Acta Physiologica

REDFORS, S.; HALLBÄCK, D.‐A.; HAGLUND, U.; JODAL, M.; LUNDGREN, O.

doi: 10.1111/j.1748-1716.1984.tb07448.xpmid: 6475548

The hemodynamic reactions of the parallel coupled vascular circuits in the cat small intestine were studied before, during and after a two‐hour period of intestinal hypotension induced by lowering the intestinal arterial inflow pressure by partially occluding the superior mesenteric artery during a continuous stimulation of the postganglionic nerves to the small intestine. Furthermore, fluid and electrolyte transport and villous tissue osmolality were measured. A histological examination of biopsies taken during and after the hypotensive period was also carried out. The animals were divided into two groups (undamaged and damaged) according to the histological appearance of the intestinal mucosa. The hemodynamic reactions were investigated with a method that made it possible to study total intestinal, absorptive site (“villous”), nonabsorptive site (“crypt”) and muscle layer blood flow. Total intestinal blood flow was lower in the damaged group than in the undamaged group during the arterial hypotension. However, absorptive site blood flow was similar in the two groups. Consequently, a significantly larger fraction of blood flow was distributed to the “villi” in the damaged group. Morover, absorptive site red blood cell flow was only slightly reduced despite the development of mucosal ulcerations. These findings are discussed in relation to the pathophysiology of the mucosal lesions. Net fluid, net sodium and net chloride absorption was unchanged in the undamaged group whereas in the damaged group a marked decrease was observed after lowering the perfusion pressure. The decrease in net sodium absorption was due to a decrease in the lumen to tissue transport of sodium. Thus, the capacity of the small intestine to absorb fluid and electrolytes is unchanged even during a marked arterial hypotension with a pronounced decrease of intestinal blood flow as long as no mucosal damage has developed.

REDFORS, S.; HALLBÄCK, D.‐A.; SJÖVALL, H.; JODAL, M.; LUNDGREN, O.

doi: 10.1111/j.1748-1716.1984.tb07449.xpmid: 6475549

The hemodynamic response in the parallel‐coupled vascular sections of the cat small intestine were studied before, during and after a two hour period of hemorrhage (about 30 per cent of estimated blood volume). Fluid and electrolyte transport and villous tissue osmolality were also measured. Biopsies for histology were taken at the end of all experiments. The animals were divided in two groups, undamaged and damaged, according to the degree of mucosal damage observed. The hemodynamic reactions were investigated with a method that made it possible to study total intestinal, absorptive site (“villous”), nonabsorptive site (“crypt”) and muscle layer blood flows. Total intestinal blood flow was lower in the damaged as compared to the undamaged group during hypovolemia. No difference in absorptive site blood flow was observed between the two groups during hypovolemia. Furthermore, no decrease of red blood cell flow in the “villi” was recorded in either group after hemorrhage. Consequently, mucosal lesions developed despite an unchanged oxygen transport capacity to the villi. The pathophysiology of the mucosal lesions is briefly discussed. Net fluid and sodium absorption was after hemorrhage increased in the undamaged group reflecting a decrease in the tissue to lumen transport of sodium. After retransfusion net fluid and sodium absorption returned to control. In the damaged group, however, net fluid and sodium absorption was decreased after hemorrhage. The increased rate of fluid and electrolyte transport observed in the undamaged small intestine after hemorrhage, is proposed to be an important mechanism for fluid replacement after hemorrhage.

BURHOL, PER G.; LYGREN, IDAR; JENSSEN, TROND G.; FLORHOLMEN, JON; JORDE, ROLF

doi: 10.1111/j.1748-1716.1984.tb07450.xpmid: 6433648

The present paper describes a sensitive, precise and specific radioimmunoassay method for measurements of plasma somatostatin; significant rises in plasma somatostatin following a test meal, intraduodenal infusion of fat and HCl, and intravenous injection of insulin; and separation of immunoreactive plasma somatostatin into two components probably representing bound and free molecular forms of somatostatin both in fasting and postprandial human plasmas.

JOHANSSON, G.; LAAKSO, M.‐L.; PORKKA‐HEISKANEN, T.; PEDER, M.; LINDROOS, F.

doi: 10.1111/j.1748-1716.1984.tb07451.xpmid: 6433649

Plasma levels of LH and FSH were measured in castrated male rats kept in a 12/12 h light/dark cycle (control lighting), continuous light or continuous darkness. In Experiment I, the animals were kept in the three illumination conditions for 5 weeks. They were then decapitated for blood collection. In Experiment II, the blood samples were collected daily via permanently implanted aortic cannulae after 7 days of adaptation to the experimental lighting condition. In both experiments, the plasma levels of LH and FSH were higher in the rats kept in continuous light than in those kept in control conditions. After exposure to darkness for 5 weeks, the gonadotropin levels did not differ from the control values. In Experiment II, the levels of FSH were lower in darkness than in the control lighting, but the levels of LH did not change.

LAAKSO, MAIJA‐LIISA; JOHANSSON, GUNNAR; PORKKA‐HEISKANEN, TARJA; PEDER, MIKAEL

doi: 10.1111/j.1748-1716.1984.tb07452.xpmid: 6433650

Plasma levels of LH and FSH in male rats were compared in blood samples collected by decapitation or through permanently implanted aortic cannulae. The hormone levels were higher in the samples taken by decapitation. After cannulation, the gonadotropin levels remained unchanged when sampling occurred only once a day and each rat was bled 1–3 times over a period of 7 days (sample volume 2.3 ml). The hematocrits of these rats decreased from 42% to 34% after two samplings. In another experiment the LH and FSH levels increased when seven samples had been taken during 24 h. In this experiment the blood cells were reinfused into the circulation, and as a result after 5 samples the hematocrit decreased only from 45% to 40%. A drop in food consumption was observed after cannulation. It is suggested that the increase in gonadotropin levels may be due to the acute stress caused by handling during and before decapitation or decrease in gonadotropin levels may be due to the chronic stress caused by the implanted cannula. The frequent bleedings and cell infusions into the cannulated rats may stimulate the secretion of gonadotropins, opposing the effect of chronic stress.

FREDRIKSSON, KENT; NORDBORG, CLAES; JOHANSSON, BARBRO B.

doi: 10.1111/j.1748-1716.1984.tb07453.xpmid: 6475550

After reducing the number of patent conduit arteries to the brain by bilateral ligation of the carotid artery, the percentage decrease in blood pressure from the aorta to the internal carotid artery distal to the ligation was larger in spontaneously hypertensive rats than in normotensive rats. The pressure drop corresponded to the degree of hypertension as well as to morphometrically determined structural arterial alteration in the main communicating circuit, i.e. larger media to internal radius ratio and smaller internal radius in the posterior communicating arteries, the proximal part of the posterior cerebral arteries, the basilar artery and the vertebral arteries. The discrepancy between the sum of the luminal cross sectional areas of the communicating circuit and the luminal areas of the ligated conduit arteries was larger in the hypertensive than in the normotensive rats. It is to be expected that occlusion of conduit arteries to the brain will have a larger impact on the cerebral arterial perfusion pressure head in the presence of such hypertensive structural alterations known to increase flow resistance.

SEJERSTED, OLE M.; VIKSE, ARILD; EIDE, IVAR; KIIL, FREDRIK

doi: 10.1111/j.1748-1716.1984.tb07454.xpmid: 6433651

Inferences about total renal (venous and urinary) PGE2 output from determinations of urinary excretion rates (UPGE2V) cannot be made unless the distribution of PGE2 between renal venous plasma and urine is known. Therefore, in the present study on intact kidneys of anesthetized dogs both urinary excretion of PGE2 and the renal venous output (the product of plasma flow and venous concentration of PGE2) was determined during low and high rates of renal PGE2 synthesis. PGE2 was measured in urine and arterial and renal venous plasma by radioimmunoassay during the following conditions: (1) Hydropenia. In the control condition UPGE2V averaged 0.041±0.012 pmol/g·min and varied between 4 and 70% of the total PGE2 output. With infusion of arachidonic acid (AA, 160 μg/kg·min) into the renal artery total PGE2 output increased from 0.18±0.03 to 3.23±0.51 pmol/g·min, whereas arterial concentrations of PGE2 were unchanged. The urinary fraction still varied between 6 and 46% of total renal PGE2 output. (2) High urine flows caused by mannitol, saline or saline and ethacrynic acid (ECA) infusion. These procedures did not stimulate total renal PGE2 output and the urinary fraction varied between 4 and 49%. ECA combined with saline infusion increased the urinary fraction significantly to 34.7±4.0%. AA increased the total PGE2 output as during hydropenia, but the urinary fraction fell to 13% in 13 dogs and was unchanged at about 8% in six dogs. On average the urinary fraction of total PGE2 output was significantly lower than in hydropenia. Thus, the urinary fraction of total renal PGE2 output is not constant, and urinary excretion of PGE2 does not give reliable information about renal synthetic rates of prostaglandins.

VIKSE, ARILD; HOLDAAS, HALLVARD; SEJERSTED, OLE M.; KIIL, FREDRIK

doi: 10.1111/j.1748-1716.1984.tb07455.xpmid: 6382924

To study the relationship between PGE2 and renin release from the kidney, examinations were performed on anesthetized dogs during afferent arteriolar dilation. This condition is known to increase renin release and enhance the stimulatory effects on renin release of β‐adrenergic agonists, such as isoproterenol. Afferent arteriolar dilation induced by constricting the renal artery or occluding the ureter increased PGE2 and renin release before, but not after, indomethacin administration. Isoproterenol infusion during afferent arteriolar dilation increased renin release but not PGE2 release both before and after indomethacin administration. Phenylephrine, an α‐adrenergic agonist, which also induces afferent arteriolar dilation, increased PGE2 and renin release at control blood pressure but not when the afferent arterioles already were dilated by ureteral occlusion. We conclude that afferent arteriolar dilation caused by renal arterial constriction, ureteral occlusion or infusion of phenylephrine increases prostaglandin synthesis which stimulates renin release. The effect of isoproterenol on renin release is independent of prostaglandin synthesis.

BRÅTVEIT, M.; HELLE, K. B.

doi: 10.1111/j.1748-1716.1984.tb07456.xpmid: 6147957

Exogenous VIP caused a concentration dependent inhibition of the spontaneous mechanical activity in the isolated rat mesenteric‐portal vein preparation via a mechanism which was completely independent of the propranolol‐blocked β‐adrenoceptor, of high K+ in the medium and of exogenous bovine pancreatic polypeptide, neurotensin and opioids. The potency of VIP ((pD2=7.52±0.18, n=6) was about 30 times higher than that of isoprenaline in the atropine and phentolamine‐blocked preparation. The isoprenaline inhibition was mediated via a β2‐type of adrenoceptor with low apparent affinity for noradrenaline (intrinsic activity (a) = 0.27±0.01, n=8). Opposite effects of exogenous VIP and noradrenaline were on the other hand observed in the atropinized and β‐blocked preparation. These results suggest that in the rat portal vein neuronal VIP and circulating adrenaline may be complementary in their antagonism of the α‐adrenoceptor mediated increase in contractility.

LUNDBLAD, LARS; HUA, XIAO‐YING; LUNDBERG, JAN M.

doi: 10.1111/j.1748-1716.1984.tb07457.xpmid: 6475551

The cardiovascular effects of locally applied nicotine and capsaicin to the nasal mucosa were studied in anaesthetized guinea‐pigs. Local application of capsaicin (0.3–30 μM) or nicotine (0.3–30 mM) induced dose‐dependent increases in arterial blood pressure, mainly due to an increase in peripheral vascular resistance. The capsaicin and nicotine responses were abolished after local anaesthesia and markedly reduced (to about 20% of control) by combined pretreatment with phentolamine and propranolol, suggesting reflexogenic sympathetic activation. Systemic capsaicin pretreatment abolished the hypertensive effect of capsaicin (30 μM) and reduced the response to nicotine application to about 25% of control (p<0.001). Local capsaicin pretreatment of the nasal mucosa one week earlier also significantly reduced the capsaicin response (p<0.05), while the nicotine‐induced increase in blood pressure was not significantly changed. The present findings suggest the presence of two afferent mechanisms in the nasal mucosa which induce hypertension upon chemical irritation. The capsaicin response is dependent upon capsaicin‐sensitive afferents. The nicotine response involves mainly capsaicin‐sensitive neurons and, in addition, a minor component which is resistant to capsaicin pretreatment. Thus, the hypertensive effect of nicotine applied locally to the nasal mucosa seems to be mainly mediated via sensory mechanisms other than the sneezing response which is not dependent on capsaicin sensitive nerves.