Role of cardiac lymph and interstitial fluid in lipid metabolism of canine heart

1978 ◽  
Vol 56 (6) ◽  
pp. 1041-1046 ◽  
Author(s):  
Pierre Julien ◽  
Gilles R. Dagenais ◽  
Laimonis Gailis ◽  
Paul-E. Roy

To determine whether cardiac interstitial spaces participate in cardiac fatty acid pool, the relationship between cardiac lymph and arterial plasma free palmitate and triglycerides was studied in anesthetized dogs. [14C]Sucrose, infused at a constant rate in a femoral vein, appeared in the lymph at 90% of its arterial concentration within 60 min. On the other hand, when [1-14C]palmitate was infused at the same rate and at the same site, the ratio of lymph to arterial plasma 14C-labelled free fatty acids (FFA) was only 21% at 60 min and 25% at 120 min, even though the concentrations of endogenous FFA in lymph and arterial plasma were the same. The ratio reached 90% only 24 h after a bolus injection of [3H]palmitate. [1-14C]Palmitate in the lymph triglyceride fraction was only 8% of that in plasma. Although the lymph composition may be influenced by the metabolism of heart muscle, cardiac adipose tissue, and serum lipoproteins, these results indicate the presence of a pool of myocardial fatty acids which may be partly located in the interstitial spaces.

1961 ◽  
Vol 200 (5) ◽  
pp. 1095-1098 ◽  
Author(s):  
Frank J. Hohenleitner ◽  
John J. Spitzer

To measure the renal removal of free fatty acids from the plasma, simultaneous determinations of this metabolite were performed in a systemic artery and a renal vein in the anesthetized dogs. Renal plasma flow was also determined by the PAH method, and the renal uptake of free fatty acids was calculated. Concentrations of free fatty acids in renal venous plasma were usually lower than the arterial concentrations. The arteriovenous differences were statistically highly significant. The results also suggested that the degree of free fatty acid removal was proportional to the arterial concentration of this metabolite.


2001 ◽  
Vol 4 (2b) ◽  
pp. 459-474 ◽  
Author(s):  
Serge Renaud ◽  
Dominique Lanzmann-Petithory

AbstractFor decades it has been postulated that the main environmental factor for coronary heart disease (CHD) was the intake of saturated fatty acids (SFA). Nevertheless, confirmation of the role of SFA in CHD through intervention trials has been disappointing. It was only when the diet was enriched in n-3 fatty acids that CHD was significantly prevented, especially cardiac death.In addition to n-3 fatty acids, many other foodstuffs or nutrients such as fibers, antioxidants, folic acid, calcium and even alcohol contribute to prevent CHD. Thus the relationship between diet and CHD morbidity and mortality appears to be much more complex than formerly suspected considering as key factors only SFA, linoleic acid, cholesterol and atherosclerosis. Some of the mechanisms are briefly described, but many additional nutrients (or non nutrients) may also play an important role in the pathogenesis of CHD.Finally, as a result of the most recent epidemiologic studies the ideal diet may comprise: 8% energy from SFA, 5% from polyunsaturated fatty acids with a ratio 5/1 of linoleic/alpha-linolenic acid+longer chains n-3, oleic acid as desired, large intake of cereals, vegetables, legumes and fruits, fish twice a week, cheese and yogurt as dairy products, rapeseed and olive oils as edible fat. Without side effects, such a diet can be highly palatable, easily enjoyed by many populations and may prevent effectively and rapidly (within a few weeks or months) CHD.


1992 ◽  
Vol 262 (5) ◽  
pp. H1579-H1584 ◽  
Author(s):  
T. P. Broten ◽  
J. K. Miyashiro ◽  
S. Moncada ◽  
E. O. Feigl

Vasodilation following the infusion of acetylcholine is due to the release of endothelium-derived relaxing factor (EDRF). However, the role of EDRF in neurogenic coronary vasodilation, when acetylcholine is released outside the vessel at the adventitial-medial junction, has not been established. The action of EDRF in parasympathetic coronary vasodilation was tested in the present study using a specific inhibitor of EDRF synthesis, nitro-L-arginine methyl ester (L-NAME). Experiments were conducted on closed-chest, alpha-chloralose-anesthetized dogs with the heart paced at a constant rate. Phentolamine and propranolol were administered to block alpha- and beta-adrenergic receptors, and ibuprofen was given to inhibit prostaglandin synthesis. Intracoronary infusion of L-NAME decreased the coronary vasodilation in response to intracoronary acetylcholine or vagal stimulation. The coronary response to the endothelium-independent vasodilator nitroglycerin was unaffected by L-NAME. These data demonstrate that L-NAME specifically inhibits coronary vasodilation caused by acetylcholine and vagal stimulation, indicating that parasympathetic coronary vasodilation is dependent on EDRF.


1984 ◽  
Vol 246 (1) ◽  
pp. F32-F38
Author(s):  
E. T. Pierce ◽  
R. J. Grekin ◽  
D. R. Mouw

Ventriculocisternal perfusion (VCP) of artificial cerebrospinal fluid (CSF) was performed in pentobarbital-anesthetized dogs. Renal function was studied in protocols consisting of a 1-h experimental period in which the animals received either CSF with an elevated sodium concentration (300 mM, high Na) via VCP or antidiuretic hormone (ADH) intravenously, bracketed by 1-h control and recovery periods. High Na VCP caused an increase in plasma ADH measured by radioimmunoassay (to 176% of control) that coincided with a natriuresis (to 180% of control). In a second set of experiments, these changes in endogenous ADH were mimicked experimentally with intravenous infusions of synthetic ADH in animals receiving continuous VCP with normal sodium artificial CSF. The dose-response relationship between log ADH and urinary sodium excretion for the intravenous ADH experiments was not different from the relationship for those experiments in which ADH was elevated as a consequence of high Na VCP. These results suggest that ADH causes part, if not all, the natriuresis induced by high Na VCP.


1964 ◽  
Vol 42 (5) ◽  
pp. 671-677 ◽  
Author(s):  
Kristen B. Eik-Nes

The concentration of testosterone has been measured in spermatic vein blood from the left testis in 25 anesthetized dogs, stimulated with human chorionic gonadotrophin and infused with arterial blood via the left spermatic artery at different rates. The secretion of testosterone varied with the rate at which arterial blood was infused and at a constant infusion rate of 3.81 ml/min, animals weighing from 19 to 23 kg produced testosterone at a constant rate over 90 minutes. Infusion rates lower than this decreased the secretion of testosterone, and if arterial blood was infused at a rate of 0.76 ml/min for the first 30 minutes of experimentation, the capacity of the infused testis to secrete testosterone in the ensuing 60 minutes was impaired even in animals given large doses of human chorionic gonadotrophin via the left spermatic artery. A relationship between the arterial blood flow to the testis and its ability to secrete testosterone under the influence of human chorionic gonadotrophin is thus established.


1996 ◽  
Vol 6 (4) ◽  
pp. 290-298 ◽  
Author(s):  
Lan Lan L. Yeh ◽  
Lewis H. Kuller ◽  
Clareann H. Bunker ◽  
Flora A. Ukoli ◽  
Sara L. Huston ◽  
...  

1988 ◽  
Vol 254 (6) ◽  
pp. G814-G818 ◽  
Author(s):  
K. Ito ◽  
T. Yukimura ◽  
T. Takenaga ◽  
K. Yamamoto ◽  
K. Kangawa ◽  
...  

A synthetic alpha-human atrial natriuretic peptide (alpha-hANP) was infused into the renal artery of anesthetized dogs, and the urine flow, renal hemodynamics, and plasma guanosine 3',5'-cyclic monophosphate (cGMP) were determined. alpha-hANP led to a natriuresis accompanied by an increase in renal blood flow in the infused kidney but not in the contralateral kidney. The systemic blood pressure remained unchanged. The arterial plasma cGMP significantly increased after alpha-hANP administration. The plasma cGMP in the renal vein was significantly lower than that in the aorta throughout the experiment; therefore the elevated circulating cGMP was probably of extrarenal origin. The plasma cGMP in the right ventricle and femoral vein was also increased to the same extent seen in the aorta. On the other hand, plasma cGMP in the superior mesenteric vein was remarkably increased over that in the aorta. After the administration of alpha-hANP, the increased circulating cGMP seems to be the result of an enhancement of production of this nucleotide from the small intestine or organs drained by the superior mesenteric venous circulation.


1984 ◽  
Vol 57 (4) ◽  
pp. 1254-1260 ◽  
Author(s):  
M. Decramer ◽  
A. De Troyer

In an attempt to understand the role of the parasternal intercostals in respiration, we measured the changes in length of these muscles during a variety of static and dynamic respiratory maneuvers. Studies were performed on 39 intercostal spaces from 10 anesthetized dogs, and changes in parasternal intercostal length were assessed with pairs of piezoelectric crystals (sonomicrometry). During static maneuvers (passive inflation-deflation, isovolume maneuvers, changes in body position), the parasternal intercostals shortened whenever the rib cage inflated, and they lengthened whenever the rib cage contracted. The changes in parasternal intercostal length, however, were much smaller than the changes in diaphragmatic length, averaging 9.2% of the resting length during inflation from residual volume to total lung capacity and 1.3% during tilting from supine to upright. During quiet breathing the parasternal intercostals always shortened during inspiration and lengthened during expiration. In the intact animals the inspiratory parasternal shortening was close to that seen for the same increase in lung volume during passive inflation and averaged 3.5%. After bilateral phrenicotomy, however, the parasternal intercostal shortening during inspiration markedly increased, whereas tidal volume diminished. These results indicate that 1) the parasternal intercostals in the dog are real agonists (as opposed to fixators) and actively contribute to expand the rib cage and the lung during quiet inspiration, 2) the relationship between lung volume and parasternal length is not unique but depends on the relative contribution of the various inspiratory muscles to tidal volume, and 3) the physiological range of operating length of the parasternal intercostals is considerably smaller than that of the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)


PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245038
Author(s):  
Yee Teng Lee ◽  
Nor Ismaliza Mohd Ismail ◽  
Loo Keat Wei

Background Ischemic stroke is one of the non-communicable diseases that contribute to the significant number of deaths worldwide. However, the relationship between microbiome and ischemic stroke remained unknown. Hence, the objective of this study was to perform systematic review on the relationship between human microbiome and ischemic stroke. Methods A systematic review on ischemic stroke was carried out for all articles obtained from databases until 22nd October 2020. Main findings were extracted from all the eligible studies. Results Eighteen eligible studies were included in the systematic review. These studies suggested that aging, inflammation, and different microbial compositions could contribute to ischemic stroke. Phyla Firmicutes and Bacteroidetes also appeared to manipulate post-stroke outcome. The important role of microbiota-derived short-chain fatty acids and trimethylamine N-oxide in ischemic stroke were also highlighted. Conclusions This is the first systematic review that investigates the relationship between microbiome and ischemic stroke. Aging and inflammation contribute to differential microbial compositions and predispose individuals to ischemic stroke.


2001 ◽  
Vol 281 (4) ◽  
pp. E742-E748 ◽  
Author(s):  
Yoshiharu Koyama ◽  
Robert H. Coker ◽  
Joshua C. Denny ◽  
D. Brooks Lacy ◽  
Kareem Jabbour ◽  
...  

This study was aimed at assessing the role of carotid body function in neuroendocrine and glucoregulatory responses to exercise. The carotid bodies and associated nerves were removed (CBR, n = 6) or left intact (Sham, n = 6) in anesthetized dogs >16 days before experiments, and infusion and sampling catheters were implanted. Conscious dogs were studied at rest and during 150 min of exercise. Isotopic dilution was used to assess glucose production (Ra) and disappearance (Rd). Arterial glucagon was reduced in CBR compared with Sham at rest (29 ± 3 vs. 47 ± 3 pg/ml). During exercise, glucagon increased more in Sham than in CBR (47 ± 9 vs. 15 ± 2 pg/ml). Cortisol and epinephrine levels were similar in the two groups at rest and during exercise. Basal norepinephrine was similar in CBR and Sham. During exercise, norepinephrine increased by 432 ± 124 pg/ml in Sham, but by only 201 ± 28 pg/ml in CBR. Basal arterial plasma glucose was 108 ± 2 and 105 ± 2 mg/dl in CBR and Sham, respectively. Arterial glucose dropped by 10 ± 3 mg/dl at onset of exercise in CBR ( P < 0.01) but was unchanged in Sham (decrease of 3 ± 2 mg/dl, not significant). Basal glucose kinetics were equal in Sham and CBR. At onset of exercise, Raand Rdwere transiently uncoupled in CBR (i.e., Rd> Ra) but were closely matched in Sham. In steady-state exercise, Raand Rdwere closely matched in both groups. Insulin was equal in the basal period and decreased similarly during exercise. These studies suggest that input from the carotid bodies, or receptors anatomically close to them, 1) is important in control of basal glucagon and the exercise-induced increment in glucagon, 2) is involved in the sympathetic response to exercise, and 3) participates in the non-steady-state coupling of Rato Rd, but 4) is not essential to glucoregulation during sustained exercise.


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