE overflow. 2. The sympatho-inhibitory effect of DU-1227 in the above experiment was shown to be caused by DU-1227 per se, since no captopril was detected in either the perfusate or tissues perfused with DU-1227. 3. In pithed SHR, alacepril (3 mg/kg) caused as potent an inhibitory effect as captopril (3 mg/kg) on the pressor response to the electrical sympathetic nerve stimulation (3 Hz) at an oral dose about half as that of captopril on the molar basis. The effect of alacepril tended to last longer than that of captopril. However, at higher oral dose levels, the inhibitory effect of alacepril (30 mg/kg) was of the similar extent to that of captopril (30 mg/kg). 4. In pithed SHR which had received bilateral nephrectomy 2 to 8 h previously, alacepril (30 mg/kg p.o.) significantly attenuated the vasopressor response induced by electrical stimulation (1-30 Hz) 1 and 3 h after administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1986

Effects of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in hypertension.

The purpose of the present study was to analyse the regulatory mechanisms of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in the resistance vessels in hypertension. The perfused mesenteric arteries were used for the experiment in spontaneously hypertensive rats (SHR; 7-10 weeks old) and age-matched normotensive Wistar-Kyoto (WKY) rats. Norepinephrine overflow during electrical nerve stimulation was significantly greater in SHR than in WKY rats. A low concentration of epinephrine (5.5 X 10(-9) mol/l) potentiated norepinephrine overflow from the nerve endings in SHR, and this was antagonized by propranolol, while this overflow was reduced by the same concentration of epinephrine in WKY rats. Higher concentrations of epinephrine decreased the norepinephrine overflow both in SHR and WKY rats, and this was antagonized by yohimbine. Dopamine reduced the norepinephrine overflow during electrical nerve stimulation, suppression being significantly less in SHR than in WKY rats. These results suggest that in SHR the increased norepinephrine overflow from sympathetic nerve endings may be partly caused by the facilitatory effect of epinephrine (through presynaptic beta-adrenoceptors) and impaired dopamine-mediated inhibition on the nerve terminals, which might contribute to the enhanced adrenergic activity in hypertension.

Animals↗

PubMed1981

[Influence of lymphostasis on healing processes of intestinal anastomoses. Experimental research].

The Authors studied the healing of the intestinal anastomoses in rats with mesenteric and celiac lymph-vessels coagulated and cut. The experiment was realized utilizing 104 rats, divided in fours groups: after the induction of the lymphostasis, in the first group an end-to-end ileal anastomosis was made by polyglycolic acid suture, 6/0 in diameter. The control groups consisted of rats with ileal anastomoses, with lymphostasis solely and sham operated. The macroscopic observation and the histological findings were studied 7 and 14 days after the anastomoses' performance. Only in the animals with lymphostasis was observed an anastomosal leakage of 19% at 7th day control. In the same period the histologic sections showed a modified anastomosal healing, related to the significant reduction of the granulomatous tissue formation in presence of the lymphostasis.

Animals↗

PubMed2000

Rat small mesenteric artery function after hindlimb suspension.

To determine whether simulated microgravity in rats is associated with vascular dysfunction, we measured responses of isolated, pressurized mesenteric resistance artery segments (157- to 388-microm ID) to vasoconstrictors, pressure, and shear stress after 28-day hindlimb suspension (HS). Results indicated no differences between HS and control (C) groups in 1) sensitivity or maximal responses to vasoconstrictors (norepinephrine, phenylephrine, serotonin, KCl); 2) ID, external diameter, or ratio of wall thickness to ID; 3) distensibility; or 4) vasodilatory responses to shear stress. Myogenic tone was attenuated (P < 0.05) in HS arteries vs. C, as evidenced by 1) decreased magnitude of tone in larger vessels (second-order branch off superior mesenteric artery, 261- to 388-microm ID) at pressures >/=40 mmHg in the presence of phenylephrine (10(-7) M) and 2) decreased magnitude of tone in smaller vessels (third-order branch off superior mesenteric artery, 157- to 277-microm ID), which exhibited spontaneous tone, at pressures > or =70 mmHg. This attenuation of myogenic tone after HS could contribute to orthostatic intolerance because myogenic tone contributes to the overall tone of resistance arteries.

Acetylcholine↗

PubMed1995

In situ hybridization shows increased endothelin-1 mRNA levels in endothelial cells of blood vessels of deoxycorticosterone acetate-salt hypertensive rats.

Endothelin-1 is a potent vasoconstrictor peptide produced in blood vessels and other tissues that may play an important role in the control of local blood flow and could be involved in the pathogenesis of hypertension. Our previous studies have documented increases in endothelin-1 peptide content and gene expression in mesenteric arteries and thoracic aorta of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Although changes in endothelin-1 were observed in the blood vessels of hypertensive rats, the exact cellular sites of these changes were not identified clearly. In the present study we investigated endothelin-1 gene expression in DOCA-salt hypertensive rats by in situ hybridization histochemistry using a high specific activity 35S-labeled complementary RNA probe. Robust increases in endothelin-1 mRNA levels were observed in both mesenteric blood vessels and aorta of DOCA-salt hypertensive rats as compared with the vessels from the uninephrectomized control rats. In both cases it was shown clearly that these increased endothelin-1 mRNA levels only originated in the endothelial cell layer, not in the underlying smooth muscle cells. Higher expression levels of endothelin-1 mRNA by the endothelial cells of DOCA-salt hypertensive rats may play an important role in vascular hypertrophy and in the maintenance of elevated blood pressure in this and perhaps other models of experimental hypertension.

Animals↗

PubMed2004

Disruption of smooth muscle gap junctions attenuates myogenic vasoconstriction of mesenteric resistance arteries.

Communication between vascular smooth muscle (VSM) cells via low-resistance gap junctions may facilitate vascular function by synchronizing the contractile state of individual cells within the vessel wall. We hypothesized that inhibition of gap junctional communication would impair constrictor responses of mesenteric resistance arteries. Immunohistochemical experiments revealed positive staining for connexin 37 (Cx37) in both endothelium and smooth muscle of rat mesenteric arterioles, whereas connexin 43 (Cx43) immunoreactivity was not detected in the mesenteric vasculature. Administration of the gap junction inhibitory peptide Gap27, which targets Cx37 and Cx43, significantly diminished myogenic vasoconstriction (8.6 +/- 3.8% of passive diameter at 100 Torr) and changes in vessel wall intracellular [Ca2+] of mesenteric resistance arteries compared with vessels treated with either vehicle (physiological saline solution) (33.5 +/- 6.1%) or a control peptide (32.1 +/- 6.5%). Administration of 18alpha-glycyrrhetinic acid, structurally distinct from Gap27, also significantly attenuated myogenic constriction compared with its vehicle control (DMSO) (9.6 +/- 3.2% vs. 23.8 +/- 4.6%). In contrast, phenylephrine-induced vasoconstriction was not altered by gap junction blockers. Attenuated myogenic vasoconstriction resulting from inhibition of gap junctions persisted after disruption of the endothelium. In additional experiments, VSM cell membrane potential was recorded in mesenteric resistance arteries pressurized to 20 or 100 Torr. VSM membrane potential was depolarized at 100 Torr compared with 20 Torr. However, VSM cells in arteries treated with Gap27 were significantly hyperpolarized (-48.6 +/- 1.4 mV) at the higher pressure compared with vehicle (-41.4 +/- 1.5 mV) and Gap20-treated (-38.4 +/- 0.7 mV) vessels. Our findings suggest that inhibition of smooth muscle gap junctions attenuates pressure-induced VSM cell depolarization and myogenic vasoconstriction.

Animals↗

PubMed1991

Sympathetic neural control of vascular muscle in reduced renal mass hypertension.

Vascular smooth muscle (VSM) transmembrane potentials (Em) were measured in situ in small branch arteries (150-300-microns o.d.), small branch veins (300-400-microns o.d.), arterioles (90-150-microns o.d.), and venules (80-250-microns o.d.) in the mesenteric and gracilis muscle and the arterioles and venules of cremaster muscle vascular beds in anesthetized rats with reduced renal mass hypertension (HT-RRM) and normotensive sham-operated RRM control rats. All rats were given a 4% NaCl diet for 2 weeks with water ad libitum. Relative to sham, HT-RRM mesenteric and gracilis arterial and venous vessels, but not the microvessels of the cremaster muscle bed, were less polarized during superfusion with normal physiological salt solution. Also relative to sham, hyperpolarization responses to local sympathetic neural (SNS) denervation with 6-hydroxydopamine were greater in mesenteric and gracilis small arteries, arterioles, veins, and venules but not in cremaster microvessels. The immediate (less than 5-minute) electrogenic depolarization response to local blockade of VSM Na(+)-K+ pump activity with 10(-3) M ouabain was similar between each respective HT-RRM and sham vessel pair in each vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Responses of femoral resistance vessels to angiotensin in vitro.

The effect of angiotensin II and angiotensin I on isolated rat resistance vessels (inner diameter ca. 200 micron) was investigated. Angiotensin II caused a contraction (ED50 = 0.58 +/- 0.17 X 10(-8) M) of rat femoral and cerebral arteries and to a lesser extent of mesenteric and renal arteries. However, all vessels showed strong tachyphylaxis on repeated stimulation with angiotensin II. Tachyphylaxis was avoided by inducing submaximal tone in the vessels with either K, noradrenaline or serotonin. The response to angiotensin II was inhibited by saralasin but not by captopril. Angiotensin I also caused contraction of the femoral arteries (ED50 = 2.68 +/- 0.32 X 10(-8) M). These responses were inhibited by captopril and saralasin. Functional removal of the endothelium had little effect on the contractile responses to either angiotensin I or II. These results indicate that there are functional receptors to angiotensin II in the resistance vessels of the rat and that, in the presence of tone (a more physiological condition), the vessels contract to angiotensin II without tachyphylaxis. In addition, angiotensin II may be formed from angiotensin I by the angiotensin converting enzyme which may be situated in the vessel wall as well as in the endothelium.

Angiotensin II↗

PubMed2001

Temporal variation in endotoxin-induced vascular hyporeactivity in a rat mesenteric artery organ culture model.

Endotoxin-induced vascular hyporeactivity to phenylephrine (PE) is well described in rodent aorta, but has not been investigated in smaller vessels in vitro. Segments of rat superior mesenteric artery were incubated in culture medium with or without foetal bovine serum (10%) for 6, 20 or 46 h in the presence or absence of bacterial lipopolysaccharide (LPS; 1 - 100 microg ml(-1)). Contractions to PE were measured with or without nitric oxide synthase (NOS) inhibitors: L-NAME (300 microM), aminoguanidine (AMG; 400 microM) 1400W (10 microM) and GW273629 (10 microM); the guanylyl cyclase inhibitor, ODQ (3 microM); the COX-2 inhibitor, NS-398 (10 microM). Contractile responses to the thromboxane A2 mimetic, U46619 were also assessed. In the presence of serum, LPS induced hyporeactivity at all time points. In its absence, hyporeactivity only occurred at 6 and 20 h. L-NAME and AMG fully reversed hyporeactivity at 6 h, whereas they were only partially effective at 20 h and not at all at 46 h. In contrast partial reversal of peak contraction was observed with 1400W (62% at 46 h), GW273629 (57% at 46 h) and ODQ (75% at 46 h). COX-2 inhibition produced no reversal. In contrast to PE, contractions to U46619 were substantially less affected by LPS. We describe a well-characterized reproducible model of LPS-induced hyporeactivity, which is largely mediated by the NO-cyclic GMP-dependent pathway. Importantly, long-term (2-day) production of NO via iNOS is demonstrated. Moreover, conventional doses of L-NAME and AMG became increasingly ineffective over time. Thus, the choice of inhibitor merits careful consideration in long-term models.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2001

Modulation by 20-HETE of phenylephrine-induced mesenteric artery contraction in spontaneously hypertensive and Wistar-Kyoto rats.

Small mesenteric arteries of spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY) were compared for the production of 20-HETE and the effects of 20-HETE and N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS, 30 micromol/L), a 20-HETE synthesis inhibitor, on contractile responsiveness to phenylephrine (0.1 to 50.0 micromol/L). 20-HETE production was higher in vessels of SHR compared with WKY (1.34+/-0.16 versus 0.27+/-0.09 pmol/mg tissue, P<0.05). Phenylephrine elicited concentration-dependent vascular contraction; the R(max) was similar in vessels of SHR and WKY, but the former were more sensitive as denoted by the lower EC(50) (1.10+/-0.14 versus 1.89+/-0.33 micromol/L, P<0.05). DDMS caused a rightward shift in the concentration-response curve to phenylephrine, increasing (P<0.05) the EC(50) by 258% and 134% in vessels of SHR and WKY, respectively. In contrast, in DDMS-treated vessels, 20-HETE (0.01 to 10.0 micromol/L) caused a leftward shift in the phenylephrine concentration-response curve, decreasing (P<0.05) the EC(50) without affecting the R(max). Importantly, the minimal concentration of 20-HETE that decreased the EC(50) of phenylephrine was much smaller in vessels of SHR that of WKY (0.01 versus 1.0 micromol/L). We conclude that 20-HETE increases the sensitivity of mesenteric arterial vessels to phenylephrine, vessels of SHR are more sensitive to this action of the eicosanoid than vessels of WKY, and vessels of SHR produce more 20-HETE than do vessels of WKY. Hence, 20-HETE of vascular origin may be a determinant of the increased reactivity to constrictor agonists in the vasculature of SHR.

Amides↗

PubMed2000

Characterization of endothelial factors involved in the vasodilatory effect of simvastatin in aorta and small mesenteric artery of the rat.

1. Vascular effects of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, simvastatin, were studied in conductance (aorta) and resistance vessels (branch II or III of superior mesenteric artery, SMA) of the rat (12 - 14 weeks old). 2. Simvastatin produced relaxation of both aorta and SMA, with and without functional endothelium. These responses were inhibited by the product of HMG-CoA reductase, mevalonate (1 mmol l(-1)). 3. In vessels with functional endothelium, the NO-synthase inhibitor, L-N(G)-nitroarginine (L-NOARG, 30 micromol l(-1)), inhibited simvastatin-induced relaxation. In the presence of L-NOARG, relaxation to simvastatin was lower in vessels with endothelium than in endothelium-denuded arteries without L-NOARG. 4. The cyclo-oxygenase inhibitor, indomethacin (10 micromol l(-1)), abolished endothelium-dependent component of the response to simvastatin in both arteries. The combination of L-NOARG plus indomethacin did not produce further inhibition. The T(p) receptor antagonist, GR 32191B (3 micromol l(-1)), did not affect relaxation in aorta but it reduced response to low concentrations of simvastatin in SMA. However, the inhibitory effect of L-NOARG was less marked in the presence of GR 32191B in aorta but not in SMA. 5. The endothelium-dependent relaxation to simvastatin was inhibited by the superoxide dismutase (SOD, 100 u ml(-1)) or by the tyrosine kinase inhibitor, genistein (30 micromol l(-1)) in the two arteries. 6. The present study shows that simvastatin produces relaxation of conductance and small arteries through mevalonate-sensitive pathway. The endothelium-dependent relaxation to simvastatin involves both NO and vasodilator eicosanoids by a mechanism sensitive to SOD, and to genistein. Also, the results highlighted participation in the aorta of endothelial vasoconstrictor eicosanoids acting on the T(p) receptor after blockage of NO synthase only.

Animals↗

PubMed1992

The effect of neonatal treatment of rats with nerve growth factor on the blood pressure and structure of the mesenteric arteries.

Newborn male Wistar rats were treated with nerve growth factor daily by subcutaneous injection for 2 weeks, and control rats were treated with either cytochrome c or buffered saline. Average body weight of the treated animals was lower than that of the controls during the 2 weeks of treatment, but became similar to that of the controls thereafter. Tissue levels of norepinephrine were elevated in the brain, adrenal glands, mesenteric arteries, and vas deferens of the treated animals immediately after the treatment, but became similar in the three groups 2 weeks after the termination of the treatment. Blood pressure and heart rate were measured beginning at 4 weeks of age until 28 weeks, when the rats were sacrificed and the mesenteric arteries sampled for morphometric measurements of vessel wall dimensions. Pretreatment with nerve growth factor did not affect blood pressure, nor heart rate. Structural alteration of the three types of mesenteric arteries was also absent in the treated animals. We conclude that even though neonatal treatment of normal Wistar rats with nerve growth factor for 2 weeks induced an elevation of the norepinephrine levels in several tissues at the end of the treatment period, it was not sufficient to produce hypertension and structural alterations in the blood vessels.

Aging↗

PubMed1999

Human chorionic gonadotropin dilates uterine and mesenteric resistance arteries in pregnant and nonpregnant rats.

Membrane receptors for human chorionic gonadotropin (hCG) are expressed in a variety of steroidogenic cells, and also in extragonadal tissues such as vessels of the female genital tract. We examined the possible contribution of hCG to the endocrine control of prearteriolar mesenteric and uterine vessels before and during pregnancy. Lumen diameters of isolated pressurized resistance arteries from Sprague-Dawley rats were measured using a video-electronic system. hCG produced marked and dose-dependent vasodilation. Uterine radial arteries were found to be highly sensitive to hCG (EC50 approximately =60 mU/ml) before and throughout gestation. Second-order mesenteric arteries from nonpregnant animals were even more sensitive (EC50=38 mU/ml), but, in these vessels, responsiveness to hCG was significantly attenuated by the pregnant state. Mechanical removal of the vascular endothelium did not reduce the degree of vasodilation mediated by hCG. The expression of hCG receptor mRNA in intact vessels could be demonstrated using reverse transcriptase polymerase chain reaction (RT-PCR). hCG appears to be an important embryonic signal, which could trigger adaptive cardiovascular changes in early pregnancy, simultaneously preserving a sufficient utero-placental perfusion during the entire gestation period by an endothelium-independent mechanism.

Acetylcholine↗

PubMed1995

Echocardiographic size of conductance vessels in athletes and sedentary people.

The purpose of the present study was to assess the size of great and medium caliber arterial and venous vessels (conductance vessels) in athletes of different sports and sedentary people. Vessel size was measured by two-dimensional echocardiography in 15 professional cyclists, 15 highly-trained long-distance runners, 15 professional volley-ball players, 10 wheelchair basketball players, 11 wheelchair distance runners and 20 sedentary controls. The following vessels were imaged and measured: aortic arch, left carotid and left subclavian artery, right pulmonary artery, abdominal aorta and mesenteric artery, superior and inferior vena cava. Vessel size was considered in absolute value and normalized for body surface area (BSA). Among the able-bodied athletes, both cyclists and long-distance runners showed a generalized increase in vessels size in respect to controls, either absolute or normalized for BSA. The increase was highly significant for normalized inferior vena cava: cyclists, mean 15.1 mm, 95% confidence intervals 14.2 to 15.8 mm; long-distance runners, 15.8 mm, 15.3 to 16.4; controls, 10.5 mm, 9.8 to 11.3. Volleyball players also showed larger vessels than controls, but this feature was clearly related to their greater body size because statistical differences were attenuated or abolished by normalization for BSA. Wheelchair athletes exhibited significantly larger upper-body vessels but significantly smaller lower-body vessels than controls when normalized for BSA. In addition, wheelchair distance runners, who trained more intensively, had larger abdominal aorta and inferior vena cava than wheelchair basket players. Long-term endurance training leads to a generalized increase in arterial and venous conductance vessels size.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1992

Immunoperoxidase labelling of albumin at the endothelial cell surface of frog mesenteric microvessels.

Albumin was visualised at the endothelial cell surface of perfused frog mesenteric microvessels using immuno-peroxidase labelling. Vessels in the mesenteries of pithed frogs were washed free of blood and then perfused with frog Ringer solutions containing bovine serum albumin (BSA) at a concentration of 20 mg BSA ml-1, followed by a brief Ringer flush to remove excess albumin from the vessel lumen. The tissues were fixed in 1% glutaraldehyde and a double antibody labelling technique used to identify albumin within the tissue. A dense layer of peroxidase reaction product was seen, which extended 25-50 nm into the vessel lumen. It appeared as a continuous layer lining the luminal openings of interendothelial cell clefts and vesicles open to the luminal cell surface. In some vessels a more irregular layer of peroxidase labelled albumin was seen extending 150 to 200 nm into the vessel lumen, whilst in others clumps of peroxidase labelled albumin were also seen within the vessel lumen. These data offer direct evidence that BSA does interact with the endothelial cell surface of perfused frog mesenteric microvessels but suggest that a proportion is loosley or non-specifically bound to the cell surface and can be removed by a brief Ringer flush. The remainder appears more tightly bound and resistant to Ringer flush.

Animals↗

PubMed1989

Vascular changes associated with deoxycorticosterone-NaCl-induced hypertension.

Rats were injected with deoxycorticosterone (DOC) and salt was added to the drinking water (DOC/NaCl) for 3 weeks. Approximately half of the animals became hypertensive (DOC-H), whereas the remainder showed no increase in blood pressure (DOC-N) compared to age-matched, untreated controls. Morphometric analysis of the alterations in the arteries of the mesenteric bed was carried out in vessels fixed at maximum relaxation. Alterations were observed in the arteries, some of which were related to hypertension, but not to treatment, and some were due to treatment alone. The alterations within the arteries of the mesenteric bed depended in part on the type of artery, i.e. elastic, muscular or arteriolar. An increase in lumen area, in intimal area, and in the area of the media was seen in all types of arteries from DOC-H, but not in either group of normotensive animals. The medial hypertrophy was positively correlated with the increase in blood pressure; and was due to an increase in the number of smooth muscle cell layers in the elastic and muscular arteries, and probably to smooth muscle cell hypertrophy in the arterioles. The adventitial area was increased only in the elastic and muscular arteries. Endothelial injury, degeneration of the basement membrane, loss of heparan sulfate proteoglycan and intimal edema was observed in all the DOC/NaCl-treated animals, but was more severe in those which were also hypertensive. Hypertrophy of the heart and kidneys were observed in both normotensive and hypertensive DOC/NaCl-treated animals. These data indicate that changes in the rat cardiovascular system can be induced by DOC/NaCl treatment in the absence of hypertension, but also that hypertension is associated with specific arterial structural alterations, which vary according to the type of artery.

Animals↗

PubMed1998

Laparoscopic surgery and splanchnic vessel thrombosis.

We report a case of fatal mesenteric artery thrombosis following laparoscopic cholecystectomy in a 60-year-old hypertensive woman, whose preoperative complaints were not typical of calculous biliary disease. Two previous case reports have associated laparoscopic cholecystectomy and acute intestinal ischemia; one of these patients died. Experimental and clinical data indicate that carbon dioxide pneumoperitoneum reduces splanchnic blood flow through several mechanical and physiologic mechanisms. Consequently, we believe that, when laparoscopic surgery is contemplated, physicians and patients should be aware of the risk of splanchnic vessel thrombosis, especially when certain pre-existing conditions are present (e.g., impairment of splanchnic vessel flow, hypercoagulable states, etc.). For such high-risk patients, especially when the planned laparoscopic procedure may be lengthy, gasless or low-pressure laparoscopic surgery, or even reversion to traditional open surgery should be considered.

Carbon Dioxide↗