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Biomedical subjects

J Iriuchijima

Publications and source records attributed to J Iriuchijima.

At least 37 records · Page 2Linked to original sources
PubMed1988

Adrenomedullary origin of the hindquarter vasodilation during the transposition response of the rat.

Transposing a rat from the home cage to a new cage produces a cardiovascular response (transposition response) characterized by an increase in hindquarter blood flow with unchanged systemic arterial pressure. Arterial blood samples were collected from rats before and during this response for radioenzymatic assay of catecholamines. During the transposition response, the concentration of adrenaline and noradrenaline in plasma increased about six- and two-fold, respectively. Ablation of the adrenal medulla prevented these changes in plasma catecholamine concentration. Constant i.v. infusion of adrenaline, at rates producing a hindquarter flow approximately matching that observed during the transposition response, evoked an increase in plasma adrenaline concentration also approximately matching the increase observed during the transposition response. It is concluded that the increase in plasma adrenaline secreted from the adrenal medulla is the main cause of the increase in hindquarter blood flow in the transposition response.

Adrenal Medulla↗
PubMed1988

Regional blood flows and resistances in conscious one-kidney, one-clip renovascular hypertensive rats.

Three regional blood flows were measured in one-kidney, one-clip renovascular hypertensive (one-kidney hypertensive) rats with chronically implanted electromagnetic flow probe. One-kidney hypertensive rats showed about 30% greater superior mesenteric flow, about 20% greater hindquarter flow at the terminal aorta, and an almost unchanged renal flow at the clipped renal artery when compared with control rats, but the sum of the mean values of these three regional blood flows in one-kidney hypertensive rats was almost the same as that of control rats. One-kidney hypertensive rats had a higher peripheral resistance in all the investigated vascular areas. The increase in peripheral resistance of the renal area including the clipped and removed arteries was greater than that in peripheral resistance of the superior mesenteric area or hindquarter area. These findings suggest that the remaining renal area which failed to compensate for the flow deprived by uni-nephrectomy plays a role in the etiology of this kind of hypertension.

Animals↗
PubMed1988

Abnormal hindquarter vasoconstrictor tone, a feature common to various kinds of hypertensive rats.

Hindquarter peripheral resistance, calculated as arterial pressure divided by hindquarter blood flow, decreased significantly on ganglionic blockade with hexamethonium bromide in four kinds of experimentally hypertensive rats, i.e. spontaneously hypertensive rats (SHR), DOCA-salt hypertensive rats, and one-kidney, one-clip and two-kidney, one-clip renovascular hypertensive rats, but not in normotensive control rats in the conscious state. Abnormal hindquarter vasoconstrictor tone seems to be a feature common to various kinds of hypertensive rats.

Animals↗
PubMed1988

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

Mean arterial pressure and three regional blood flows--renal, superior mesenteric, and hindquarter flows--were monitored in conscious normotensive control rats (NCR), in two-kidney, one-clip (two-kidney), and in one-kidney, one-clip (one-kidney) hypertensive rats. After administering captopril, an angiotensin-converting enzyme inhibitor, mean arterial pressure decreased in all three groups. However, lowering of arterial pressure was not statistically significant in any of the groups. Renal flow increased significantly in the intact artery of two-kidney hypertensive rats, whereas it did not significantly increase in the clipped artery of one-kidney hypertensive rats and in the intact artery of NCR. Superior mesenteric flow increased significantly only in one-kidney hypertensive rats. Hindquarter flow did not significantly change in the three groups. Regional resistance reduced significantly in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it did not reduce significantly in these two vascular areas in one-kidney hypertensive rats and in NCR. The present findings show that the renin-angiotensin-mediated vasoconstriction plays a role in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it hardly plays a role in these three vascular beds in one-kidney hypertensive rats.

Animals↗
PubMed1987

Hemodynamic characteristics of conscious deoxycorticosterone acetate hypertensive rats.

An electromagnetic flow probe was chronically implanted around the common carotid, superior mesenteric, or renal artery or the terminal aorta in deoxycorticosterone acetate (DOCA) hypertensive rats (prepared with DOCA and saline after uninephrectomy) and uninephrectomized control rats. A catheter for pressure measurement was inserted into the terminal aorta through a femoral artery. At rest the carotid and hindquarter (measured at the terminal aorta) blood flows in DOCA hypertensive rats were similar to the respective, corresponding values in normal rats with intact bilateral kidneys. The group mean of superior mesenteric flow was about 70% and that of renal flow about 40% larger than in normal rats. Cardiac output was estimated to be greater in DOCA hypertensive rats than in normal rats. In uninephrectomized control rats, superior mesenteric flow was larger than in normal rats to such an extent that an increase in cardiac output was assumed as in DOCA hypertensive rats, but renal flow was normal (about twice the unilateral renal flow in normal rats). Estimation of regional sympathetic vasoconstrictor tone from the decrease in peripheral resistance with hexamethonium and vasopressin antagonist revealed a substantial tone also in the superior mesenteric and hindquarter areas, where the tone was estimated to be almost absent in normal rats and uninephrectomized rats. It is suggested that hypertension in DOCA hypertensive rats is sustained by an increase in cardiac output and an elevation of vasoconstrictor tone in resistance vessels. Since increase in cardiac output appears to be similarly present in uninephrectomized control rats, the elevation of sympathetic tone due to administration of DOCA and salt seems to be indispensable for DOCA hypertension.

Animals↗
PubMed1987

Redistribution of cardiac output during grooming of the rat.

Changes in blood flow in the carotid, superior mesenteric, or renal artery or terminal aorta during grooming were measured in the conscious rat with a chronically implanted electromagnetic flow probe. Arterial pressure was measured simultaneously with an indwelling catheter. During grooming, carotid flow almost doubled and arterial pressure rose slightly, while hindquarter (terminal aortic) flow decreased by an average of about 20%. Superior mesenteric flow decreased occasionally and renal flow remained almost unchanged. Heart rate increased by an average of about 10%. An increase in carotid flow during grooming was similarly observed after cervical sympathectomy. After ganglion blockade with hexamethonium, grooming did not decrease hindquarter flow any more. These findings suggest that during grooming a substantial amount of blood flow is switched from the hindquarters to the carotid areas, to achieve a redistribution of cardiac output largely by excitation of the respective regional sympathetic and parasympathetic fibers and that sympathetic vasoconstrictor fibers supplying different vascular areas are controlled by separate pathways from separate neuron groups.

Animals↗
PubMed1986

Regional distribution of sympathetic vasoconstrictor tone in conscious spontaneously hypertensive rats.

An electromagnetic flow probe was chronically implanted around the common carotid, superior mesenteric, or renal artery in spontaneously hypertensive rats (SHR). An indwelling catheter was inserted into the terminal aorta for measurement of arterial pressure. Peripheral resistance was calculated by dividing arterial pressure by flow. Decrease in peripheral resistance on ganglion blockade with hexa-methonium bromide was assumed to indicate the presence of vasoconstrictor tone to regional resistance vessels. In the conscious, resting state, peripheral resistance decreased significantly on ganglion blockade in the carotid and renal areas but not in the superior mesenteric area. The magnitudes of the decrease in peripheral resistance in the carotid and renal areas were not greater than the respective, corresponding values in normal rats. Presumably, vasoconstrictor tone in these three vascular regions, being quite different from that in the hindquarters, is not higher in SHR than in normal rats. Venomotor tone does not seem to be elevated in conscious SHR either, because the decrease in the sum of the mean peripheral flows on ganglion blockade, which was assumed to reflect the decrease in cardiac output, was not larger in SHR than in normal rats. Pentobarbital anesthesia did not abolish renal vasoconstrictor tone in SHR as it does in normal rats.

Animals↗
PubMed1985

Regional difference in sympathetic vasoconstrictor tone in conscious rats.

Regional differences in sympathetic vasoconstrictor tone were studied in conscious rats. In each rat an electromagnetic flow probe was chronically implanted around the common carotid, superior mesenteric, or renal artery, or the terminal aorta. An indwelling catheter for the measurement of arterial pressure was inserted into the terminal aorta via the right femoral artery. Peripheral resistance was calculated by dividing arterial pressure by flow. The per cent decrease in peripheral resistance on the ganglion blockade with hexamethonium bromide was used as a measure of regional sympathetic vasoconstrictor tone. A significant decrease in peripheral resistance, assumed to indicate a substantial tonic discharge to resistance vessels, was observed in conscious rats only in the carotid and renal areas and not in the superior mesenteric and hindquarter (supplied by the terminal aorta) areas. Since ganglion blockade also diminished the sum of the mean regional flows, cardiac output was estimated to decrease on the ganglion blockade. This suggests that capacitance vessels are also receiving a sizable vasoconstrictor tone, because the ganglion blockade did not elevate right atrial pressure. Pentobarbital anesthesia markedly inhibited the assumed tone to the renal area and was estimated to newly generate a tone to the hindquarters.

Animals↗
PubMed1985

Vascular area with marked resistance elevation in one-clip, two-kidney renovascular hypertensive rats.

Blood flow in the terminal aorta or superior mesenteric artery was recorded in conscious one-clip, two-kidney renovascular hypertensive rats and normal control rats with a chronically implanted electromagnetic flow probe. An indwelling catheter for direct measurement of arterial pressure was inserted into the terminal aorta in rats with a flow probe around the superior mesenteric artery. In the hindquarter area supplied by the terminal aorta, the elevation of vascular resistance in hypertensive rats in relation to normal rats was close to the average over the whole body. However, it was about 40% more intense than the average in the superior mesenteric area. Quantitatively, the hindquarter and superior mesenteric beds in hypertensive rats contributed about a quarter and a third of the decrease in total vascular conductance, respectively. Plots of superior mesenteric flow per body weight against arterial pressure at rest for 51 measurements in 9 hypertensive rats revealed an inverse relation between these two variables. These findings indicate that elevation of vascular resistance in the superior mesenteric area and probably the splanchnic area in general play an important role in one-clip, two-kidney renovascular hypertension.

Animals↗
PubMed1985

A pressor response to vibration in conscious rats.

Cardiovascular response in an alerted state induced by vibration was studied in conscious rats by giving a to-and-fro movement to their cages for 30 sec. Cardiac output, superior mesenteric flow, and hindquarter flow were observed with chronically implanted electromagnetic flow probes and arterial pressure with an indwelling catheter. Arterial pressure, heart rate, cardiac output and hindquarter flow increased and superior mesenteric flow decreased with vibration. The increase in heart rate was still present after adrenalectomy, but was abolished by beta-adrenoceptor blockade propranolol. The increase in hindquarter flow was greatly diminished by propranolol or after adrenalectomy, but was still present in adrenalectomized rats after alpha-adrenoceptor blockade phentolamine. The decrease in superior mesenteric flow in vibration was abolished by phentolamine. It was diminished by adrenalectomy. These findings indicate that the cardiovascular response to vibration includes excitation of the cardiac sympathetic nerves, adrenomedullary secretion, and excitation of sympathetic vasoconstrictor fibers and exercise hyperemia in skeletal muscles.

Animals↗
PubMed1985

Mechanism of elevation of hindquarter vascular resistance in spontaneously hypertensive rats.

In spontaneously hypertensive rats and normotensive control rats in the conscious state, hindquarter flow was observed with an electromagnetic flow probe chronically implanted around the terminal aorta. In separate groups of hypertensive and control rats, arterial pressure was observed with an indwelling catheter inserted into the terminal aorta. On ganglion blockade with hexamethonium bromide, hindquarter flow tended to increase in hypertensive rats and to decrease in normal rats. The percent change of hindquarter flow on ganglion blockade was significantly greater in the former than in the latter (p less than 0.05). Hindquarter peripheral resistance, estimated from flow and pressure values obtained in separate rat groups, was greater in hypertensive rats than in normal rats before ganglion blockade, but there was no difference between the groups after blockade. Presumably, an elevated sympathetic tone is responsible for the higher hindquarter peripheral resistance in spontaneously hypertensive rats, which plays an important part in the elevation of total peripheral resistance. However, bilateral lumbar sympathectomy did not induce chronic lowering of arterial pressure in hypertensive rats. This was at least partly due to the development of denervation supersensitivity.

Animals↗
PubMed1984

Changes in cardiac output and peripheral flows on pentobarbital anesthesia in the rat.

In rats chronically implanted with an electromagnetic flow probe around the ascending aorta, terminal aorta, or superior mesenteric artery as well as arterial and venous indwelling catheters, changes in cardiac output, hindquarter flow, splanchnic flow, and arterial pressure on pentobarbital anesthesia were observed. On intravenous injection of pentobarbital sodium at 30 mg/kg, arterial pressure dropped acutely from an average value of about 105 mmHg to a minimum of about 75 mmHg in about 5 min and then gradually recovered to an average level of about 90 mmHg in 30 min. Cardiac index gradually decreased about 30% on the average in 30 min. Hindquarter flow decreased about 25%. Superior mesenteric flow first increased about 40% within 5 min and then returned almost to the premedication level in 30 min. In adrenalectomized rats there was no decrease of hindquarter flow on pentobarbital anesthesia. The increase in superior mesenteric flow immediately after pentobarbital injection remained almost unchanged after adrenalectomy or splanchnicectomy. It is concluded that an appreciable portion of the decrease in cardiac output on pentobarbital anesthesia is induced by inhibition of tonic adrenomedullary secretion which has a dilating effect on muscle blood vessels through stimulation of beta-receptors. The marked increase in splanchnic flow immediately after pentobarbital injection, which is responsible for the concomitant drop in arterial pressure, is considered to be induced by a direct inhibitory effect of the anesthetic on splanchnic blood vessels.

Anesthesia, General↗
PubMed1983

Regional blood flow in conscious spontaneously hypertensive rats.

In spontaneously hypertensive and normal control rats in the conscious state, blood flow was observed in the carotid artery, superior mesenteric artery, renal artery, and terminal aorta with a chronically implanted electromagnetic flow probe. At rest, flow per body weight was not different between the two groups except at the terminal aorta where it was significantly smaller in hypertensive rats (P less than 0.05). Regional peripheral resistance was higher in hypertensive rats than in normal rats in all the four arteries, but its elevation in the former was not uniform but most marked in the hindquarter area supplied by the terminal aorta. Quantitatively, this area was estimated to contribute about 40% of the total conductance decrease in hypertensive rats in comparison with the control. This suggests the importance of elevation of resistance in muscle blood vessels in hypertension. The contributions from the superior mesenteric area and the bilateral kidneys were estimated to be about 15% each. In the transposition response induced by transposing rats from their home cage to a new cage, the increase in hindquarter flow was significantly greater in hypertensive rats than in normal rats (P less than 0.01). The sum of the mean flows of the four arteries, a measure of cardiac output, was not different between hypertensive and normal rats at rest but greater in the former during transposition response. Elevation of arterial pressure in the response in hypertensive rats but not in the normal rats was ascribable largely to a greater increase in cardiac output in the former than the latter.

Animals↗
PubMed1983

Conditions for secretion of vasopressin in pressor amounts in water-replete rats.

Conditions for secretion of pressor amounts of vasopressin were sought in conscious, water-replete rats. The characteristic lowering of arterial pressure on injection of a vasopressin antagonist was used to detect vasopressin secretion in pressor amounts. The absence or marked abatement of both baroreceptor impulses and adrenomedullary secretion were found necessary for secretion of vasopressin in pressor amounts: the vasopressin antagonist lowered arterial pressure in rats with sinoaortic denervation and ganglion blockade or adrenalectomy. Besides baroreceptor activity and adrenomedullary secretion, anesthetics were also found inhibitory on vasopressin release in pressor amounts. The adrenomedullary hormone signaling the presence of adrenomedullary activity to the vasopressin releasing mechanism was identified as noradrenaline and not adrenaline. It is suggested that the vasopressin pressor mechanism is recruited to sustain arterial pressure when the sympathoadrenal system fails.

Adrenal Medulla↗