Reference sample microsphere method: cardiac output and blood flows in conscious rat

Ishise, Shozo; Pegram, Barbara L.; Yamamoto, J.; Kitamura, Yoshihisa; Fröhlich, Edward D.

doi:10.1152/ajpheart.1980.239.4.h443

Cited by 166 publications

(129 citation statements)

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“…The results of our cardiac output studies are similar to those that have been published previously (eg Foster & Frydman, 1977;Tsuchiya et al, 1978;Ishise et al, 1980). However, the eventual pattern of tumour growth does not bear any relation to the pattern of tumour cell arrest or rate of autolysis.…”

Section: Discussionsupporting

confidence: 89%

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Mechanisms of organ selective tumour growth by bloodborne cancer cells

Murphy

Alexander²,

Senior³

et al. 1988

Br J Cancer

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Summary The sites of tumour development for 6 rat tumours injected into syngeneic rats via different vascular routes was determined. Xenografts of human tumours were also injected intra-arterially (i.a.) into immunosuppressed rats.Following intravenous (i.v.) In explaining the mechanism of site selectivity by bloodborne metastasis the haemodynamic theory of Ewing (1928) stressed the importance of the mechanics of the circulation whereas the Soil/Seed hypothesis of Paget (1889) emphasized the importance of the environment in which the trapped emboli found themselves. The eventual sites of metastasis are, however, determined by both haemodynamic and soil/seed factors. Haemodynamic factors are important following the venous discharge of tumour cells since the 'organs of first encounter' are the commonest site for bloodborne metastasis -the lung after systemic venous discharge of tumour cells and the liver after portal venous discharge (Viadana et al., 1978). The present study emphasizes that the 'soil' becomes important when tumour cells have entered the systemic arterial circulation and are thereby delivered to all organs. Clinically this situation can occur when cells are released from primary or secondary lung tumours or possibly when cells released into the venous circulation manage to traverse the lung capillaries.In this paper we extend earlier data (Murphy et al., 1986) on the pattern of spread of rat syngeneic non-lymphoid and non-haemopoietic tumours following intravenous (i.v.), intraportal (i.ptl.) and intra-arterial (i.a.) injection. In our i.v. and i.ptl. studies as well as previously reported studies tumour growth is essentially limited to the 'organs of first encounter' and the study of mechanisms of site selectivity is therefore limited. In order to deliver tumour cells to all organs we have injected them intra-arterially via the intracardiac (i.c.) route. Labelled cell distribution after i.c. injection has been compared with the distribution of cardiac output (measured using the microsphere technique) in order to establish whether cells disseminate and arrest passively or whether they recirculate and localise in certain organs. The 'arterial pattern' of tumour growth after unlabelled cell injection has then been compared with the arterial distribution of labelled tumour cells to establish and quantitate the 'soil effect'.Having established a 'soil effect' after arterial injection of tumour cells we have attempted to determine the mechanisms using several approaches. Firstly a correlation of site selectivity with organ vascularity (using data obtained from the microsphere studies) was sought since there have been reports that more vascular organs might be more susceptible to metastasis (Weiss et al., 1981). Secondly the rate of autolysis of trapped labelled cells in different organs has been compared with the organs susceptibility to tumour growth. Thirdly we have intervened pharmacologically to see if site preference can be altered and finally we have rendered refractory organs susceptible to tum...

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Section: Discussionsupporting

confidence: 89%

“…Six chemically induced syngeneic to the hooded Lister rat were used in the intravascular experiments (Table I) (Ishise et al, 1980 (Tables II and III). However, after i.a.…”

Section: Tumoursmentioning

confidence: 99%

Mechanisms of organ selective tumour growth by bloodborne cancer cells

Murphy

Alexander²,

Senior³

et al. 1988

Br J Cancer

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“…The estimated portal vein glucose concentration (G P V ) was calculated as G P V = G A + (GINF/ PVPF), where GINF P O R = portal vein glucose infusion rate (micromoles per minute), and PVPF = portal vein plasma flow rate (milliliters per minute). Hepatic plasma flow was assumed to be 1.3 m l · g -1 l i v e r · min -1 liver weight (g), with portal vein flow rate assumed to be 80% of the HPF (19,20). Analytical procedures.…”

Section: Methodsmentioning

confidence: 99%

Portal vein afferents are critical for the sympathoadrenal response to hypoglycemia.

2000

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We sought to elucidate the role of the portal vein a fferents in the sympathetic response to hypoglycemia. Laparotomy was performed on 27 male Wi s t a r rats. Portal veins were painted with either 90% phenol (denervation group [PDN]) or 0.9% saline solution (sham-operated group [SHAM]). Rats were chronically cannulated in the carotid artery (sampling), jugular vein (infusion), and portal vein (infusion). After a recovery period of 5 days, animals were exposed to a hyperinsulinemic-hypoglycemic clamp, with glucose infused either portally (POR) or peripherally (PER). In all animals, systemic hypoglycemia (2.48 ± 0 . 0 9 mmol/l) was induced via jugular vein insulin infusion (50 mU · k g -1 · min -1 ). Arterial plasma catecholamines were assessed at basal (-30 and 0 m i n ) and during sustained hypoglycemia (60, 75, 90, and 105 min). By design, portal vein glucose concentrations were significantly elevated during POR versus PER (4.4 ± 0.14 vs. 2.5 ± 0.07 mmol/l; P < 0.01, respectively) for both PDN and SHAM. There were no significant differences in arterial glucose or insulin concentration between the four experimental conditions at any point in time. When portal glycemia and systemic glycemia fell concomitantly (SHAM-PER), epinephrine increased 12-fold above basal (3.75 ± 0.34 and 44.56 ± 6.1 nmol/l; P < 0.001). However, maintenance of portal normoglycemia (SHAM-POR) caused a 50% suppression of the epinephrine response, despite cerebral hypoglycemia (22.2 ± 3.1 nmol/l, P < 0.001). Portal denervation resulted in a significant blunting of the sympathoadrenal response to whole-body hypoglycemia (PDN-PER 27.6 ± 3.8 nmol/l vs. SHAM-PER; P < 0.002). In contrast to the sham experiments, there was no further suppression in arterial epinephrine concentrations observed during PDN-POR versus PDN-PER (P = 0.8). These findings indicate that portal vein afferent innervation is critical for hypoglycemic detection and normal sympathoadrenal counterregulation. D i a b e t e s 4 9 :8-12, 2000 C atecholamines constitute the primary defense against hypoglycemia for individuals with type 1 diabetes, in which the ability to suppress insulin is absent and the capacity to secrete glucagon is diminished. The catecholamine response has been well characterized for both normal and diabetic individuals (1-4). Under normal conditions, this sympathetic response appears sufficient to compensate for the loss of other counterregulatory measures (1,2). Unfortunately, over time, the catecholamine response for individuals with type 1 diabetes diminishes relative to the fall in blood glucose (1,2). The diminished catecholamine response appears to have been further exacerbated by increasingly aggressive attempts to control blood glucose levels in type 1 diabetic patients (3,4).Although iatrogenic hypoglycemia has been invoked as a partial explanation, in general, the pathology of the diminished sympathetic response in patients with type 1 diabetes remains poorly understood. In part, this can be attributed to the lack of knowledge concerning the locus f...

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“…Cardiac output was determined by the radioactive microsphere technique described by Ishise et al 25 The difference in oxygen content of arterial and mixed venous blood (a-v02) was calculated from the Fick equation with use of the measured t2 and the simultaneously measured cardiac output under each exercise condition. Mean arterial pressure and left ventricular end-diastolic pressure were measured via the tail artery catheter and the indwelling left ventricular catheter, respectively.…”

Section: Methodsmentioning

confidence: 99%

Endurance training in rats with chronic heart failure induced by myocardial infarction.

et al. 1986

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The response to exercise was investigated in trained and sedentary rats with moderate compensated heart failure produced by myocardial infarction (MI) and in rats that underwent sham operations. Trained rats ran on a treadmill (10% grade at 20 m/min) for 60 min/day, 5 days/week for 10 to 12 weeks, whereas sedentary rats had only limited activity. Maximal oxygen consumption normalized for body weight (ml kg min`) was determined for each rat and found to be (1) greater in trained rats when compared with sedentary rats and (2) greater in sham-operated rats when compared with their counterparts that suffered infarction. In addition, skeletal muscle succinate dehydrogenase activities were greater and the blood lactic acid response to submaximal exercise was lower in trained rats compared with sedentary rats. Left ventricular infarct size for sedentary and trained rats with infarction was 36 3% and 34 + 3% of the total endocardial circumference, respectively, and resulted in (1) elevated left ventricular end-diastolic pressures at rest and during exercise, (2) lower mean arterial pressures at rest, and (3) lower maximal heart rates when compared with those in their sham-operated counterparts. However, normalization of mean arterial pressures during submaximal and maximal exercise was found along with a trend toward normalization of maximal heart rate when trained rats with infarction were compared with their sedentary counterparts. Blood flows to the kidneys, organs of the gut, and skeletal muscle during both submaximal and maximal exercise were unaffected by either myocardial infarction or training; no differences between sedentary and trained rats with infarction and sedentary and trained sham-operated rats were found. These results demonstrate that an exercise training program of moderate intensity produces beneficial hemodynamic and metabolic effects in rats with moderate compensated heart failure. Circulation 74, No. 2, [431][432][433][434][435][436][437][438][439][440][441] 1986

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Reference sample microsphere method: cardiac output and blood flows in conscious rat

Cited by 166 publications

References 0 publications

Mechanisms of organ selective tumour growth by bloodborne cancer cells

Mechanisms of organ selective tumour growth by bloodborne cancer cells

Portal vein afferents are critical for the sympathoadrenal response to hypoglycemia.

Endurance training in rats with chronic heart failure induced by myocardial infarction.

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