Biomedical subjects

H Matsuguchi

Publications and source records attributed to H Matsuguchi.

23 records · Page 2Linked to original sources

PubMedDate not supplied

The effect of graded coronary stenosis on myocardial blood flow and left ventricular wall motion.

The effect of graded coronary stenosis on resting regional myocardial flow and left ventricular (LV) wall motion was studied in 18 anesthetized dogs. The left circumflex coronaary artery (LC) was constricted. The degree of LC stenosis and the changes in LV wall motion were determined by cineangiography of the coronary artery and LV. Regional myocardial flow was determined by tracer microspheres (TM), labeled with two different isotopes, Sr85, Sc46 or Ce141. The first TM1 and the second TM2 were infused after LC stenosis, and during a temporary complete LC occlusion respectively. Resting flow in areas with 70% stenosis was reduced, with a greater reduction of subendocardium and posterior papillary muscle, but minimum impairment of LV wall motion. No ST elevation was found. Animals with 80--90% stenosis showed a marked reduction of flow and wall motion, a significant ST-elevation and a delayed antegrade run-off in coronary arteriography.

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PubMedDate not supplied

Effects of collateral circulation on regional myocardial blood flow and left ventricular wall motion (A preliminary note).

The effect of collateral circulation on regional myocardial flow and wall motion of left ventricle was studied on 5 anesthetized dogs with a surgically implanted constrictor on the left circumflex coronary artery (LC). The grade of LC stenosis and wall motion of left ventricle (LV) were determined by cineangiography of the coronary artery and LV at the period of acute and chronic occlusion. Regional myocardial flow was determined by tracer microspheres (TM), labeled with four different isotopes, Sr85, Cr51, Sc46, Ce141. The first TM1 was infused after LC stenosis, TM2 during a temporary complete LC occlusion at the period of acute occlusion; TM3 and TM4 in a similar way 3 to 4 weeks after the acute LC stenosis. Three to four weeks after LC stenosis, i.e. chronic period of occlusion, the degree of LC stenosis progressed from 70--80% to 100% occlusion, but collateral flow and collateral vessels to the ischemic LC area were increased together with an improvement of wall motion of the ischemic LC area. The results may support the idea that collaterals may be an effective compensatory mechanism for ischemia. In contrast to an increase of collateral flow to the ischemic LV free wall in all five dogs, an increase to the posterior papillary muscle was found only in two out of five dogs.

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PubMedDate not supplied

Does vasopressin contribute to salt-induced hypertension in the Dahl strain?

A humoral factor has been implicated in Dahl salt-sensitive genetically hypertensive rats. The goal of this study was to evaluate the pressor role of vasopressin (AVP) in Dahl rats. Salt-sensitive (S) and resistant (R) rats were fed either high (8%) or low (.04%) NaCl diets for 6 to 8 weeks. Blood pressure was elevated in S rats fed high salt diets (p less than 0.05). Plasma AVP increased with high salt diet in both groups (p less than 0.05), but was higher in S than R rats (2.0 +/- 0.3 and 1.3 +/- 0.2 microU/ml respectively, mean +/- SE, p less than 0.05). With low salt diet, plasma AVP did not differ significantly in S and R rats (1.0 +/- 0.2 and 0.7 +/- 0.2 microU/ml respectively). Pressor responses to intravenous injection of AVP were greater in S than R rats (p less than 0.05), but this difference was also observed with pressor responses to norepinephrine (S greater than R, p less than 0.05); there was no difference in pressor responses to AVP in S rats fed high vs low salt diet. Injection of 50 micrograms of d(CH2)5 VDAVP, which selectively inhibits vasoconstrictor effects of AVP, failed to lower blood pressure in S and R rats fed high or low salt diets despite the fact that this dose decreased pressor responses to 8 microU of AVP more than 90%. Although plasma AVP and vasopressor responses to AVP and NE are slightly elevated in S rats fed high salt, results with d(CH2)5 VDAVP suggest that vasoconstrictor effects of AVP do not play an important role in the maintenance of hypertension in Dahl S rats.

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PubMedDate not supplied

Abnormal baroreflex control of heart rate in prehypertensive and hypertensive Dahl genetically salt-sensitive rats.

This study tested the hypothesis that in the Dahl model of genetic hypertension abnormal baroreflex function may precede and contribute to the development of hypertension. Sensitivity of baroreflex control of heart rate was assessed in conscious sensitive (S) and resistant (R) Dahl rats fed a high or low salt diet. Sensitivity of baroreflex control of heart rate was lower in S rats fed low salt although arterial pressure was not different from that of R rats. Hypertensive S rats showed resetting of baroreflexes to the higher pressure level without any further change in sensitivity. Pressor responses to phenylephrine were augmented in both prehypertensive and hypertensive S rats compared to R rats. Ganglionic blockade abolished this difference. In hypertensive S rats, ganglionic blockade decreased arterial pressure to levels not different than similarly treated R rats, indicating that neurogenic mechanisms contribute importantly to the early stages of hypertension in the Dahl model. These studies have identified impaired baroreflex function in prehypertensive and hypertensive Dahl S rats. This defect augments responses to pressor stimuli and may contribute to the development of salt-induced hypertension in the Dahl strain.

Animals↗

PubMedDate not supplied

Effect of graded coronary stenosis on regional myocardial blood flow and left ventricular function.

Dogs with 70% stenosis of the left circumflex coronary artery showed a reduction of myocardial blood flow with a minimal impairment of left ventricular wall motion. Eighty to ninety percent stenosis produced a marked reduction of flow and wall motion, and ST elevation close to 100% occlusion, but delayed antegrade run-off was found. The effectiveness of collaterals to protect against left ventricular dysfunction was supported.

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