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Biomedical subjects

J Iriuchijima

Publications and source records attributed to J Iriuchijima.

At least 19 recordsLinked to original sources
PubMed2001

Differential effects of chlorpromazine on two vasoconstrictor tones in the rat.

Hindquarter compensator tone (HCT) is referred to as the sympathetic vasoconstrictor tone to the hindquarters of the rat induced by such hypotensive interventions as pentobarbital anesthesia, nitrate administration and blood loss. The aim of this study is to observe whether chlorpromazine (CPZ) injected intravenously in rats (0.5 mg/kg) inhibits the following two different kinds of vasoconstrictor tone: HCT induced by pentobarbital and the renal tone which is normally present in the conscious state. Rats were implanted with an electromagnetic flow probe around the terminal aorta or the left renal artery. The right common carotid was cannulated for mean arterial pressure (AP). Regional peripheral resistance (hind-quarter resistance [HQR] or renal resistance [RR]) was calculated as AP divided by regional flow. In rats under pentobarbital anesthesia, after CPZ, ganglionic blockade with hexamethonium bromide (25 mg/kg) did not decrease HQR. However, in conscious rats after CPZ, blockade decreased RR significantly. These findings indicate that CPZ inhibits HCT almost completely but scarcely decreases the renal tone and further suggest that HCT and the renal tone are generated by different mechanisms.

Animals↗
PubMed2000

Inhibition of abnormal hindquarter vascular tone in spontaneously hypertensive rats with chlorpromazine.

The presence of an abnormal sympathetic vascular tone is assumed in the hindquarters of spontaneously hypertensive rats (SHR) on the basis that ganglionic blockade decreases hindquarter vascular resistance (HQR) in them but not in normotensive control rats (NCR). Hindquarter blood flow (HQF) was observed with an electromagnetic flow probe implanted around the terminal aorta in SHR and NCR in the conscious state. Mean arterial pressure (AP) was also recorded with an indwelling catheter. HQR was calculated as AP divided by HQF. Intravenous bolus injection of chlorpromazine-HCl at 0.5 mg/kg significantly decreased HQR in SHR but not in NCR. Thereafter, in SHR, ganglionic blockade with hexamethonium bromide did not decrease HQR further. Chlorpromazine given to SHR after ganglionic blockade did not decrease HQR either. These findings indicate that the abnormal hindquarter tone in SHR was inhibited by chlorpromazine. It is suggested that dopaminergic neurons are involved in the hindquarter sympathetic tone generation.

Animals↗
PubMed1999

Vascular areas where clonidine induces vasodilation in hypertensive and normotensive rats.

The aim of this study was to find vascular areas where clonidine decreases the regional vascular resistance when this drug lowers arterial pressure in conscious spontaneously hypertensive rats and normotensive control rats. Arterial pressure was observed with an indwelling catheter at a carotid. Blood flow was measured with an electromagnetic flow probe implanted around the renal artery or the superior mesenteric artery. Regional vascular resistance was calculated as arterial pressure divided by blood flow. Intravenous bolus injection of clonidine at a dose to decrease arterial pressure decreased renal resistance and superior mesenteric resistance. Quantitatively, the combined effect of the decrease in these two resistances was enough to account for the decrease in arterial pressure. Although clonidine is thought to inhibit sympathetic nerve activity centrally, the above vasodilator effect is not ascribable to this inhibitory mechanism: Sympathetic activity to be inhibited does not seem to be present in the superior mesenteric area and clonidine similarly decreased renal vascular resistance even after renal denervation.

Animals↗
PubMed1998

Peripheral blood flow response to step-wise increase of arterial pressure in conscious rats.

In conscious rats, changes in renal or superior mesenteric flow were observed when arterial pressure was elevated by occluding the terminal aorta. Blood flow was measured with an implanted electromagnetic flow probe and terminal aorta occlusion (TAO) was induced with an implanted pneumatic occluder. Arterial pressure was recorded with an indwelling catheter in the common carotid. Each TAO lasted for 20 seconds and flow and pressure at the end of this period were noted as those during TAO. After elimination of the reflexive compensation of arterial pressure by ganglionic blockade, the renal flow increase during TAO was slight but significant (p <0.01), although the relative increase in flow was less than that in pressure. In other words, renal autoregulation, constancy of renal blood flow in the face of arterial pressure change, was imperfect. After further pentobarbital anesthesia, however, renal autoregulation was more complete to such an extent that the renal flow increase was insignificant during TAO. In contrast, the relative increase in superior mesenteric flow during TAO was larger than that in pressure with or without anesthesia.

Animals↗
PubMed1997

Why is the hypotensive effect of clonidine greater in hypertensive rats?

The original aim of this study was to observe whether the depressor drug clonidine inhibited the abnormal hindquarter tone in spontaneously hypertensive rats (SHR). In conscious SHR and normotensive control rats (NCR), hindquarter (terminal aortic) blood flow was observed with an implanted electromagnetic flow probe and mean arterial pressure with an indwelling catheter. Twenty minutes after intravenous injection of clonidine (5 micrograms/kg) when arterial pressure reached a steady lower level, hindquarter resistance (HQR), calculated as mean arterial pressure divided by hindquarter flow, did not decrease in SHR. Thus we were unable to obtain evidence for an inhibitory effect of clonidine on the abnormal hindquarter tone in SHR. In NCR, HQR increased significantly by clonidine. The decrease in arterial pressure on clonidine was greater in SHR than in NCR, presumably because the increase in HQR partially offset the hypotensive effect in NCR. It seems that the increase in HQR in NCR was induced by a reflexive excitation of regional sympathetic vasoconstrictor fibers, which, being the final common path for the abnormal hindquarter tone also, were already being excited in SHR before clonidine administration. This point was quantitatively verified.

Animals↗
PubMed1997

Hindquarter sympathetic tone induced by small blood loss in conscious rats.

We have designated the hindquarter (or terminal aortic) vascular resistance (HQR) of the rat as hindquarter compensator (HC) because it increases after such hypotensive interventions as pentobarbital anesthesia and nitrate administration, presumably due to reflex excitation of regional vasoconstrictor fibers. The aim of the present study was to observe whether the HC mechanism is also mobilized in response to hemorrhage. Rats were implanted with a 1.5 or 2 mm diameter electromagnetic flow probe at the terminal aorta for measurement of hindquarter flow (HQF). An indwelling catheter was placed in the right common carotid artery to measure arterial pressure (AP) and withdraw blood. Experiments were performed in conscious rats two or three days after implantation. HQR was calculated by dividing AP by HQF. About 10 min after withdrawing blood (0.3 ml/100 g body weight), ganglionic blockade with hexamethonium bromide significantly decreased HQR, which indicated a mobilization of the HC mechanism, a change not observed with superior mesenteric resistance. A quantitatively similar change was observed in HQR after withdrawing double the amount of blood, i.e., 0.6 ml/100 g body weight, suggesting that the HC mechanism is activated almost fully by the relatively small amount of blood loss of 0.3 ml/100 g body weight.

Animals↗
PubMed1994

Hindquarter vascular resistance as compensator for hypotension in conscious rats.

The purpose of this study was to test whether hindquarter (terminal aortic) vascular resistance uniquely increases in order to compensate for interventions which result in a lowering of arterial pressure. Changes in hindquarter resistance were compared to changes in superior mesenteric resistance after the administration of the nitrovasodilator drug, molsidomine. Hindquarter blood flow or superior mesenteric flow was measured in conscious rats using an electromagnetic flow probe implanted around the terminal aorta or the superior mesenteric artery, respectively. Twenty minutes after an intravenous bolus injection of molsidomine (1 mg/kg), ganglionic blockade with hexamethonium bromide (25 mg/kg, i.v.) significantly decreased hindquarter resistance, but not superior mesenteric resistance. In the absence of molsidomine, ganglionic blockade has no effect on resistance in either vascular bed. These findings suggest that excitation of sympathetic vasoconstrictor fibers supplying the hindquarters but not those supplying the superior mesenteric area occurred in response to the hypotensive effect of molsidomine. This is consistent with the hypothesis that augmenting-hindquarter resistance is the first line of defense against hypotensive interventions.

Animals↗
PubMed1992

Supraspinal origin of abnormal hindquarter vasoconstrictor tone in spontaneously hypertensive rats.

The object of this study was to determine whether the abnormal hindquarter tone in spontaneously hypertensive rats (SHR) is of spinal origin or not. SHR were implanted with a catheter in the left common carotid and an electromagnetic flow probe around the terminal aorta. About three days after implantation, the spinal cord was transected at Th 1 under ether anesthesia. One hour later, when the rat restored consciousness and the arterial pressure recovered partially to a new plateau level which was significantly higher than that in similarly treated normal rats, ganglionic blockade with hexamethonium did not significantly decrease hindquarter (terminal aortic) resistance, calculated as arterial pressure divided by hindquarter flow. It was concluded that there was no appreciable sympathetic vasoconstrictor tone in the hindquarters of SHR after spinal transection and that the origin of the abnormal tone was at the supraspinal level.

Animals↗
PubMed1992

Sympathetic vasoconstrictor tone induced by pentobarbital anesthesia in hindquarters of rats.

Hindquarter (terminal aortic) blood flow (HQF) and arterial pressure (AP) were observed in rats with an electromagnetic flow probe implanted around the terminal aorta and an arterial indwelling cannula. Hindquarter peripheral resistance (HQR) was calculated by dividing mean AP by HQF. Under pentobarbital anesthesia, HQR was decreased significantly (p less than 0.001) by ganglionic blockade with hexamethonium bromide (C6). Since C6 does not change HQR significantly without anesthesia, we interpret that pentobarbital anesthesia generated a sympathetic vasoconstrictor tone in hindquarter resistance vessels. This was further substantiated by the observation that the increase in HQR on infusion of vasopressin was obscure under pentobarbital anesthesia: Presumably, the increase was offset by reflex inhibition of the hindquarter tone induced by anesthesia. The generation of hindquarter vasoconstrictor tone by pentobarbital was for the most part ascribable to the baroreceptor reflex to compensate for the depressor effect of this anesthetic, because it was greatly diminished after severance of the buffer nerves.

Anesthesia↗
PubMed1992

[Postural changes in finger and toe pulse waves].

Finger and toe pulse waves were simultaneously recorded in medical students and outpatient hypertensive patients. The delay of the rise of toe pulse to that of finger pulse (t) was almost halved in students on postural change from the supine position to the sitting position. This was mainly due to an increase in the pulse wave velocity in the aorta, which was thought to be induced by the increase in hydrostatic pressure in the aorta. In students a marked dicrotic wave was observed in both finger and toe pulse waves. That the interval between the main and dicrotic waves (T) was shorter for finger pulse than toe pulse also seems to be ascribable to the influence of the intraaortic pressure: Pulse was transmitted faster in the systolic phase than in the diastolic phase. The features of pulse waves of hypertensive patients were that (t) was short even in the supine position, and that dicrotic wave was small or absent especially for toe pulse. These differences were considered to be accounted for by the high blood pressure and the structural change of arterial wall in the hypertensive patients.

Aged↗
PubMed1990

Further evidence for abnormal hindquarter tone in spontaneously hypertensive rats.

In spontaneously hypertensive rats (SHR) and normotensive control rats (NCR), hindquarter flow was observed in the conscious state with an electromagnetic flow probe chronically implanted around the terminal aorta. Arterial pressure was recorded with an indwelling catheter in the common carotid. When arginine vasopressin was infused intravenously at a rate of 12.5 ng/(kg.min), the increase in hindquarter resistance, calculated as arterial pressure divided by hindquarter flow, was significantly (p less than 0.005) augmented after ganglionic blockade with hexamethonium in SHR but not in NCR. This is explicable by assuming a tonic sympathetic vasoconstrictor activity in the hindquarters of SHR, reflexive inhibition of which partially offsets vasoconstrictor effect of infused vasopressin.

Animals↗
PubMed1990

Regional distribution of vasoconstrictor tone in acute spinal rats.

Rats, chronically instrumented with an electromagnetic flow probe around the carotid, superior mesenteric, or renal artery, or the terminal aorta as well as having an arterial and venous catheter, were anesthetized with either and submitted to high spinal cord transection. One hour later, when the rats had recovered consciousness and the arterial pressure had recovered partially, hexamethonium was intravenously injected for ganglionic blockade. Peripheral resistance (arterial pressure/regional flow) was decreased significantly by ganglionic blockade in the carotid and renal areas but not in the superior mesenteric and hindquarter (terminal aortic) areas. This suggests the presence of sizable vasoconstrictor tone to resistance vessels in the carotid and renal areas but not in the superior mesenteric and hindquarter areas in the acute spinal rat. This distribution of vasoconstrictor tone is similar to that in intact conscious rats in the resting state and suggests the possibility that the vasoconstrictor tone for resistance vessels in intact rats is also for the most part generated in the spinal cord. Spinal transection decreased blood flow in all the four regions, suggesting a decrease in cardiac output due to dilation of capacitance vessels. It is possible that, in intact rats at rest, the so-called medullary vasomotor center is sending tonic impulses for the most part to capacitance vessels.

Animals↗
PubMed1989

Superior mesenteric sympathetic tone in conscious renovascular hypertensive rats.

Blood flow in the superior mesenteric artery was observed with a chronically implanted electromagnetic flow probe in two-kidney, one-clip renovascular hypertensive rats (2K1C), one-kidney, one-clip renovascular hypertensive rats (1K1C), and normotensive control rats (NCR) in the conscious state. Arterial pressure was recorded with an indwelling catheter. Superior mesenteric resistance was calculated as arterial pressure divided by superior mesenteric flow. In all three groups of rats, superior mesenteric resistance remained almost unchanged when arterial pressure decreased markedly on ganglionic blockade with hexamethonium bromide. However, subsequent injection of a vasopressin antagonist (Manning compound) decreased superior mesenteric resistance significantly in 2K1C but not in 1K1C and NCR. Injection of vasopressin antagonist alone was without effect on arterial pressure and superior mesenteric flow in the three rat groups. Only 2K1C were judged to have appreciable sympathetic tone in resistance vessels of the superior mesenteric area, which was blocked by hexamethonium but compensated for by secondarily secreted vasopressin.

Animals↗
PubMed1989

Blood flow redistribution during spontaneous wheel walk of the rat.

Changes in regional blood flow and arterial pressure in the rat during spontaneous walk in a wheel were observed. An electromagnetic flow probe was implanted around the carotid, superior mesenteric, or renal artery, or the terminal aorta and a catheter for pressure measurement was inserted into the terminal aorta or the common carotid artery. The wheel had a diameter of 35 cm and rotated passively as the rat walked. When hindquarter (terminal aortic) flow increased markedly during wheel walk, carotid flow decreased, superior mesenteric flow decreased or remained unchanged, and renal flow did not change. Arterial pressure remained almost unchanged and heart rate increased an average of about 10%. Semiquantitative considerations indicated that arterial pressure was maintained in the face of the profuse increase in hindquarter flow during wheel walk by an increase in cardiac output rather than shifts of blood flow from other regions.

Animals↗