Separate hemodynamic roles for chloride and sodium in deoxycorticosterone acetate-salt hypertension

It has been reported that both sodium and chloride ions must be ingested to induce the elevated blood pressure of deoxycorticosterone acetate (DOCA)-salt-sensitive hypertension. This study was designed to determine the separate roles of the sodium and chloride ions in the altered hemodynamics underlying the high blood pressure. DOCA pellets (75 mg) were implanted in uninephrectomized rats and the animals were then fed one of four diets: (i) high sodium chloride, (ii) high sodium-low chloride, (iii) high chloride-low sodium, or (iv) low sodium chloride. Blood pressures were measured weekly by tail-cuff plethysmography for 5 weeks and the animals were then subjected to a terminal experiment to measure cardiac output by thermodilution technique, renal blood flow by electromagnetic flow probe, and direct arterial pressure. Blood pressure in the DOCA-high NaCl group was significantly greater (P less than 0.05) compared with that of the DOCA-low NaCl group (160 +/- 3 mm Hg vs 124 +/- 2 mm Hg, respectively) at 5 weeks after treatment; all other groups were not significantly different from the DOCA-low NaCl group. Cardiac output was significantly greater in DOCA-treated rats consuming diets high in sodium (44 +/- 2 ml/min/100 g) or sodium chloride (40 +/- 2 ml/min/100 g) compared with animals consuming low sodium chloride (31 +/- 2 ml/min/100 g; P less than 0.01 for each comparison). Direct intraarterial blood pressure and renal blood flow were used to calculate renal vascular resistance. Renal vascular resistance was increased in those DOCA-treated rats consuming diets high in chloride (42 +/- 3 mm Hg/ml/min/100 g) and high sodium chloride (54 +/- 3 mm Hg/ml/min/100 g) compared with rats consuming low sodium chloride (30 +/- 3 mm Hg/ml/min/100 g; P less than 0.01 for each). It appears that elevations in cardiac output are associated with increased dietary sodium and act in synergy with the elevations in renal vascular resistance associated with increased dietary chloride. Increases in both cardiac output and renal vascular resistance are involved in the maintenance of elevated blood pressure in the DOCA-salt-sensitive model of hypertension.     

Seasonal variation of cardiovascular function in the marmot, Marmota flaviventris

Monthly measurements of heart rate, mean arterial pressure, and cardiac output were made on active and hibernating marmots from the time of emergence from hibernation through the next hibernation period. From these measurements cardiac index, stroke index, and total peripheral resistance were calculated on the basis of estimated lean body mass. Heart rate was low after emergence (132 +/- 9.5 beats (B)/min), peaked in August (160 +/- 9.3 B/min), and then fell slightly in September and October. During hibernation heart rate fell to 9 +/- 1.1 B/min. Mean arterial pressure, which was low in early spring (101 +/- 6.9 mm Hg), rose to a peak value in June (131 +/- 7.7 mm Hg) and remained essentially unchanged until hibernation when it fell to 52 +/- 4.0 mm Hg. Cardiac index (61 +/- 4.9 ml/kg min) in March rose to a peak in May (83 +/- 8.5 ml/kg min) and fell linearly until October. There was an additional drop in cardiac index during hibernation (7.6 +/- 0.9 ml/kg min). Total peripheral resistance increased linearly from the time of emergence until October. Most of this change was due to the decrease in cardiac index. Stroke index showed no significant changes in the prehibernation period, but increased by 55% during hibernation. Maintenance of arterial pressure in the months preceding hibernation in the face of diminishing cardiac index indicate that alterations in vasomotor tone or shifts in patterns of blood flow occurred prior to the hibernation period.     

Impaired vascular dynamics in normotensive diabetic rats induced by streptozotocin: tapered T-tube model analysis

This study is to explore the changes of arterial mechanical properties in streptozotocin (STZ)-diabetic rats, based on the exponentially tapered T-tube model. Rats given STZ 65 mg kg(-1)i.v. are compared with untreated weight- and age-matched controls. A high-fidelity pressure sensor and electromagnetic flow probe measured pulsatile pressure and flow waves in the ascending aorta, respectively. Diabetic rats exhibit isobaric vasodilatation that is characterized by an increase in cardiac output and no significant changes in aortic pressure. Total peripheral resistance of diabetic rats is lower than that of weight- and age-matched controls. Diabetic rats have higher total peripheral compliance (2.86+/-0.70 microl mm Hg(-1)) than do weight- (1.77+/-0.34 microl mm Hg(-1)) and age-matched (1.87+/-0.69 microl mm Hg(-1)) controls. Aortic characteristic impedance is reduced from 0.017+/-0.003 mm Hg min kg ml(-1)in weight- and 0.020+/-0.004 mm Hg min kg ml(-1)in age-matched controls to 0.010+/-0.004 mm Hg min kg ml(-1)in diabetic rats. Moreover, diabetic rats show shorter wave transit time in lower body circulation (17.86+/-1.91 ms) than do weight- (20.45+/-1.91) and age-matched (23.05+/-2.04 ms) controls. Under isobaric vasodilatation, the decreased resistance and increased compliance in peripheral circulation suggest that the contractile dysfunction of the smooth muscle cells may occur in resistance arterioles in diabetes. With unaltered aortic pressure, an impairment in aortic distensibility of STZ-diabetic rats is manifest on the reduced wave transit time rather than on the diminished aortic characteristic impedance.     

Initial cardiovascular response on change of posture from squatting to standing

The immediate cardiovascular responses on active change from the squatting (control) to the standing position differ from those obtained in the lying-to-standing manoeuvre. Without exception, the first beat after changing from squatting to standing showed a decrease in systolic, diastolic and mean pressure by 2.0 +/- 1.1 kPa (14.6 +/- 8.3 mm Hg), 1.4 +/- 1.7 kPa (10.6 +/- 12.6 mm Hg) and 1.9 +/- 1.0 kPa (13.9 +/- 7.3 mm Hg), respectively. During the 4th or 5th pulse after standing the pulse pressure was significantly higher than when lying (P less than 0.01). Mean pressure reached a minimum of 7.7 +/- 1.9 kPa (57.8 +/- 14.4 mm Hg) after 7.1 +/- 1.1 s. Thereafter the blood pressure increased to a new level within about 15 s. 11 of 16 subjects demonstrated a biphasic heart rate (HR) response. The maximum HR was reached after 11.0 +/- 2.4 s of standing. In all experiments, the peaks in HR were distinctly delayed after the blood pressure dips. We conclude that an arterial baroreflex could be implicated in the immediate HR increase after a squatting-to-standing manoeuvre. The subsequent time course of the initial HR response, however, might be induced by other mechanisms.     

Effects of forskolin on placental vascular resistance in rabbits

Forskolin is a direct stimulant of adenylate cyclase and increases cAMP production. It also acts as a vasodilator. To study the effect of forskolin infusion on rabbit maternal vascular resistance, we instrumented 11 pregnant rabbits with catheters in the left ventricle, jugular vein, and left and right femoral arteries. After a 2-day recovery period, one of two protocols was performed. In the control period of the first protocol (N = 6), 50% ethanol in saline was infused at 0.103 ml.min-1 for 5-min. Forskolin (10(-3) M) in 50% ethanol was then infused for 5 min at 0.103 ml.min-1. After each infusion period, regional blood flows were measured by microsphere injection. Data are expressed as means +/- SEM. Blood pressure decreased from 81 +/- 3 to 79 +/- 3 mm Hg, (P less than 0.05, N = 10) during forskolin infusion. Total placental resistance fell from 180.3 +/- 10.7 to 133.8 +/- 12.0 mm Hg.min.ml-1 per gram, P less than 0.05. Cerebral, coronary, and renal vascular resistance fell significantly. During the second protocol (N = 5), angiotensin II (0.05 microgram.min-1) was infused for 5 min followed by the addition of forskolin (10(-3) M at 0.103 ml.min-1) to the infusate. Regional blood flows, vascular resistances and blood pressures were determined. Blood pressure fell from 99 +/- 6 to 92 +/- 7 mm Hg (P less than 0.05) when forskolin was added to the infusate. Placental resistance fell from 202.5 +/- 21.6 to 158.0 +/- 29.0 mm Hg.min.ml-1 per gram (P less than 0.05). While cerebral vascular resistance did not change, renal and coronary resistances fell in response to forskolin. This study demonstrates that forskolin is able to dilate rabbit placental vessels alone and in the presence of the vasoconstrictive agent angiotensin II.     

Cardiopulmonary response to an induced pulse in intracranial pressure

Increased intracranial pressure may result in the Cushing response. We applied a short pulse of pressure to the cranial cavity of anesthetized cats which were intubated, curarized, ventilated, and the cranium exposed to an 80- to 100-msec pulse of pressure at 5.3 atm. The following significant increases developed: Intracranial pressure rose from 7.4 +/- 1.5 to 150.6 +/- 19.4 mm Hg, systolic arterial peak pressure from 130.7 +/- 8.1 to 299.0 +/- 11.4, pulmonary peak pressure from 18.9 +/- 1.9 to 42.9 +/- 4.9. Alveolar lavage protein in controls was 6.7 +/- 0.4 mg/g lung compared to 11.9 +/- 2.0 in the experimental group. Extravascular lung water/dry weight ratios increased from 3.36 +/- 0.04 in controls to 3.51 +/- 0.09 but varied inversely with pulmonary systolic peak pressure (r = 0.59). These results showed that a pulse of pressure applied to the cranium of cats produced lung edema which was inversely related to pulmonary artery pressures.     

Systemic blood pressure response to the inhibition of two hyperpolarizing pathways: a comparison to NO-synthase inhibition

The impact on blood pressure of two vasodilating mechanisms, underlied by vascular smooth muscle hyperpolarization, was studied and compared to that induced by nitric oxide NO mechanism. Systemic blood pressure, after inhibitory intervention in arachidonic acid metabolism cytochrome P-450 inhibition by miconazole 0.5 mg/100 g b.w. , one of the hyperpolarizing pathways, did not change. After the inhibition of the action voltage-dependent K(+) channels operator by 4-aminopyridine 0.1 mg/100 g b.w. , the other hyperpolarizing pathway, blood pressure declined slightly from 132.3+/-3.2 mm Hg to 116.5+/-5.0 mm Hg, P<0.05 . Inhibition of nitric oxide production L-NAME 5 mg/100 g b.w. increased blood pressure considerably 123.5+/-2.7 mm Hg to 155.4+/-3.1 mm Hg, P<0.001 . After inhibition of the hyperpolarizing pathway by miconazole, hypotension induced by acetylcholine (Ach, 10 microg represented 63.0+/-1.9 mm Hg vs control value 78.6+/-5.2 mm Hg P<0.001 , by bradykinin (BK) 100 microg 59.4+/-3.9 mm Hg vs control value 71.2+/-6.1 mm Hg P<0.05 . After inhibition of the hyperpolarizing pathway by 4-aminopyridine, hypotension induced by ACh 10 microg achieved 64.6+/-2.5 mm Hg vs control value 78.4+/-2.8 mm Hg P<0.001 and that induced by BK 100 microg 56.6+/-5.3 mm Hg vs control value 72.3+/-2.5 mm Hg P<0.001 . ACh or BK hypotension after the inhibition of the above hyperpolarizing pathways was significantly attenuated. On the contrary, after NO-synthase inhibition the hypotension to ACh was significantly enhanced. Blood pressure decrease after ACh 10 microg hypotension was 91.8+/-4.1 mm Hg vs control value 79.3+/-3.3 mm Hg P<0.01 , and after BK 100 microg it was 78.4+/-7.1 mm Hg vs control value 68.3+/-5.2 mm Hg. A different basal BP response, but equally attenuated hypotension to Ach and BK, was detected after the inhibition of two selected hyperpolarizing pathways. In cotrast, the inhibition of NO production elicited an increase in systemic BP and augmentation of ACh and BK hypotension. The effectiveness of further hyperpolarizing mechanisms in relation to systemic BP regulation and nitric oxide level remains open.     

Interrelationships among cardiohaemodynamic parameters in human postnatal ontogenesis

In one-day old humans and to 20 years of age, the stroke volume (SV) increases from 5.4 +/- 0.4 to 70 +/- 5 ml, the arterial systolic pressure (ASP)--from 60 +/- 5 to 120 +/- 10 mm Hg. Heart rate decreases to 70 +/- 4/min from 136 +/- 10/min at birth. The N coefficient as the SV/ASP ratio parameter grows from 0.1 in children to 0.6 by 20 years of age. The peripheral resistance in the arterial system scope from the left ventricle exit tract to the middle of the humeral artery amounts up to 76 mm Hg x ml(-1) x min(-1) in newborn infants and in adults it is reduced to 28. Reduction of post-load decreases 6-fold the total amount of the heart mechanical work of pumping the SV into the vascular system.     

Cardiovascular responses to catecholamines at 12 degrees C in the American bullfrog (Rana catesbeiana)

The effects of epinephrine, norepinephrine, phenylephrine, and isoproterenol on blood pressure and heart rate were studied in cannulated American bullfrogs, Rana catesbeiana. The bullfrogs were chronically cannulated with a T cannula in the right sciatic artery. In warm-acclimated (22 degrees C) bullfrogs, preinjection mean systemic arterial pressure (SAP) prior to experimental treatment was 13.1 +/- 0.7 mm Hg. Preinjection heart rate was 34.8 +/- 1.8 beats per minute. These parameters were lower in cold-acclimated (12 degrees C) bullfrogs. Cold-acclimated animals had mean SAP values of 8.2 +/- 0.3 mm Hg, and heart rate was 11.1 +/- 1.1 beats per minute. Epinephrine, norepinephrine, and phenylephrine increased blood pressure to an equivalent degree in warm- and cold-acclimated animals. Dose-related decreases in heart rate in response to these catecholamines were observed in warm- but not in cold-acclimated bullfrogs. Warm-acclimated animals were more responsive to isoproterenol from 0.03 micrograms/kg body weight (bw) to 10 micrograms/kg bw than were cold-acclimated animals. The response to isoproterenol was effectively blocked by propranolol (5 mg/kg bw) in both warm- and cold-acclimated animals. Propranolol alone decreased mean SAP in both warm- and cold-acclimated animals, suggesting blockade of endogenous sympathetic activity. Beta receptor response thus appears diminished, but not absent at 12 degrees C. However, the alpha receptors responsible for elevation of blood pressure equally responsive at 12 degrees and 22 degrees C.     

Effects of calcitonin gene-related peptide on renal blood flow in the rat

The effects of alpha-rat calcitonin gene-related peptide (alpha-rCGRP) on systemic and renal hemodynamics and on renal electrolyte excretion were examined in normal anesthetized rats. In one group of rats (n = 7), infusions of alpha-rCGRP at doses of 10, 50, 100, and 500 ng/kg/min for 15 min each produced dose-related and significant decreases in mean arterial pressure from a control of 130 +/- 3 mm Hg to a maximal depressor response of 91 +/- 2 mm Hg. During the first three doses of alpha-rCGRP, renal blood flow progressively and significantly increased from a control of 5.0 +/- 0.3 ml/min to a peak level of 6.3 +/- 0.3 ml/min achieved during the 100 ng/kg/min infusion. With the highest infusion rate of 500 ng/kg/min, renal blood flow fell below the control level to 4.5 +/- 0.2 ml/min (P less than 0.05). The responses in renal blood flow and mean arterial pressure were associated with reductions in renal vascular resistance. After cessation of alpha-rCGRP infusions, arterial pressure, renal blood flow, and renal vascular resistance gradually returned toward the baseline values. In another group of rats (n = 9), infusion of alpha-rCGRP for 30 min at 100 ng/kg/min produced a significant reduction in urinary sodium excretion from 0.28 +/- 0.06 to 0.14 +/- 0.5 muEq/min (P less than 0.05). Urine flow and urinary potassium excretion also appeared to decrease, but the changes were not significantly different (P greater than 0.05) from their respective baselines. These results demonstrate that alpha-rCGRP is a potent and reversible hypotensive and renal vasodilatory agent in the anesthetized rat. The data also suggest that alpha-rCGRP may have significant effects on the excretory function of the kidney.     

Haemodynamics in the first seconds after coronary artery occlusion.

The changes in cardiac and in total haemodynamics, occurring during the first seconds of occlusion and the subsequent desocclusion of coronary arteries were studied on 28 dogs. The most intensive changes were observed after the trunk occlusion of the left coronary artery. Simultaneously with decreasing blood inflow into the myocardium its contractility and the systolic pressure in the left ventricle and the outflow from the coronary sinus began to fall rapidly. The systolic pressure in the left ventricle decreased within the first 10 s from 24 to 13-15 kPa (180 to 100-110 mm Hg), which means that the systolic pressure fell about 1 kPa (7-8 mm Hg) per second, or 0.5-0.6 kPa (4-5 mm Hg) per systole. At the same time the end-diastolic pressure in the left ventricle also increased from zero to 3-4 kPa (25-30 mm Hg). After the trunk desocclusion of the left coronary artery the systolic pressure in the left ventricle proceeded to fall by about 2-3 kPa (15-22 mm Hg). Only then, 20-25 s after the desocclusion, blood flow in the left coronary artery began to rise intensively and 4-6 s later the myocardial contractility and the systolic pressure in the left ventricle also increased. After unclamping (50-60 s), there was an overshoot of haemodynamic values above preocclusive values and then followed the compensatory phase. This phase lasted 80-90 s and on its peak the pressure and flow parameters increased by about 50-60% above preocclusive values. During the occlusion of ramus interventricularis anterior or ramus circumflexus for 30-60 s the haemodynamic parameters changed only slightly. The same was observed during trunk occlusion of the right coronary artery (30-60 s), but in that case many extrasystoles occurred.     

The red wine antioxidant resveratrol protects isolated rat hearts from ischemia reperfusion injury.

The consumption of red wine has been reported to impart a greater benefit in the prevention of coronary heart disease than the consumption of other alcoholic beverages. This beneficial effect is increasingly being attributed to certain antioxidants comprising the polyphenol fraction of red wine such as transresveratrol. In the present study, we investigated the potential cardioprotective effects of resveratrol in the face of ischemia reperfusion (I/R) injury. Isolated perfused working rat hearts after stabilization were perfused with Krebs-Henseleit Bicarbonate buffer (KHB) either in the presence or absence of transresveratrol (RVT) at a concentration of 10 microM for 15 min prior to subjecting them to 30 min of global ischemia followed by 2 h of reperfusion. Left ventricular functions were monitored at various timepoints throughout the reperfusion period to assess the extent of postischemic recovery in comparison with baseline values. Coronary perfusate samples were also collected to determine malonaldehyde (MDA) levels. The results demonstrated that RVT exhibited significant myocardial protection. This was evidenced by improved recovery of post-ischemic ventricular function including developed pressure and aortic flow as compared to the control group (KHB). Values for developed pressure in the RVT-treated group were significantly higher than those in the control group throughout the reperfusion period (71.09+/-4.88 mm Hg vs. 58.47+/-3.88 mm Hg, 68.87+/-5.07 mm Hg vs. 49.74+/-2.65 mm Hg and 51.67+/-3.95 mm Hg vs. 30.50+/-4.80 mm Hg at reperfusion timepoints R-15, R-60, and R-120, respectively). From R-30 onwards, aortic flow was markedly higher in the RVT treated group as compared with the control group, the differences being most significant at R-90 (32.45+/-2.19 ml/min vs. 19.83+/-1.62 ml/min) and R-120 (27.15+/-2.27 ml/min vs. 14.10+/-1.69 ml/min). In contrast to the KHB treated group, the RVT-treated group displayed significant reduction in MDA formation especially in the immediate early reperfusion period (63.71+/-8.19 pM/ml vs. 130.86+/-4.76 pM/ml, 63.84+/-15.62 pM/ml vs. 156.99+/-18.93 pM/ml, 71.29+/-2.80 pM/ml vs. 129.5+/-10.30 pM/ml and 56.25+/-5.79 pM/ml vs. 127.99+/-3.50 pM/ml at timepoints R-1, R-3, R-5, and R-7, respectively) indicating a reduction in I/R injury related oxidative stress. Infarct size was markedly reduced in the RVT group when compared with the control group (10.57+/-0.35% vs. 36.27+/-5.28%). In vitro studies revealed RVT to be a potent scavenger of peroxyl radicals suggestive of a probable mechanism involved in the protective ability of RVT. The results of this study indicate that resveratrol possesses cardioprotective effects which may be attributed to its peroxyl radical scavenging activity.     

Relative influence of carotid baroreceptors and muscle receptors in the control of renal and hindlimb circulations.

In vagotomized dogs, a comparison was made of the relative ability of the carotid baroreceptors and of the receptors in skeletal muscles to cause constriction of the renal and hindlimb resistance vessels. With kidney and hindlimb perfused at constant pressure a decrease in pressure in the carotid sinuses from 250 to 40-45 mm Hg (1 mm Hg = 133 N/m2) caused the respective blood flows to increase by 19 +/- 6% and 80 +/- 4% (mean +/- SE), and stimulating muscle receptors with capsaicin caused a further decrease of 49 +/- 9% and 4 +/- 2%, respectively. With perfusion at constant flow, the baroreflex caused an increase of 34 +/- 4 mm Hg in the renal perfusion pressure and of 99 +/- 10 mm Hg in the hindlimb; capsaicin caused further increases of 203 +/- 17 and 35 +/- 9 mm Hg; respectively. These responses were abolished by sympathectomy. Capsaicin injection increased mean renal sympathetic nerve activity by 111 +/- 16% over the maximal impulse frequency recorded when the carotid sinus pressure was 40-45 mm Hg. Thus, withdrawal of the restraint exerted by the carotid baroreceptors on the pool of central neurons controlling the vascular beds of the hindlimb and kidney leads to near maximal constriction of the resistance vessels in the former bu not the latter; with strong activation of muscle receptors, near maximal constriction occurs in both beds.     

Accuracy of interface pressure measurement systems

Interface pressure measurement is needed to assess beds designed to prevent pressure sores, so it is therefore important to establish the accuracy of interface pressure measuring systems. In this study, the Talley SA500 pressure evaluator (with 28 mm and 100 mm sensor pads), the DIPE (with 100 mm sensor pad), and a water-filled bladder system (with 0.1 ml and 0.3 ml water) were assessed. Measurement errors were evaluated using a loading system with pressures up to 7.4 kPa (55 mm Hg) in steps of 0.9 kPa (6.9 mm Hg). All systems tested over-measured interface pressure, the error being approximately linearly proportional to the loading pressure. The repeatability for a given system was approximately constant. The mean error (± SD) (%) and repeatability (kPa) for the systems were: 28 mm Talley 12 ± 1%, ± 0.07 kPa; 100 mm Talley 15 ± 1%, ± 0.07 kPa; DIPE 27 ± 3%, ± 0.12 kPa; 0.1 ml water bladder 17 ± 1%, ± 0.13 kPa; 0.3 ml water bladder 26 ± 3%, ± 0.07 kPa. Different interfaces affected accuracy markedly, and repeatability was affected when an inhomogeneous interface was used. The study shows that the errors associated with interface pressure measurement systems can be substantial, and can vary from one system to another.     

Dependence of the parameters of microcirculation and lymph flow in the liver on the value of venous pressure

In experiments on cats the perfusion (at a constant flow and controlled venous outflow) of haemodynamic isolated liver was carried out. It was shown that at the levels of venous pressure in the liver 0, 2, and 4 mm Hg, the lymph flow (22.8 +/- 3.5, 41.8 +/- 5.7 and 57.6 +/- 8.6 mkl.min-1.100 g-1, respectively) was depended on the value of hydrostatic pressures in the sinusoids (1.4 +/- 0.1, 3.3 +/- 0.1, and 5.4 +/- 0.1 mm Hg, respectively) and did not depend on the value of sinusoidal filtration coefficient (0.421 +/- 0.029, 0.473 +/- 0.036, and 0.474 +/- 0.034 ml.min-1.mm Hg-1.100 g-1, respectively).     

Losartan decreases glomerular filtration rate in isolated perfused porcine slaughterhouse kidneys

We investigated whether Losartan, an angiotensin II (Ang II) AT1 receptor antagonist, decreases renal vascular resistance (RVR) and increases glomerular filtration rate (GFR) in isolated perfused porcine slaughterhouse kidneys (11 control experiments and 11 Losartan experiments with 7.5mg Losartan in the preservation solution and 100(g/minute Losartan infused during perfusion). With perfusion, plasma renin activity (PRA) increased markedly from 3 +/- 1 to 90 +/- 17 ng Ang I/ml/h (control), and from 4 +/- 1 to 70 +/- 8 ng Ang I/ml/h (Losartan), plasma Ang II increased from 86 +/- 63 to 482 +/- 111 pg/ml (control), and from 73 +/- 42 to 410 +/- 91 pg/ml (Losartan). The GFR was decreased in Losartan experiments as compared with control experiments (5 +/- 1 versus 10 +/- 2 ml/min/100g kidney wt; p < 0.05). The RVR was the same in both groups (0.2 +/- 0.01 mm Hg/100g kidney wt/min/ml). Tubular sodium reabsorption was decreased in Losartan experiments as compared with control experiments (0.7 +/- 0.1 versus 1.4 +/- 0.3 mmol/min/100g kidney wt). Overall, Losartan accentuated pathophysiological signs of acute renal failure. Although other drugs have to be investigated, these results suggest that porcine slaughterhouse kidneys could be useful as a tool for research in areas such as transplantation and intensive-care medicine.     

The strength of the aortic media and its role in the propagation of aortic dissection

The elastic properties of the thoracic aorta are well known, but this is the first study of the inherent strength of the tunica media. The latter is crucial to understand how dissecting aneurysms occur. Pressure-volume (P-V) measurements were recorded as a dilute suspension of India ink was infused into the tunica media using a constant flow pump (0.21 or 0.88 ml min-1) attached to a 20 G needle inserted into the media. Tests done on 31 opened pig upper descending thoracic aortas showed the peak pressure to tear the media averaged 77.2 +/- 1.5 kPa (579 mm Hg). The initial slope of the P-V curve revealed the average distensibility of the media of 3.02 +/- 0.28 (MPa)-1. The work per unit area of tissue required to propagate a tear in the aorta was 15.9 +/- 0.9 mJ cm-2. These values were independent of the tear depth at the 95% confidence interval.     

Cardiovascular responses to an isosterically modified prostaglandin analog in conscious dogs

The cardiovascular effects of oral and intravenous administration of 0.05 and 0.1 mg/kg of the isosterically modified prostaglandin (PG) analog, (+)- 4-(3-[3-[2-(1-hydroxycyclohexyl)ethyl]-4-oxo-thiazolidinyl] propyl) benzoic acid were ascertained in conscious mongrels. After 0.05 mg/kg p.o., mean arterial pressure (MAP), obtained from indwelling catheters, fell from 105 +/- 1 to 100 +/- 4 mm Hg and total peripheral resistance (TPR) decreased from 0.062 +/- 0.006 to 0.039 +/- 0.002 mm Hg/ml/min. Cardiac output (CO), measured via electromagnetic flow probes, rose from 1.8 +/- 0.2 to 2.6 +/- 0.1 l/min and heart rate from 109 +/- 13 to 128 +/- 8 beats/min. The 0.1 mg/kg p.o. dose produced similar results. Intravenous injection of 0.1 mg/kg immediately dropped MAP from 103 +/- 6 to 58 +/- 3 mm Hg and TPR from 0.049 +/- .006 to .014 +/- .002 mm Hg/ml/min. CO climbed from 2.3 +/- 0.2 to 5.3 +/- 0.5 l/min and HR increased from 126 +/- 9 to 254 +/- 14 beats/min. Stroke volume was not affected by either oral or intravenous administration of the PG analog. Pretreatment with 100 micrograms/kg timolol blunted the CO and HR responses to 0.1 mg/kg iv of the PG analog without affecting the depressor response. Metaraminol infused during injection of 0.1 mg/kg iv of the PG analog diminished all responses. When compared to the cardiovascular effects of hydralazine and nitroprusside, the profile of the PG analog activity closely resembled that produced by the arterial vasodilator, hydralazine; in contrast, nitroprusside (which also dilates veins) reduced stroke volume, but did not significantly affect HR. In conclusion, dilation of the resistance vessels by the PG analog decreased MAP and TPR and reflexly elevated CO and HR in conscious dogs.     

Long-term effects of betamethasone on blood pressure and hypothalamo-pituitary-adrenocortical function in spontaneously hypertensive and normotensive rats

An enhanced hypothalamo-pituitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure in spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 weeks of age, the rats were treated with 0.1 and 0.5 microgram betamethasone per milliliter drinking water for 7 weeks. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 +/- 3.9 (mean +/- SEM) to 203.1 +/- 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 +/- 4.0 mm Hg in response to 0.5 microgram betamethasone per milliliter drinking water. In WKY, blood pressure increased from 134.4 +/- 3.3 to 148.2 +/- 3.0 and 157.9 +/- 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 +/- 2.1 to 136.3 +/- 3.2 and 135.6 +/- 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all three strains. Stress-induced secretion of adrenocorticotropin was markedly reduced by 0.5 microgram betamethasone per milliliter in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.     

Baseline pulmonary physiologic values for the squirrel monkey (Saimiri sciureus).

Baseline pulmonary physiologic values were determined on 43 (421-910 g) male and 47 (425-604 g) female squirrel monkeys (Saimiri sciureus). Respiratory rate was found to be 55 +/- 1.9 (SE) breaths per minute for males and 58 +/- 1.7 breaths per minute for females. Tidal volume was 8.9 +/- 0.37 ml for males and 7.5 +/- 0.28 ml for females. Airway resistance for the male was 0.052 +/- 0.006 cm H2O/ml/second; while for the female it was 0.086 +/- 0.011 cm H2O/ml/second. Dynamic compliance was found to be 1.78 +/- 0.15 ml/cm H2O for males and 1.48 +/- 0.124 ml/cm H2O for females. An index of distribution of ventilation was 48 +/- 2.5 breaths for males and 42 +/- 1.7 breaths for females.