摘要:

Administration of the γ-aminobutyric acid (GABA) receptor agonist, muscimol, into the third ventricle of anesthetized cats causes decreases in blood pressure and heart rate. To determine the brain areas involved, we administered muscimol into the (1) entire ventricular system, (2) lateral and 3rd ventricles, and (3) 4th ventricle. Muscimol 0.05-16.65 μg administered into the entire ventricular system resulted in dose-dependent decreases in blood pressure, and at the two highest doses of 6.65 and 16.65μg, significant reductions in heart rate. These changes in blood pressure and heart rate were mimicked when muscimol was localized to the 4th ventricle. Pressure and rate changes were not observed when muscimol was restricted to the lateral and 3rd ventricles. To determine the autonomic nerves involved in mediating the responses produced by muscimol administered into the 4th ventricle, bilateral vagotomy and bilateral stellate ganglionectomy were performed. Vagotomy had no effect on the responses evoked by muscimol, whereas stellate ganglionectomy prevented the decrease in heart rate without altering the effect of muscimol on blood pressure. To determine the efficacy of muscimol, the hypotensive and bradycardic effects of this agent were compared to those obtained with clonidine. The depressor response obtained with muscimol was greater than that seen with clonidine. In addition, muscimol produced an additional fall in pressure after a plateau effect had been obtained with clonidine; the converse was not observed. Pretreatment with the GABA receptor antagonist, bicuculline (25-100μg) administered into the fourth ventricle in doses which had no effects on blood pressure or heart rate prevented the effect of muscimol. Treatment with bicuculline after a peak response had been obtained with muscimol restored pressure and rate to normal. These results indicate that activation of GABA receptors in the region of the hindbrain causes hypotension and bradycardia, and that both of these responses are mediated by a reduction in sympathetic outflow to the vasculature and heart.Circ Res 47: 80-88, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Instantaneous femoral artery pressure-flow (P/Q) relations were evaluated in consecu-tive 50-msec intervals of the pulseless flow changes during cardiac arrest in six anesthetized dogs and in two anesthetized dogs with a-adrenergic blockade. In all 245 P/Q graphs obtained under conditions of normal or elevated venous pressure, either with or without a blockade, the pressure-flow relations are linear, and the zero-flow intercept on the pressure axis—reached in less than 3 seconds after the onset of cardiac arrest—is markedly higher than the simultaneous venous pressure. We believe that the zero-flow intercept is the effective downstream pressure to arterial flow and that the reciprocal of the slope of the pressure-flow line indicates the arterial resistance. The elevation of femoral venous pressure raises the effective downstream pressure and the resistance to arterial flow in the same leg. The effective downstream pressure in the contralateral leg is raised also. a-Adrenergic blockade abolishes the reflex change in the contralateral leg, but a change in P/Q relations in the manipulated leg remains. We believe that the.central reflex change could be triggered by stretch receptors in the wall of the small veins transmitted to the arterioles through a-adrenergic receptors. The encroachment on the smallest arterioles by distended small veins and by the rise in interstitial fluid pressure might be the local mechanism by which venous pressure elevation directly changes arterial P/Q relations in the manipulated leg.CircRes 47: 88-98, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the control of renin release and renal hemodynamic function by administering prostaglandin synthetase inhibitors to conscious sodium-depleted dogs with blockade of the adrenergic nervous system induced by bilateral renal denervation and propranolol administration. Indomethacin (10 mg/kg) reduced plasma renin activity (PRA) by 59% from a high sodium-depleted value, but PRA was still 3 times the normal sodium-repleted level. Arterial pressure, Ccr, CPAH, urine flow, and potassium excretion fell strikingly. Similar results were obtained with meclofenamate. When SQ 14,225 was given to another group of conscious, sodium-depleted dogs with adrenergic nervous system blockade, PRA increased from the high sodium-depleted level of 5.7 to 29.3 ng of Angiotensin I (AI)/ml per hour; indomethacin (10 mg/kg) appeared to reduce PRA (0.05 <P< 0.1) but to only 12.1 ng of AI/ ml per hour, which is 17 times the normal level. This high level of PRA after blockade of the adrenergic nervous system and injection of indomethacin suggests that important mechanisms other than norepi-nephrine and renal prostaglandins control renin release; it is proposed that both the renal vascular receptor and the macula densa are involved. The marked decreases in Ccrand CPAHin response to indomethacin emphasize the important role of renal prostaglandins in the control of renal hemodynamic function during sodium depletion.Circ Res 47: 99-107, 1980.

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We measured epicardial S-T segment elevation and blood flow to the subjacent myocar-dium in 8-12 samples from anesthetized, open-chest dogs with coronary occlusion. The response to iv adenosine of blood flow to “ischemic” myocardium/mean aortic pressure depended on which criterion (among criteria I-V) was used to select samples as “ischemic”: I—(S-T ⩾ 2 mV), 125 ± 47% increase(P< 0.08); II—(S-T ⩾ 4 mV), 58 ± 48% increase [not significant (NS)]; III—(myocardial blood flow < 50% of control zone), 6 ± 19% decrease (NS); IV—(flow < 25% of control), 13 ± 16% decrease (NS); V—(< 2% normal zone tissue, labeled by a special microsphere technique), 46 ± 8% decrease(P< 0.03). Peripheral coronary pressure and retrograde flow/mean aortic pressure decreased by 23 and 28%, respectively(P< 0.05), to suggest that criterion V was correct in identifying as ischemic a group of samples in which adenosine decreased collateral flow. The higher apparent control collateral flow values (criteria I-III) and unchanged or increased flow to samples of supposedly ischemic myocardium (criteria I-IV) could be explained by their larger fractions of normal zone tissue mixed in with ischemic tissue: absolute flow change during adenosine = 3.85 (fraction of normal zone tissue in sample)—0.156 ml/min per g,r= 0.94,n =64. We conclude that criteria which fail to exclude contamination of supposedly ischemic samples by normal zone tissue can lead to misinterpretation of the direction and/or magnitude of changes in collateral flow to ischemic myocardium during vasodilation. Changes in flow to samples containing mixtures of normal and ischemic tissue may not be relevant to attempts to salvage truly ischemic myocardium by increasing actual collateral myocardial blood flow.Circ Res 47:108-116,1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

This paper presents a multipole analysis of the QRS complex of the normal magnetocar-diogram (MCG) of six normal subjects. The multipole strengths up to the octupole term were determined from the measured distribution of the z-component of the cardiac magnetic field (the component perpendicular to the frontal plane). This equivalent magnetic multipole generator was found to represent the cardiac magnetic field with a minimum error of <10%. The dipolar term of the expansion was found to represent the field distribution with reasonable accuracy early during ventricular activation, whereas late during activation, the higher multipole terms were clearly more significant.CircRes 47:117-130, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The purpose of this study was to examine the ultrastructure of the sarcolemma in the normal and severely anoxic rabbit heart with the technique of freeze-fracture. Severe anoxia and subsequent reoxygenation cause a significant decrease (31%) in intramembranous particles (IMP) in the P face of the membrane and a 25% decrease in the E face. P face IMP's are severely aggregated. The decrease in density and the redistribution of IMP's indicate a severely altered Upoprotein structure of the sarcolemma. In addition, the necks of caveolae open and the caveolae become flattened in the plane of the membrane. With reoxygenation, many rupture. Spherical projections of cytoplasmic vesicles appear in the membrane (possibly of sarcoplasmic reticulum or lysosomal origin) and also can be seen to rupture after reoxygenation. When glucose is present in the perfusate, it affords some protec-tion against these structural defects. We propose that the fragmentation or holes in the sarco-lemma reported in severe anoxia are directly related to the structural changes reported in this study.CircRes 47:131-143, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID