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Biomedical subjects

N Hasebe

Publications and source records attributed to N Hasebe.

At least 55 records · Page 3Linked to original sources
PubMed1992

Mechanisms of subendocardial dysfunction in response to exercise in dogs with severe left ventricular hypertrophy.

The effects of exercise on regional myocardial blood flow and function were examined in the presence and absence of beta-adrenergic receptor blockade in 10 adult conscious dogs with severe left ventricular (LV) hypertrophy induced by aortic banding in puppies, which increased the LV weight/body weight ratio by 87%. Exercise at the most intense level studied increased LV systolic (+87 +/- 8 mm Hg) and end-diastolic (+28 +/- 5 mm Hg) pressures, systolic (+85 +/- 12 g/cm2) and diastolic (+49 +/- 11 g/cm2) wall stresses, and subepicardial wall thickening (+0.18 +/- 0.05 mm) but reduced subendocardial wall thickening (-0.45 +/- 0.12 mm) and full wall thickening (-0.42 +/- 0.13 mm). This was associated with a fall in the subendocardial/subepicardial (endo/epi) blood flow ratio to 0.87 +/- 0.06 from 1.24 +/- 0.08. Subendocardial dysfunction persisted during recovery, at a time when transmural blood flow distribution returned to baseline, suggesting myocardial stunning. At the least intense level of exercise studied, the endo/epi blood flow ratio did not fall (1.27 +/- 0.14), but increases in heart rate (+73 +/- 8 beats per minute) and LV systolic (+35 +/- 8 g/cm2) and diastolic (+27 +/- 3 g/cm2) wall stresses were observed, and subendocardial wall thickening fell significantly (-0.21 +/- 0.08 mm, p less than 0.05). With anticipation of exercise, subendocardial wall thickening was not changed. However, subendocardial dysfunction was even evident after 10 beats, i.e., the first 3 seconds of exercise, at a time when LV pressures and stresses had not increased. After beta-adrenergic receptor blockade with propranolol, the most intense level of exercise was associated with lesser increases in systolic and diastolic LV wall stresses, heart rate, and LV dP/dt, and the endo/epi blood flow ratio was no longer reduced below unity (1.17 +/- 0.09). In addition, there were no decreases in subendocardial or full wall thickening, and myocardial stunning was no longer observed. Thus, the subendocardial hypoperfusion and depression in subendocardial wall thickening observed during exercise in dogs with LV hypertrophy was prevented by pretreatment with beta-adrenergic receptor blockade. Furthermore, the subendocardial dysfunction occurred rapidly, before alterations in LV systolic or diastolic wall stress or an alteration in the endo/epi blood flow ratio.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

Mechanisms of alpha 1-adrenergic vascular desensitization in conscious dogs.

To investigate the mechanisms of alpha 1-adrenergic vascular desensitization, osmotic minipumps containing either saline (n = 9) or amidephrine mesylate (AMD) (n = 9), a selective alpha 1-adrenergic receptor agonist, were implanted subcutaneously in dogs with chronically implanted arterial and right atrial pressure catheters and aortic flow probes. After chronic alpha 1-adrenergic receptor stimulation, significant physiological desensitization to acute AMD challenges was observed, i.e., pressor and vasoconstrictor responses to the alpha 1-adrenergic agonist were significantly depressed (p < 0.01) compared with responses in the same dogs studied in the conscious state before pump implantation. However, physiological desensitization to acute challenges of the neurotransmitter norepinephrine (NE) (0.1 micrograms/kg per minute) in the presence of beta-adrenergic receptor blockade was not observed for either mean arterial pressure (MAP) (30 +/- 7 versus 28 +/- 5 mm Hg) or total peripheral resistance (TPR) (29.8 +/- 4.9 versus 28.9 +/- 7.3 mm Hg/l per minute). In the presence of beta-adrenergic receptor plus ganglionic blockade after AMD pump implantation, physiological desensitization to NE was unmasked since the control responses to NE (0.1 micrograms/kg per minute) before the AMD pumps were now greater (p < 0.01) than after chronic AMD administration for both MAP (66 +/- 5 versus 32 +/- 2 mm Hg) and TPR (42.6 +/- 10.3 versus 23.9 +/- 4.4 mm Hg/l per minute). In the presence of beta-adrenergic receptor, ganglionic, plus NE-uptake blockade after AMD pump implantation, desensitization was even more apparent, since NE (0.1 micrograms/kg per minute) induced even greater differences in MAP (33 +/- 5 versus 109 +/- 6 mm Hg) and TPR (28.1 +/- 1.8 versus 111.8 +/- 14.7 mm Hg/l per minute). The maximal force of contraction induced by NE in the presence or absence of endothelium was significantly decreased (p < 0.05) in vitro in mesenteric artery rings from AMD pump dogs compared with saline control dogs. Furthermore, alpha 1-adrenergic receptor density, as determined by [3H]prazosin binding in membrane preparations from vessels in the mesentery, was decreased (8.2 +/- 1.0 versus 18.4 +/- 1.4 fmol/mg protein, p < 0.001) without any change in Kd in the AMD pump dogs compared with the saline pump dogs.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Agonists↗
PubMed1992

The effect of intermittent coronary sinus occlusion on coronary sinus pressure dynamics and coronary arterial flow.

The effect of intermittent coronary sinus occlusion (ICSO) with a balloon-tipped catheter on coronary arterial flow and coronary sinus pressure (CSP) dynamics were studied in open-chest dogs. During coronary sinus occlusion (CSO), CSP gradually rose and finally reached a plateau, while left coronary arterial mean flow velocities decreased. After the release of CSO, CSP immediately returned to baseline values, and the flow velocities correspondingly increased over the baseline values (hyperemic response). The decrease in ratios of flow velocities during CSO were unrelated to the duration of CSO, whereas hyperemic responses were positively correlated with the CSO duration. In the repetitive application of CSO (ICSO), inadequately short duration of release period decreased the net volume of coronary arterial flow significantly. Moreover, hyperemic responses were abolished by maximal coronary vasodilation with intravenous adenosine, augmented by combination with coronary sinus retroperfusion and reduced by coronary arterial ischemia. These findings indicate the presence of a compensatory regulating mechanism in the coronary circulation during ICSO. We should attach much importance to this mechanism for the effectiveness of ICSO. To be accurate, the changes in coronary arterial flow as well as CSP dynamics should be considered when choosing adequate occlusion-release intervals of ICSO.

Adenosine↗
PubMed1992

Site of hypoxic pulmonary vasoconstriction in pulsatile perfused canine lung lobes.

To elucidate the site of hypoxic pulmonary vasoconstriction (HPV) in the dynamic lung, we studied the effect of alveolar hypoxia (0 approximately 4% O2) on excised canine lung lobes with pulsatile perfusion from artery to vein (antegrade perfusion: AP) or vein to artery (retrograde perfusion: RP), and compared responses to hypoxia with those to serotonin and histamine. In our preparation, increases in the pulmonary vascular resistance (R) resulted in a wide range of decreases in the flow wave amplitude at the lobar inflow site (FA). These decreases in FA reflected reductions in the compliance of the vasculature proximal to the main site of resistance. The FA/R ratios of serotonin were 2.29 in AP and 0.24 in RP indicating the predominant arterial constriction, those of histamine were 0.07 in AP and 1.24 in RP indicating the selective venous constriction. In contrast, the responses to hypoxia were 0.38 in AP and 0.42 in RP. These results suggest that HPV occurs not only on the arterial side but on the venous side in the dynamic lung, and the main site of HPV is located in the peripheral pulmonary vasculature, between muscular arteries and veins which are constricted by serotonin and histamine.

Animals↗
PubMed1991

Transient pulsus alternans induced by isosorbide dinitrate: echocardiographic and hemodynamic evidence of reduced venous return--a case report.

Transient pulsus alternans was induced by isosorbide dinitrate (ISDN) in a patient with postmyocarditis congestive heart failure under diuretic therapy. The severity and duration of pulsus alternans depended on the dose of ISDN. According to the echocardiographic and hemodynamic examinations, the superimposed preload reduction caused by ISDN combined with decreased blood volume owing to diuretic therapy most likely contributed to the development of pulsus alternans.

Adult↗
PubMed1991

Experimental studies on the mechanism of reversible pressor response in pulmonary microembolism in the dog.

In the present study, we examined the difference in hemodynamic responses between groups of canine lung lobes which received latex particles of different sizes (50 microns and 300 microns in diameter). We also assayed prostaglandin I2 (PGI2) and thromboxane A2 in the effluent blood of the lobes. Reversible pressor response was clear in embolization by 50 micron particles whereas it was not in that by 300 microns. No difference in PGI2 between two embolizations was seen. We conclude that a local contractile mechanism exists in the pulmonary arterial wall of about 50 microns in diameter whereas participation of the same mechanism is minimal in 300 microns, and that this difference cannot be explained from the change in PGI2.

Animals↗
PubMed1991

[Acute and chronic effects of vasodilators in a case of chronic recurrent pulmonary embolism].

A 65-year-old man was admitted to our hospital because of shortness of breath on exertion. As the results of examinations including pulmonary angiography, pulmonary perfusion scan and pulmonary ventilation scan, we diagnosed the case as chronic recurrent pulmonary embolism. Although the patient received thrombolytic therapy by a tissue plasminogen activator (t-PA), there was no noticeable improvement. However, oxygen and vasodilator therapy had marked effective on the hemodynamics. In chronic pulmonary embolism, vasodilators are generally not considered to be effective for improvement of hemodynamics. However, if the acute effects of vasodilators were confirmed, we should try to administer them while paying attention to possible adverse effects.

Aged↗
PubMed1984

[Studies on experimental miliary pulmonary embolism with special reference to the mechanism of initial elevation in pulmonary arterial pressure. Significance of myogenic factor].

It is generally accepted that a vasoconstrictive mechanism participates in transient pulmonary hypertension observed in miliary embolism, in addition to the mechanical blockade of pulmonary vascular tree. For the explanation, some neural and humoral factors, especially those released from adhesion-aggregation process of platelets, have been emphasized. In our previous reports, we have stressed the importance of some local vascular factors in this vasoconstrictive mechanism. Present study was undertaken to elucidate those local factors extensively. Miliary pulmonary embolism in the isolated perfused canine lung lobe was produced by injecting lycopodium spore suspension in saline, in which hepalinized autologous blood and three different artificial solutions were employed as the perfusate. Although each perfusate made a slight difference in perfusing condition, probably owing to its viscosity and oncotic pressure, all preparations showed definite response to embolization. After each embolization, pulmonary inflow pressure was raised rapidly and reached to a maximal level after 30-60 sec., then fell gradually. Repeated embolization at an interval of 6 min., before pulmonary inflow pressure returned to the control level, produced a cumulative effect. There was no significant difference between perfusations with autologous blood and artificial perfusates at the first and the second embolizations, but it was more distinct in those with autologous blood at the third and the fourth embolizations. The results have showed that the initial pulmonary pressure elevation in miliary embolism is observed apparently even under the bloodless and denervated conditions. It was concluded that "Myogenic Factor" (existing locally in the pulmonary arterial and arteriolar endothelium-smooth muscle) must play a very important role as to initial elevation in pulmonary arterial pressure induced by miliary embolizations. Further advanced studies on the myogenic factor is expected.

Animals↗