Mechanism of blood pressure elevation during angiotensin infusion

The mechanism of increased preload and its contribution to the rise in blood pressure during intravenous angiotensin infusion were studied in anesthetized dogs. In open-chest dogs angiotensin increased mean aortic blood pressure by 58±12 mmHg. Left ventricular end-diastolic dimension, measured as myocardial chord length (MCL) by ultrasonic technique, increased by 7±1 %. By inflating a balloon in the inferior vena cava, end-diastolic MCL was reduced to control value and the rise in mean aortic blood pressure was almost halved to 32±10 mmHg above control value. A similar preload effect was recorded in closed-chest dogs using end-diastolic left ventricular pressure as an estimate of left ventricular volume. During angiotensin infusion to the upper body only, end-diastolic MCL did not increase. When redistribution of the splanchnic blood volume was prevented, the effect of angiotensin on end-diastolic MCL was reduced to 1/3. Angiotensin reduced liver but not splenic dimension measured by ultrasonic technique. We conclude that about half of the rise in blood pressure during angiotensin infusion is due to increased end-diastolic volume caused by blood redistribution. About 2/3 of this increase in preload is due to redistribution from the splanchnic bed, mainly from the liver.     

Determinants of pulmonary blood volume. Effects of acute changes in pulmonary vascular pressures and flow

To examine the effects of pulmonary vascular pressures and flow on pulmonary blood volume (PBV), experiments were performed at constant heart rate and zone 3 conditions (mean left atrial pressure (LAP) above airway pressure) in six anesthetized, open-chest dogs. PBV was calculated as the product of electromagnetic aortic flow and pulmonary mean transit time for ascorbate, obtained without blood withdrawal by polarographic recording of aortic ascorbate changes. In three series of experiments LAP was raised similarly in three steps, from 4.5 to 14.8 mmHg: by mitral constriction which reduced pulmonary blood flow, by blood volume expansion which more than doubled pulmonary blood flow, or by a combination of the two procedures which kept pulmonary blood flow constant. In all three series, LAP and mean pulmonary arterial pressure (PAP) rose in proportion, but PBV was better correlated to PAP (r=0.87±0.02) than to LAP (r=0.66±0.09). These experiments suggest that PAP is the most important factor in determining PBV under zone 3 conditions, whether PAP is raised by increasing pulmonary blood flow or by mitral constriction.     

Hypothalamic laterality in regulating gonadotropic function: unilateral hypothalamic lesion and ovarian compensatory hypertrophy

Regardless of the side of hemiovariectomy, unilateral lesion placed in the right-side medial anterior hypothalamus suppressed ovarian compensatory hypertrophy, but the lesion made in the left side failed to suppress it. This suggests the presence of a hypothalamic laterality in regulating gonadotropin secretion.     

Positive correlation between aortic valve pressure gradient and mitochondrial respiratory chain capacity in hypertrophied human left ventricle

Summary The effect of chronic left ventricular pressure overload on the activities of mitochondrial respiratory chain enzymes was investigated in myocardial biopsies from the left ventricular apex of 13 patients undergoing aortic valve replacement for aortic valve stenosis. Transvalvular pressure gradients measured by left-sided heart catheterization ranged from 52 to 100 mmHg. The specific activity of mitochondrial respiratory chain enzyme complexes I + III (antimycin A sensitive NADH cytochrome c oxidoreductase) and the myocardial concentrations of coenzyme Q₁₀ (CoQ₁₀) increased significantly (P < 0.05) with increasing aortic valve pressure gradient. In contrast, the specific activities of complex IV (cytochrome c oxidase), succinate dehydrogenase, and citrate synthase, a mitochondrial matrix enzyme, showed no significant correlation with the pressure gradient. Since (CoQ₁₀) is the rate-limiting compound of the activity of complexes 1+111 but not of cytochrome c oxidase, succinate dehydrogenase, or citrate synthase, these data suggest that the increase in the activity of complexes I+III is due to the increase in (CoQ₁₀) content.Abbreviations CoQ coenzyme Q - CoQ₉ coenzyme Q₉ - CoQ₁₀ coenzyme Q₁₀ - SDH succinate dehydrogenase - NCP noncollagen protein     

Changes in isometric force- and relaxation-time,electromyographic and muscle fibre characteristics of human skeletal muscle during strength training and detraining

HÄKKINEN, K., ALÉN, M. & KOMI, P.V. 1985. Changes in isometric force- and relaxation-time, electromyographic and muscle fibre characteristics of human skeletal muscle during strength training and detraining. Acta Physiol Scand 125, 573–585. Received 26 January 1985, accepted 9 May 1985. ISSN 0001–6772. Department of Biology of Physical Activity and Department of Health Sciences, University of Jyväskylä, Jyväskylä, Finland. Eleven male subjects (20–32 years) accustomed to strength training went through progressive, high-load strength training for 24 weeks with intensities ranging variably between 70 and 120% during each month. This training was also followed by a 12-week detraining period. An increase of 26.8% (P < 0.001) in maximal isometric strength took place during the training. The increase in strength correlated (P < 0.05) with significant (P < 0.05–0.01) increases in the neural activation (IEMG) of the leg extensor muscles during the most intensive training months. During the lower-intensity training, maximum IEMG decreased (P < 0.05). Enlargements of muscle-fibre areas, especially of fast-twitch type (P < 0.001), took place during the first 12 weeks of training. No hypertrophic changes were noted during the latter half of training. After initial improvements (P < 0.05) no changes or even slight worsening were noted in selected force-time parameters during later strength training. During detraining a great (P < 0.01) decrease in maximal strength was correlated (P < 0.05) with the decrease (P < 0.05) in the maximum IEMGs of the leg extensors. This period resulted also in decreases (P < 0.05) of the mean muscle-fibre areas of both fibre types. It was concluded that improvement in strength may be accounted for by neural factors during the course of very intensive strength training. Selective training-induced hypertrophy also contributed to strength development but muscle hypertrophy may have some limitations during long-lasting strength training, especially in highly trained subjects.     

Interstitial microfibrils in the myocardium of patients with rheumatic and congenital cardiac defects

Electron-microscopic investigation of biopsy specimens of heart tissue from patients with rheumatic and congenital cardiac defects revealed aperiodic microfibrils, the number of which was proportional to the fibrosis of the myocardium, on the basal membranes of the capillaries and muscle fibers and also in the lumen of the T-tubules and their vacuolar expansions. If signs of rheumatic carditis are present the myofibrils are less regular and their number somewhat greater. Microfibrils are rutheniophilic and argyrophilic and consist of elementary fibrils of reticular fibers. Their hyperplasia is the ultrastructural equivalent of the reticular skeleton of the hypertrophied myocardium in patients with cardiac defects.Institute of Rheumatism, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. I. Strukov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 8, pp. 1011–1014, August, 1976.     

Cardiovascular ‘reactivity’ to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats

Cardiovascular ‘reactivity’ to graded splanchnic nerve stimulations was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/r₁ of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.     

左肝管全程剖开胆肠吻合术的应用解剖学研究

左肝管全程剖开手术,必须熟悉左肝管与邻近血管的局部解剖关系.为此我们用 ABS 丙酮溶液灌注塑型了6具新鲜成人尸肝脏,解剖40例(成人30,儿童10)肝脏标本,测量了左肝管长度和管径,左肝管与肝总管夹角。全程剖开左肝管与右肝管,并观察左肝管与右肝管、左肝动脉、门静脉左干和肝圆韧带的关系,提出了右肝管全程剖开手术方法和注意事项。     

伊贝沙坦对血管紧张素Ⅱ所致心肌细胞蛋白质合成和肌球蛋白重链表达的影响

目的 观察伊贝沙坦对血管紧张素Ⅱ（AngⅡ）所致心肌细胞中蛋白质合成速率及肌球蛋白重链（MHC）基因表达改变的影响.方法 以AngⅡ及伊贝沙坦分别或同时作用于培养的细胞.采用放射性同位素[^3H]-leu掺入法检测培养心肌细胞蛋白质合成速率.应用荧光定量PCR方法检测心肌细胞心房利钠肽因子（ANF）以及α-MHC、β-MHC的表达.结果 AngⅡ处理使心肌细胞中[^3H]-Leu掺人增加（P＜0.05）,同时ANF mRNA的表达明显高于正常（P＜0.05）;α-MHC mRNA的表达显著低于正常（P＜0.05）,而β-MHC mRNA的表达显著高于正常（P＜0.05）,α-MHC/β-MHC的比值下降（P＜0.05）.当伊贝沙坦与AngⅡ共同作用于培养的心肌细胞时,与AngⅡ组比较,[^3H]-Leu的掺入明显下降（P＜0.05）,与正常组比无统计学意义（P＞0.05）;同时ANF的表达下降,与正常组比无统计学意义（P＞0.05）;心肌细胞中α-MHC的表达明显增高（P＜0.05）,而β-MHCmRNA的表达显著降低（P＜0.05）,α-MHC/β-MHC的比值上升（P＜0.05）.结论 伊贝沙坦能抑制AngⅡ所致的心肌细胞肥大和细胞中α-MHC向β-MHC表达的转换.