Reflex inhibition of sympathetic activity during volume load in awake normotensive and spontaneously hypertensive rats

The reflex inhibition of the sympathetic activity in the splanchnic nerves was recorded upon volume expansion with blood in awake spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto rats (WKR) at an age of 16–20 weeks. At 10% blood volume expansion SHR showed a significantly greater nerve inhibition (43 %) in comparison with WKR (33 %). This augmented reflex response was not caused by the arterial baroreceptors, because the sensitivity of the arterial baroreceptor reflex arch, if anything, tended to be lower in SHR and the increase in arterial blood pressure upon volume load was also lower in SHR. It is suggested that the reason for this increased reflex inhibition in SHR is an augmented low pressure receptor response. The mechanism behind this is discussed. The most likely explanation is a decreased distensibility of the venous system, the systemic andlor the pulmonary veins.     

Renal nerve activity and exaggerated natriuresis in conscious spontaneously hypertensive rats

Exaggerated natriuresis upon volume loading occurs in both human and animal hypertension and is mainly due to suppressed tubular reabsorption. To explore whether altered renal sympathetic activity contributes to this response, conscious male spontaneously hypertensive rats (SHR) were exposed to isotonic saline loading in comparison with normotensive male Wistar Kyoto rats (WKR). After a 60 min control hydropenic period, during which mean arterial pressure, heart rate, renal sympathetic nerve activity and urinary sodium excretion were followed, a 60 min period of intravenous volume expansion with isotonic saline (0.2 ml/minx 100 g b. w.) was started followed by a 60 min hydropenic recovery period. Already during the control period sodium excretion was significantly higher in SHR. During the volume load and subsequent recovery period a clearly exaggerated natriuresis occurred in SHR compared with WKR. Further, volume loading reduced renal sympathetic nerve activity in all animals, but significantly more in SHR. Moreover, volume loading reduced mean arterial pressure and heart rate in both groups. It is suggested that the accentuated reflex inhibition of renal sympathetic activity in SHR upon volume loading emanates from cardiac mechanoreceptors and partly explains the exaggerated natriuresis in SHR. This augmented ‘volume’ reflex response is probably due to reduced systemic venous compliance in SHR with a consequently increased central filling and cardiac receptor activation.     

Estimation of central venous pressure by measurement of proximal axillary venous pressure using a "half-way" catheter

The pressure in the proximal axillary vein (AVP) was compared with central venous pressure (CVP) in eight patients during and after elective abdominal surgery. Both pressures were recorded from soft, elastic, polyurethane catheters inserted in the basilic or cephalic veins ("half-way" catheters), punctured at the fossa cubiti (AVP), and via the right jugular vein (CVP). The AVP and CVP were recorded simultaneously using hydrostatic, conventional disposable venous pressure measurement sets. The measurements were performed during intermittent positive pressure ventilation with positive end-expiratory pressure from 0 to 7.5 cmH2O (0-0.74 kPa), as well as during spontaneous breathing. During both controlled and spontaneous respiration, small mean differences (0.2-1.0 cmH2O) (0.02-0.1 kPa), and a highly significant (P less than 0.001) positive correlation between CVP- and AVP-values were found. An increase of 1 cmH2O (0.10 kPa) in the CVP was associated with an increment of practically identical order (0.99-1.04 cmH2O) (0.10-0.11 kPa) in the AVP. The results suggest that monitoring of the AVP by a basilic "half-way" catheter produces diagnostic information similar to that from the measurement of the CVP from subclavian, external or internal jugular, as well as "long-way" brachial catheter, with no risk of the major mechanical complications which accompany the use of the latter catheters.     

Thoracic epidural anaesthesia in patients with unstable angina pectoris

The effect of high thoracic epidural anaesthesia with intermittentepidural bolus injections of bupivacaine (2.5 or 5 mg ml^-1)was studied in 28 patients with unstable angina pectoris. Themajority of the patients had a history of previous acute myocardialinfarction(s) and/or angina pectoris and severe coronary arterydisease. All patients were treated wth nitroglycerin infusionfor gt;24 h and were included in the study if they had chestpain, not caused by acute myocardial infarction, at bed restor recurrent anginal pain at rest < 2 days after infarction.4.4 ± 0.3 ml of bupivacaine induced a blockade of theupper seven sympathetic segments ( Th_1-7) for 98 ± 9min.Heart rate decreased significantly from 70 ± 3 to 64± 3 beats min^-1 while blood pressure was unaffected bythoracic epidural anaesthesia. In 27 patients (96%) the anaesthesiainduced complete analgesia. Nitroglycerin infusion was discontinueddefinitely within 3 h in 26 patients (93%) and pain was thereaftercontrolled by means of thoracic epidural anaesthesia as thesole treatment in 23 patients (82%) and as the major treatmentin 25 patients (89%). Twenty-one patients (75%) were fully mobilizedand stabilized. Treatment with thoracic epidural anaesthesialasted for 6.0 ± 1.1 days. The number of daily epiduralinjections decreased significantly with time from 2.7 ±0.3the first day to 0.9 ± 0.3 the fourth day (P>0.01,n = 19). Two patients developed acute myocardial infarctionduring the anaesthesia treatment period, and one of these patientsdied. Exercise stress testing was performed on eight patients threeto five days after the start of thoracic epidural anaesthesia.At a comparable workload, ST-segment depression was significantly(P>0.05) less pronounced during anaesthesia ( – 0.6± 0.1 mm) compared with control ( – 1.3 ±0.2mm). The respective heart rate values were 95 ± 7and 107 ± 7 beats min ^-1 (P > 0.05), while systolicor diastolic blood pressure did not differ between the two conditions. We conclude that blockade of cardiac sympathetic afferents andefferents by means of thoracic epidural anaesthesia can effectivelytreat pain and stabilize patients with unstable angina pectorisrefractory to medical treatment. Furthermore, thoracic epiduralanaesthesia attenuates stress-induced myocardial ischaemia;thus, it may be an efficient supplementary treatment for thecontrol of pain and for stabilizing patients with unstable anginapectoris during diagnostic procedures and prior to coronarysurgery or angioplasty.     

Norepinephrine causes a pressure‐dependent plasma volume decrease in clinical vasodilatory shock

Background: Recent experimental studies have shown that a norepinephrine‐induced increase in blood pressure induces a loss of plasma volume, particularly under increased microvascular permeability. We studied the effects of norepinephrine‐induced variations in the mean arterial pressure (MAP) on plasma volume changes and systemic haemodynamics in patients with vasodilatory shock. Methods: Twenty‐one mechanically ventilated patients who required norepinephrine to maintain MAP ≥70 mmHg because of septic/postcardiotomy vasodilatory shock were included. The norepinephrine dose was randomly titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, haematocrit, arterial and mixed venous oxygen content and urine flow urine were measured. Changes in the plasma volume were calculated as 100 × (Hct_pre/Hct_post?1)/ (1?Hct_pre), where Hct_pre and Hct_post are haematocrits before and after intervention. Results: Norepinephrine doses to obtain target MAPs of 60, 75 and 90 mmHg were 0.20±0.18, 0.29±0.18 and 0.42±0.31 μg/kg/min, respectively. From 60 to 90 mmHg, increases in the cardiac index (15%), systemic oxygen delivery index (25%), central venous pressure (CVP) (20%) and pulmonary artery occlusion pressure (33%) were seen, while the intrapulmonary shunt fraction was unaffected by norepinehrine. Plasma volume decreased by 6.5% and 9.4% (P<0.0001) when blood pressure was increased from 60 to 75 and 90 mmHg, respectively. MAP (P<0.02) independently predicted the decrease in plasma volume with norepinephrine but not CVP (P=0.19), cardiac index (P=0.73), norepinephrine dose (P=0.58) or urine flow (P=0.64). Conclusions: Norepinephrine causes a pressure‐dependent decrease in the plasma volume in patients with vasodilatory shock most likely caused by transcapillary fluid extravasation.     

Effects of halothane and isoflurane on left ventricular diastolic function during surgical stress in patients with coronary artery disease

Background: The effects of inhalation anesthetics on left ventricular (LV) systolic function are well documented, while the effects of these agents on LV diastolic function have mainly been evaluated in animal studies, with conflicting results.
Methods: We investigated the effects of halothane and isoflurane, when used to control the stress response to sternotomy in 33 patients with coronary artery disease (CAD). LV early diastolic relaxation and end-diastolic stiffness were evaluated from mitral Doppler flow profiles, transesophageal two-dimensional echocardiography, and central hemodynamic measurements. Measurements were performed a) after induction of anesthesia, b) after volume loading, c) prior to surgery and d) during surgery, 10 min after introduction of the inhalation anesthetic. The effects of the anesthetics on Doppler indices reflecting early diastolic relaxation, and on the left ventricular end-diastolic pressure-area (LVED P/A) relationship, were studied.
Results: When data obtained during surgical stress were compared to the control situation, we found an increase in the LV filling pressures in both groups, while only the isoflurane group showed an increase in heart rate. An increase in end-systolic LV area and decreased fractional area change was present in the halothane group, while an increase in LV end-diastolic area, and similar changes in the mitral Doppler indices (decreases of deceleration rate and time of early diastolic filling), indicating an impairment of early diastolic relaxation, was present in both groups. Isoflurane induced a displacement of the LVED P/A relationship leftwards from the baseline LVED P/A curve.
Conclusion: Both halothane and isoflurane impair early diastolic relaxation in patients with CAD, when used to control intraoperative surgical stress. In contrast to halothane, isoflurane induced a change in the LVED P/A relationship, suggestive of an increased LVED stiffness.     

Coarctation of the Abdominal Aorta in Elderly Patients

ABSTRACT Coarctation of the abdominal aorta as a congenital disease is infrequent, the diagnosis mostly being made at an early age because of renovascular hypertension. Patients who reach the age of 40 more often tend to have the problems located distally to the renal arteries. A 66-year-old female is described, who developed an aortic occlusion, renovascular hypertension and uremia. She was cured with a bifurcation graft and a patch angioplasty of a stenotic renal artery and nephrectomy of the contralateral kidney with an occluded artery without refilling. A literature survey is made of patients older than 40 years.     

Interaction between “mental stress” and baroreceptor reflexes concerning effects on heart rate,mean arterial pressure and renal sympathetic activity in conscious spontaneously hypertensive rats

Spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared concerning the interactions between cortico-hypothalamic alerting responses and baroreflex influences on neurogenic cardiovascular control. For this purpose mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were continuously recorded during night time in conscious, otherwise undisturbed rats. Baroreceptor sensitivity was assessed as percentage HR and RSNA reductions per mmHg MAP elevation when a standardized phenylephrine infusion was performed. A state of acute “mental stress” could be induced by a likewise standardized sudden blowing of air. These two opposing influences on neurogenic cardiovascular control were also experimentally superimposed in various ways and the effects on MAP, HR and RSNA followed. During “rest” RSNA was higher in SHR than in WKY and it also increased more during “mental stress”. The baroreflex sensitivity was clearly reduced in SHR and WKY concerning HR reduction (0.44±0.06 vs. 0.78±0.08%/mmHg; p<0.01) but not so concerning RSNA, which was similar in SHR and WKY (2.6±0.2 vs. 2.9±0.4%/mmHg). If expressed (HR + 1±3%; p<0.025 vs. SHR and RSNA + 11%±10, p<0.01 vs. SHR). These results) (0.10±0.02 vs. 0.06±0.01 μV/mmHg; p<0.12). Also single fibre recordings in anaesthetized rats showed the same principle difference between SHR and WKY. Addition of “mental stress” during phenylephrine baroreflex activation clearly increased both HR (24±7%) and RSNA (114±21 %) in SHR, while almost no change then occurred in WKY (HR + 1±3%; p<0.025 vs. SHR and RSNA + 11%±10, p<0.01 vs. SHR). These results suggest that a modestly accentuated cortico-hypothalamic activity ordinarily prevails in SHR, explaining the suppressed baroreflex control of heart rate and the augmented sympathetic activity to e.g. renal and splanchnic areas. Further, environmental alerting stimuli induce in SHR more powerful defence reactions which, unlike the situation in WKY, readily overcome baroreflex inhibitory influences on sympathetic activity.