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PubMed1997

Comparison of the nitric oxide and cyclo-oxygenase pathway in mesenteric resistance vessels of normotensive and spontaneously hypertensive rats.

1. The double perfused mesentery was used to compare arterial and venous KCl- and acetylcholine (ACh)-induced responses in tissues taken from normotensive (WKY) and spontaneously hypertensive rats (SHR) in the presence or absence of inhibitors of nitric oxide (NO) synthase (NG-nitro-L-arginine (L-NOARG) and NG-nitro-L-arginine methyl ester (L-NAME)) and cyclo-oxygenase (indomethacin, mefenamic acid). 2. KCl (20 to 120 mM K+) caused concentration-dependent increases in arterial and venous perfusion pressures. The maximal arterial effects were significantly higher in the SHRs than in the WKY, with no differences in the venous pressor responses. 3. L-NAME and L-NOARG (100 microM) had no effect on the basal perfusion pressures in tissues from either WKY or SHRs, and mefenamic acid only induced a significant reduction of the basal perfusion pressures in the venous mesenteric vessels isolated from WKY. 4. L-NAME and L-NOARG (100 microM) potentiated the pressor responses to KCl to the same extent in the venous and arterial beds derived from WKY and SHR, while indomethacin and mefenamic acid (5 microM) only significantly decreased these responses in WKY. 5. Acetylcholine (ACh)-induced relaxations (1 nM to 10 microM) were significantly higher in arterial beds of WKY than in SHR, without differences in the venous relaxant responses. 6. L-NAME (100 microM) inhibited ACh-induced relaxations in arterial and venous beds from both groups of rats. Mefenamic acid was without effect on ACh-induced relaxations in either the arterial or the venous beds from WKY and SHR. 7. In conclusion, the liberation of NO in the perfused mesenteric vasculatures requires an active tone and no dysfunction of NO synthase activity is functionally apparent in the mesenteries isolated from SHRs. The cyclo-oxygenase pathway is only implicated in the KCl-induced responses of tissues derived from WKY, but not in the vasodilatations induced by ACh in either the arterial or the venous vasculatures from WKY and SHR.

Acetylcholine↗

PubMed2000

Blunt thoracic and abdominal vascular trauma and organ injury caused by road traffic accident.

OBJECTIVES: To analyse the relationship between vascular trauma and associated injuries to intra-thoracic and abdominal organs caused by traffic accidents. Design retrospective study in a university hospital. MATERIALS AND METHODS: We investigated 458 consecutive patients who were admitted with blunt thoracic and/or abdominal trauma caused by road traffic accidents between 1986 and 1999. Vascular trauma was encountered in 54 patients (12%). RESULTS: The injured vessels were located in the abdomen in 45 patients and in the chest in nine patients. Mesenteric vessels were the most frequently injured vessels (33/45) in the abdomen, while the aorta and major vessels were most frequently injured (9/9) in the chest. Injury to the large/small intestine was often associated with mesenteric vessel injury (26/27). In the 190 patients with blunt abdominal organ injury, the frequency of mesenteric vessel injury was also highest, regardless of the injured organ. Vascular reconstruction was necessary only in one of 51 patients who underwent operation. CONCLUSIONS: Our results demonstrate that the mesenteric vessels are susceptible to blunt thoracic and abdominal trauma in road traffic accidents. Vascular reconstruction may be indicated for selected patients as long as the injuries to hollow organs are assessed carefully because of their strong association with vascular injury.

Abdomen↗

PubMed1988

Calcitonin gene-related peptide acts as a novel vasodilator neurotransmitter in mesenteric resistance vessels of the rat.

Systemic blood pressure is controlled by changes in the resistance of the peripheral vascular bed for example in the mesenteric blood vessels. The tone of peripheral blood vessels is primarily maintained by sympathetic vasoconstrictor nerves. Although vasodilator innervation has been identified in certain isolated elastic arteries, it is not known whether vasodilator nerves contribute to the regulation of the peripheral resistance vessels. We present pharmacological evidence for the existence of nonadrenergic, noncholinergic (NANC) vasodilator nerves in the mesenteric resistance vessel of the rat and that the resistance is controlled by not only sympathetic vasoconstrictor nerves but also NANC vasodilator nerves. We also show that the neurogenic vasodilation was selectively abolished by depleting endogenous calcitonin gene-related peptide (CGRP), a potent vasodilator neuropeptide, from perivascular nerves. This indicates that CGRP is a novel vasodilator neurotransmitter and may play a role in control of the total peripheral resistance of systemic circulation through a local reflex mechanism.

Animals↗

PubMed1995

Lengthening of the mesentery using the marginal vascular arcade of the right colon as the blood supply to the ileal pouch.

PURPOSE: Creation of a safe ileal pouch requires a tension-free anastomosis. The aim of this study was to evaluate a technical procedure that increases the length of the mesentery while preserving the blood supply to the ileal pouch. HYPOTHESIS: Preservation of the marginal vascular arcade (MVA) of the right colon will allow ligation of more mesenteric vessels and increase the mesenteric length. METHODS: Six fresh cadavers were dissected. Measurement of the apex of the terminal ileum was done in relation to the pubic symphysis. Measurements were taken after 1) complete mobilization of the terminal ileum, right colon, and hepatic flexure; 2) vascular ligation between colon wall and the MVA, preserving the latter from the right branch of the middle colic artery to the ileal branch of the ileocolic artery (ICA); 3) ligation of the distal third of the superior mesenteric artery; 4) ligation of the ICA at its origin; 5) ligation of the right colon artery; and 6) division of the terminal ileal mesentery. RESULTS: This technique enabled complete division of the terminal ileal mesentery, adding a mean additional 3.6 (range, 2.5 - 5.0) cm (36.5 +/- 16.5 percent) in length to the mesentery, compared with superior mesenteric artery, ICA, and right colic artery ligation. CONCLUSION: Patients who have a shorter mesentery and concern of excessive mesenteric tension should have colectomy performed, preserving the MVA from the middle colic artery to the ileal branch of the ICA. The preserved MVA can be a reliable alternative blood supply to the pouch if more mesenteric vessel ligations are necessary.

Anastomosis, Surgical↗

PubMed2003

Endovascular treatment of celiac and mesenteric arteries stenoses: applications and results.

PURPOSE: To evaluate the safety and assess the role of endovascular therapy in a variety of conditions related to celiac and mesenteric vascular occlusive disease. Patients and methods Our retrospective study population included 25 consecutive patients (mean age, 66 years), in whom 28 procedures were performed on 26 stenosed or occluded mesenteric vessels (superior mesenteric artery [SMA] or celiac artery [CA]). Indications included chronic mesenteric ischemia (21 patients), including 2 patients who underwent stenting prior to a planned operative repair of a juxtamesenteric AAA. Three liver transplantation patients underwent stenting of an associated CA stenosis. One patient with a splenorenal bypass underwent stenting on an associated CA stenosis. The technical and clinical success rates and the incidence of complications were determined. Follow-up parameters included maintained patency on duplex sonography and sustained clinical benefit. The need for additional interventions was noted. RESULTS: All procedures but one were technically successful (96%). Major complications occurred in three patients (one transient contrast-induced nephrotoxicity and two pseudoaneurysms). Immediate clinical success was achieved in 22 patients (88%). The three clinical failures included two patients with an excellent angiographic outcome, but with single-vessel moderate severity disease. Survival table analysis of delayed clinical outcome showed primary and primary-assisted clinical benefits at 11 months of 85% and 91%, respectively. Primary and primary-assisted stent patencies, as assessed by duplex sonography and/or angiography, at 6 months were both 92%. Angiographically documented restenosis occurred in three patients. Restenosis in two patients with CA stents was due to extrinsic compression, and it was without symptoms in one patient and was treated satisfactorily by restenting in the other patient. Restenosis in one patient with an SMA stent was successfully treated by restenting. CONCLUSIONS: Our experience suggests a potential role for endovascular therapy of celiac and mesenteric arterial occlusive disease in a variety of clinical scenarios, with a low incidence of complications and a high technical success rate.

Adult↗

PubMed2001

CYP4A1 antisense oligonucleotide reduces mesenteric vascular reactivity and blood pressure in SHR.

The cytochrome P-450 4A (CYP4A)-derived arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) affects renal tubular and vascular functions and has been implicated in the control of arterial pressure. We examined the effect of antisense oligonucleotide (ODN) to CYP4A1, the low K(m) arachidonic acid omega-hydroxylating isoform, on vascular 20-HETE synthesis, vascular reactivity, and blood pressure in the spontaneously hypertensive rat (SHR). Administration of CYP4A1 antisense ODN decreased mean arterial blood pressure from 137 +/- 3 to 121 +/- 4 mmHg (P < 0.05) after 5 days of treatment, whereas treatment with scrambled antisense ODN had no effect. Treatment with CYP4A1 antisense ODN reduced the level of CYP4A-immunoreactive proteins along with 20-HETE synthesis in mesenteric arterial vessels. Mesenteric arteries from rats treated with antisense ODN exhibited decreased sensitivity to the constrictor action of phenylephrine (EC(50) 0.69 +/- 0.17 vs. 1.77 +/- 0.40 microM). Likewise, mesenteric arterioles from antisense ODN-treated rats revealed attenuation of myogenic constrictor responses to increases of transmural pressure. The decreased vascular reactivity and myogenic responses were reversible with the addition of 20-HETE. These data suggest that CYP4A1-derived 20-HETE facilitates myogenic constrictor responses in the mesenteric microcirculation and contributes to pressor mechanisms in SHR.

Animals↗

PubMed1989

[Characteristics of the microcirculation and blood rheology in arterial and venous forms of mesenteric vascular occlusion].

The functional properties of microcirculation and rheology of blood were studied in dogs subjected to arterial and venous occlusion of mesenteric vessels (cranial mesenteric artery and cranial mesenteric vein). It was found that a local alterations of microvascular bed of intestinal wall are quite different in case of arterial or venous occlusion. The degree of hemorheological and microvascular deviations is higher in case of acute venous thrombosis than during the acute occlusion of cranial mesenteric artery.

Acute Disease↗

PubMed1989

[Disturbances of blood flow in the large bowel during acute pancreatitis].

Cases of vascular complications in the large bowel in acute pancreatitis are reported. In the light of own observations and a literature review the author classifies the complications into early (with in 3 days after onset of acute pancreatitis) and late (after more than 3 days). Depending on the mechanism of intestinal ischaemia the cases were divided into: 1) cases of thrombosis of great mesenteric vessels, 2) occlusion of mesenteric vessels caused by compression (inflammatory infiltration or abscess), 3) circulation disturbances in the intestinal wall. Despite the rarity of these complications they should be considered in the analysis of the course of acute pancreatitis, in the prognosis and in operation decisions.

Acute Disease↗

PubMed1981

Evidence against the involvement of prostaglandins in the vasoconstrictor action of calcium ion in rat mesenteric blood vessels.

1. Prostaglandin E2 (PGE2) has been claimed to be essential to the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels. Since noradrenaline acts by releasing intracellular calcium, experiments have been performed using the perfused rat superior mesenteric artery preparation to determine whether prostaglandin synthesis is necessary for the direct vasoconstrictor action of calcium. 2. The cyclo-oxygenase inhibitors, indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA), inhibited responses to noradrenaline and calcium but both were less effective in inhibiting the response to calcium than to noradrenaline. 3. PGE2 (6 ng-20 micrograms/ml) failed to overcome the inhibitory effect of indomethacin (62 micrograms/ml) and ETA (10 micrograms/ml) on the response to the EC50 of Ca2+ (100 micrograms/ml). The EC50 of Ca2+ did not significantly increase PGE2-like release by the blood vessels from the resulting value of 19 +/- 8 pg of PGE2 equivalents/min. 4. PGA1 (6 micrograms/ml) and the thromboxane A2 agonist, U-46619 (200 ng/ml), both caused full restoration of indomethacin-depressed responses to calcium, but did not restore responses depressed by ETA. U-46619 (200 ng/ml) also reversed the inhibitory effect of papaverine (4 micrograms/ml) and caused a 1.6 fold potentiation of Ca2+ responses. 5. The results do not support the hypothesis that prostaglandin synthesis is essential to the vasoconstrictor action of Ca2+ in rat mesenteric blood vessels.

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

PubMed1982

Potentiating and depressive effects of ouabain and potassium-free solutions on rat mesenteric resistance vessels.

We have investigated the in vitro effects of ouabain and K-free solutions on some pharmacological and electrophysiological properties of rat mesenteric resistance vessels (internal diameter approximately 190 micrometers). Vessels were mounted as ring preparations on a myograph capable of measuring their isometric wall tension. In normal saline solutions, vessels did not exhibit any tone and had a membrane potential of -54 mV. Both 1 mM ouabain and K-free solutions caused a transient depolarization of 5-8 mV; thereafter the membrane slowly depolarized to about -45 mV after 30 minutes. There was no mechanical response to ouabain, but K-free solutions caused a transient development of tension which could be inhibited by phentolamine (1 microM). In norepinephrine-activated vessels, exposure to ouabain or K-free solutions caused a small depolarization and an increase in tension. Long-term (30-minute) exposure to 1 mM ouabain or K-free solutions reduced the amplitude of norepinephrine responses and, for the lower (but not the higher) norepinephrine concentrations, the membranes were about 14 mV more depolarized than control. The mechanical responses to a cocktail of norepinephrine in a high potassium solution were, however, unaffected. Re-exposure to normal saline solution produced a transient hyperpolarization and transiently eliminated the norepinephrine response, but thereafter the membrane potential and response returned to normal. The results indicate that ouabain and K-free solutions can have both short-term potentiating and long-term depressive effects on the mechanical response of rat mesenteric resistance vessels to norepinephrine.

Animals↗

PubMed1987

Effects of dihydropyridines on tension and calcium-45 influx in isolated mesenteric resistance vessels from spontaneously hypertensive and normotensive rats.

Contractile tension responses to norepinephrine and depolarizing potassium (80 mM K+), as well as calcium-45 influx stimulated by these agents, were studied in isolated mesenteric resistance vessels (each 100 microM internal diameter) from spontaneously hypertensive rats (SHRs) and from normotensive Wistar Kyoto rats (WKYs). Inhibitory effects of 2 dihydropyridine Ca++ antagonists, PN 200-110 (isradipine) and nisoldipine, on these parameters were also determined. Contractile responses to 80 mM K+ were inhibited by both Ca++ antagonists with the same potency and efficacy in SHR compared with WKY vessels (PN 200-110 IC50 = 2.8 +/- 1.3 X 10(-8) M in SHRs and 2.5 +/- 1.5 X 10(-8) M in WKYs; nisoldipine IC50 = 1.1 +/- 0.4 X 10(-8) M in SHRs and 1.2 +/- 0.9 X 10(-8) M in WKYs). However, contractile responses to norepinephrine (10(-4) M) were inhibited less potently by nisoldipine in SHR vessels (IC50 = 2.2 +/- 0.3 X 10(-9) M) compared with WKY vessels (IC50 = 1.6 +/- 0.6 X 10(-10) M). Similarly, PN 200-110 tended to be less (but not significantly less) potent in SHR vessels (IC50 = 3.3 +/- 1.8 X 10(-8) M) than in WKY vessels (IC50 = 3.4 +/- 0.9 X 10(-9) M); its efficacy was significantly depressed in the SHR vessels (by approximately 20%). When norepinephrine-stimulated calcium-45 influx was determined in the presence of these Ca++ antagonists, a similar profile emerged with respect to a comparison of SHR and WKY vessels. These results support a previously hypothesized alteration in receptor-activated Ca++ influx pathways in SHR mesenteric resistance vessels.

Animals↗

PubMed1994

Regeneration of mesenteric lymphatic vessels in a new experimental model of orthotopic intestinal transplantation in rats.

A new experimental model of orthotopic intestinal transplantation was performed using microsurgical techniques in rats; the physiological flow of blood, lymph, and food was reconstructed. Regeneration of mesenteric lymphatic vessels, which plays an extremely important role in lipid absorption of the transplanted intestine, was studied by mesenteric lymphangiography. Regeneration of mesenteric lymphatic vessels was first confirmed on the seventh postoperative day by mesenteric lymphangiography, and favorable regenerative patterns, without obstruction, were observed on the 32nd, 58th, and 93rd postoperative days.

Animals↗

PubMed2000

Experimental study of lymphogenous peritoneal cancer dissemination: migration of fluorescent-labelled tumor cells in a rat model of mesenteric lymph vessel obstruction.

Primary gastrointestinal cancer frequently spreads to the mesentery, omentum and other parts of the peritoneum, and these deposits are generally considered to be induced by intraperitoneal seeding from the primary lesion. However, a few peritoneal metastatic cases or cases with positive intraperitoneal lavage cytology, without serosal infiltration, have been reported. Most of peritoneal dissemination is certainly attended with serosal involvement of gastrointestinal malignancy. Nevertheless, we observe an unusual case of peritoneal dissemination without definite serosal invasion of the malignancy. And peritoneal dissemination is likely to be concomitant with lymph node metastasis in both cases with and without definite serosal invasion. In this study, we examined peritoneal cancer dissemination from the viewpoint of lymphogenous metastasis. For the model of lymphatic invasion, we established an animal experimental model of mesenteric lymph vessel obstruction. With these models, lymphangiographical studies were made on the fourth postoperative day (ten animals each) and we obtained mesenteric lymphangiograms of extensive mesenteric lymph vessels and reflux of lymph distal to the obstruction point from all ten animals. Next, in these experimental models, fluorescent-labelled tumor cells (rat hepatoma cell line, N1-S1) were infused from the mesenteric lymph node distal to the obstruction point on the fourth postoperative day (five animals each), and the migration of these tumor cells was investigated via fluorescent micrography. Subsequently, the fluorescent-labelled tumor cells were revealed in the mesenteric lymph nodes, mesenteric lymph vessels, interstitial tissues of the mesentery, submucosal lymph nodules and mucosal layer of the small intestine. Hence, lymphatic invasion and obstruction may cause extensive peritoneal dissemination via the lymphatic route.

Animals↗

PubMed1987

Effects of atriopeptin III on isolated mesenteric resistance vessels from SHR and WKY.

The effects of atriopeptin III (AP III) were determined on agonist-induced [i.e., 10(-4) M norepinephrine (NE)] and depolarization-induced (80 mM K+) contractions of isolated mesenteric resistance vessels (ID approximately 100 microns) from spontaneously hypertensive rats (SHR) and from normotensive control Wistar-Kyoto (WKY) rats. The vessels from both groups, when activated by 80 mM K+, were unaffected by AP III. However, activation of WKY vessels by 10(-4) M NE (both phasic and tonic contraction) was inhibited quite effectively and potently by AP III, whereas that in SHR vessels was much less inhibited. In the WKY rat vessels, the concentration of AP III that inhibited contraction by 50% for NE-induced phasic tension was 3.1 +/- 1.3 nM, whereas in SHR vessels it was nearly 1 microM. Comparison of AP III inhibition of NE-induced phasic tension to that at 5 min of activation (tonic tension) indicated that the tonic contractions were less sensitive to AP III than the phasic contractions in the vessels from both strains. A similar experiment indicated that AP III was a potent inhibitor of agonist-induced activation in a human renal resistance vessel (ID 125 microns) and that this vessel depended virtually completely on extracellular Ca2+ for NE-induced contraction. These studies contrast with earlier reports (1, 30) that similar peptides inhibited tension only in rat renal resistance vessels and not in resistance vessels from other vascular beds. The decreased sensitivity and efficacy of AP III in inhibiting tension in SHR compared with WKY mesenteric resistance vessels is discussed in the context of the etiology of spontaneous hypertension.

Animals↗

PubMed2004

Expression of inducible nitric oxide synthase in cultured smooth muscle cells from rat mesenteric lymphatic vessels.

OBJECTIVE: The objective was to devise a method for establishing cultures of rat mesenteric lymphatic vessel smooth muscle cells (LSMC) and to investigate if inducible nitric oxide synthase (iNOS) expression could be activated in LSMC treated with bacterial lipopolysaccharide (LPS). METHODS: LSMC were successfully grown from explanted rat lymphatic microvessels and maintained by subculture. Treatment of LSMC for 24 h with LPS (1-100 microg/mL) activated iNOS protein induction, associated with (1) assay of increased nitrite concentrations in the medium representing cellular nitric oxide synthesis, and (2) demonstration of iNOS in cell extracts by Western blotting. RESULTS: The protein synthesis inhibitor cycloheximide (10 microM) blocked both LPS-induced nitrite formation and iNOS protein expression in LSMC. 1400 W (1 microM), a selective iNOS inhibitor, prevented LPS-induced nitrite formation but not iNOS expression. As well as induction of iNOS by LPS, "constitutive" iNOS was present in some cultures, producing nitrite in amounts that were also subsequently reduced after cell treatment with 1400 W. CONCLUSION: Rat mesenteric LSMC produce nitrite and express iNOS in response to bacterial LPS. Cultured LSMC may provide a useful model for studying mechanisms of iNOS induction in relation to possible influences of iNOS upon lymphatic vessel function.

2-Propanol↗

PubMed1992

Effects of oxodipine on isolated rabbit aorta and mesenteric resistance vessels.

The inhibitory effects of the dihydropyridine Ca2+ antagonist, oxodipine, on contractions and 45Ca2+ influx stimulated by noradrenaline (NA) and high K+ in rabbit aorta were compared to the same parameters measured in mesenteric resistance arteries. In aortic rings oxodipine, 10(-11)-10(-6) M, inhibited in a concentration-dependent manner the contractions induced by high K+ (IC50 = 9.0 +/- 4.0 x 10(-10) M) or by Ca2+ in high K+ solution (IC50 = 6.2 +/- 2.4 x 10(-9) M), while responses to NA were only slightly affected (IC50 greater than 10(-6) M). In mesenteric resistance vessels oxodipine inhibited the contractions induced by high K+ and NA but was more effective against NA- than high K(+)-induced contractions (IC50 = 5.2 +/- 3.1 x 10(-10) and 1.2 +/- 1.8 x 10(-8) M, respectively). The concentration-inhibition curves for high K(+)-induced contraction and 45Ca2+ influx in aorta were almost superimposable (I50 = 2.2 +/- 2.0 x 10(-9) M), whereas NA-induced contractions were inhibited less than 45Ca2+ influx (I50 = 8.2 +/- 2.6 x 10(-8) M). In mesenteric resistance vessels the curves for contraction and 45Ca2+ influx stimulated by high K+ and NA were also superimposable, but 45Ca2+ influx stimulated by NA was more sensitive to oxodipine than that stimulated by high K+ (I50 = 3.9 +/- 2.0 x 10(-10) and 2.2 +/- 1.2 x 10(-8) M, respectively). It is concluded that the effects of oxodipine can be attributed to its ability to inhibit Ca2+ entry through both potential- and receptor-operated pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Evidence for a decreased noradrenaline sensitivity in mesenteric resistance vessels from rats with chemical renal medullectomy.

1. Chemical renal medullectomy was performed in Wistar rats by intraperitoneal injection of 2-bromoethylamine hydrobromide (200 mg/kg body weight). The effect of this treatment upon blood pressure and mesenteric vascular reactivity and morphology was studied 3 weeks after treatment. 2. Blood pressure was significantly raised in medullectomized rats. The indirect systolic pressures (means +/- SEM) were 112 +/- 2.4 mmHg (14.9 +/- 0.32 kPa) and 123 +/- 3.5 mmHg (16.4 +/- 0.5 kPa) (P less than 0.02) for control (n = 12) and medullectomized (n = 12) rats, respectively. However, there were no significant changes in the morphology of the mesenteric resistance vessels. 3. Maximum pressor responses and Ca2+ sensitivities were unchanged in these vessels compared with controls, but the sensitivity to noradrenaline was significantly reduced. Noradrenaline pD2 (= -log ED50) values (means +/- SEM) were 5.87 +/- 0.03 and 5.69 +/- 0.08 (P less than 0.05) for control (n = 12) and medullectomized (n = 12) rats, respectively. 4. This study demonstrates that in this model of hypertension the noradrenaline sensitivity is reduced in mesenteric resistance vessels, but there are no detectable morphological changes associated with the rise in blood pressure.

Animals↗

PubMed1985

Evidence for hyperplasia in mesenteric resistance vessels of spontaneously hypertensive rats using a three-dimensional disector.

Cellular dimensions in mesenteric resistance vessels from 10 spontaneously hypertensive rats and 10 Wistar-Kyoto rats have been determined using a random volume with an unbiased counting rule as the counting unit (the disector). With this method, vessels first were mounted on a myograph. Media thickness (spontaneously hypertensive rats, 11.3 micron; Wistar-Kyoto rats, 8.6 micron; P less than 0.01), lumen diameter (spontaneously hypertensive rats, 178 micron; Wistar-Kyoto rats, 194 micron; P greater than 0.1), and maximum active wall tension response (spontaneously hypertensive rats, 3.2 N/m; Wistar-Kyoto rats, 2.5 N/m; P less than 0.05) were determined. After fixation, serial sections normal to the long axis of the smooth muscle cells were made. In each vessel, the disector was a defined volume of the vessel wall (volume ca. 25 X 10(3) micron3) which was contained in about eight of these sections. The number of nuclei within the disector was counted using an unbiased, three-dimensional counting rule. On the basis that cells were mononuclear (an assumption that was tested), the ratio of this number divided by disector volume equaled the numerical cellular density. Measurement of the fraction of media taken up by smooth muscle cells then gave mean cell volume (spontaneously hypertensive rats, 563 micron3; Wistar-Kyoto rats, 615 micron3; P greater than 0.1). From the myograph measurements, the number of cells per unit length (spontaneously hypertensive rats, 10.4/micron; Wistar-Kyoto rats, 7.4/micron; P less than 0.05) and maximum force production per cell (spontaneously hypertensive rats, 5.1 microN; Wistar-Kyoto rats, 5.7 microN; P greater than 0.1) could then be calculated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗