Runoff and leaching of atrazine and alachlor on a sandy soil as affected by application in sprinkler irrigation.

Rainfall simulation was used with small packed boxes of soil to compare runoff of herbicides applied by conventional spray and injection into sprinkler-irrigation (chemigation), under severe rainfall conditions. It was hypothesized that the larger water volumes used in chemigation would leach some of the chemicals out of the soil surface rainfall interaction zone, and thus reduce the amounts of herbicides available for runoff. A 47-mm rain falling in a 2-hour event 24 hours after application of alachlor (2-chloro-N-(2,6-diethylphenyl)-N-(methoxymethyl)-acetamide) and atrazine (6-chloro-N-ethyl-N'-(1-methylethyl)-1,3,5-triazine-2, 4-diamine) was simulated. The design of the boxes allowed a measurement of pesticide concentrations in splash water throughout the rainfall event. Initial atrazine concentrations exceeding its' solubility were observed. When the herbicides were applied in 64,000 L/ha of water (simulating chemigation in 6.4 mm irrigation water) to the surface of a Tifton loamy sand, subsequent herbicide losses in runoff water were decreased by 90% for atrazine and 91% for alachlor, as compared to losses from applications in typical carrier water volumes of 187 L/ha. However, this difference was not due to an herbicide leaching effect but to a 96% decrease in the amount of runoff from the chemigated plots. Only 0.3 mm of runoff occurred from the chemigated boxes while 7.4 mm runoff occurred from the conventionally-treated boxes, even though antecedent moisture was higher in the former. Two possible explanations for this unexpected result are (a) increased aggregate stability in the more moist condition, leading to less surface sealing during subsequent rainfall, or (b) a hydrophobic effect in the drier boxes. In the majority of these pans herbicide loss was much less in runoff than in leachate water. Thus, in this soil, application of these herbicides by chemigation would decrease their potential for pollution only in situations where runoff is a greater potential threat than leaching.

Hepatitis C antibodies in haemodialysis and pattern of end-stage renal failure in Gassim, Saudi Arabia.

As by the end of 1992, 96 (47 females; 49 females) patients were on regular dialysis treatment for end stage renal failure (ESRF) in 5 haemodialysis HD units, the Gassim region of Saudi Arabia. Because of lack of facilities, paediatric patients were under-represented, age range being 11 to 80 years. Systemic hypertension (47%), followed by hereditary/congenital conditions (23%) and non-insulin dependent diabetes mellitus NIDDM (19%) were the most common causes of ESRF in the region. One patients developed ESRF 14 years after donor nephrectomy. Overall prevalence of HCAb was 50% with a range of 17.24% to 83%. Based, especially, on the findings in two of the units which between them handle 57% (55/96) of the patients, we believe that the practice of machine isolation policy (MIP) rather than blood transfusion is largely responsible for this wide variation in prevalence between the centres. Considering the very high overall prevalence of the Kingdom, we suggest the MIP should no longer be optional and should be part of the universal infection precautions for HD patients. Comparing Gassim with findings from Taif, there may be some variation in the pattern of ESRF between different parts of the Kingdom. More reports will be needed to document this. Donor nephrectomy as a cause of ESRF is being recorded for the first time in the Kingdom. Vigilance is important. Similarly, we believe that sexual intercourse as a probable route of hepatitis C virus HCV transmission is being recorded for the first time in the Kingdom.

Gender-related differences in the baroreceptor reflex control of heart rate in normotensive humans.

The present study investigates the baroreceptor reflex control of heart rate (HR) of normotensive male and female human volunteers under two conditions: bolus- and infusion-evoked elevations of blood pressure by intravenous administration of phenylephrine. Average age and blood pressure were similar in both sexes, but females had a significantly lower heart period (HP; higher HR). A major difference existed between the two sexes when the blood pressure was elevated by the bolus method. Females had a significantly (50%) smaller baroreflex sensitivity (regression coefficient), which inferred a gender-related difference in baroreceptor reflex control of HR. However, because a positive correlation existed between basal HP and baroreflex sensitivity, it was important to investigate whether this difference was related to the significantly lower basal HP in females. This possibility was ruled out because a similar difference still existed when the data were collected from another group of females who had basal HP values similar to those of males. This gender-related difference in baroreceptor reflex control of HR seems to depend on the pattern by which the pressor stimulus is evoked. The baroreceptor HP response to a slowly developing pressor response that was maintained at a steady-state level was very similar in both sexes. Because the HP response to abrupt (bolus-evoked) pressor stimuli mainly reflects the activity of the vagal component, our findings suggest that the cardiac vagal component seems to play a substantially smaller role in the baroreflex-mediated bradycardia in females.

Vasopressin receptors in the area postrema differentially modulate baroreceptor responses in rats.

This study examined the effects of microinjection of [Arg8]vasopressin (AVP) into the area postrema (AP) on baroreceptor reflex control of heart rate (HR) and sympathetic efferent discharge (SED) in anesthetized rats. Comparable increments in blood pressure evoked by systemic AVP, as opposed to phenylephrine, were associated with significantly greater reflex bradycardia. Similarly, AVP augmented the baroreflex-mediated sympathoinhibition; however, this effect was evident only with the lower increments in arterial pressure (< 45 mm Hg) i.e. following systemic administration of small doses of AVP. Beyond 45 mm Hg there was no further augmentation of baroreflex-mediated sympathoinhibition showing the non-linearity of the response compared to phenylephrine which was linear over a wide range of induced pressure increases. Microinjection of AVP into the AP produced a differential effect on HR and SED responses to baroreceptor activation by systemically administered phenylephrine, the baroreflex slope of HR response was attenuated whereas that of SED was enhanced. Microinjection of the V1 antagonist AVPX (d(CH2)5Tyr(Me)-AVP) into the AP abolished the inhibitory effect of AVP on the baroreceptor-HR response suggesting that V1 receptors are involved in this response. Further, AVPX inhibited the baroreceptor-SED response suggesting that V1 receptors in the AP are tonically involved in modulating the baroreceptor reflex control of SED. Qualitatively similar but smaller responses were obtained following microinjection of AVP into the nucleus tractus solitarii (NTS) suggesting involvement of neural input from the AP to the NTS in AVP-evoked responses in the AP. It is concluded that the AVP receptors in the AP differentially modulates the baroreceptor reflex control of HR and SED.

Role of the sympathetic nervous system in ethanol-induced hypertension in rats.

The present study investigated the role of the sympathetic nervous system in the development of ethanol-induced hypertension (EIH) in the rat. Sympathetic nerve activity (SNA) as an index of central sympathetic tone was measured directly from the preganglionic fibers of the greater splanchnic nerve. Four weeks after starting ethanol feeding, and prior to the development of hypertension, SNA of the ethanol-fed rats was significantly greater than that of controls. The increase in SNA was also evident at the early stages of EIH, at 8 weeks, and in fully developed EIH, after 12 weeks of ethanol consumption. Baroreceptor reflex control of heart rate (HR) but not SNA was impaired prior to the development of EIH at 4 weeks. However, at 8 and 12 weeks, baroreflex control of HR and SNA was normal or slightly greater than that of control rats. Because arterial pressure of ethanol-fed rats was significantly higher than that of controls at 8 and 12 weeks, the data suggest that ethanol feeding caused baroreceptor resetting. Pressor responsiveness to phenylephrine was depressed before the development of EIH but was similar to that of control rats following the development of EIH. The data also shows that blood and plasma volumes of ethanol-fed rats at the times that coincided with the pre- and posthypertensive states were similar to those of control rats which suggests that the development of EIH does not involve an increase in plasma volume. It is concluded that an increase in SNA contributes to the development of EIH and that baroreceptor resetting evoked by ethanol feeding plays a permissive role in maintaining an elevated blood pressure in ethanol-fed rats.

Inadequate blockade by hexamethonium of the baroreceptor heart rate response in anesthetized and conscious rats.

The ability of hexamethonium (HEX) alone or in combination with atropine methylbromide (AMB) to block the heart rate (HR) response to baroreceptor activation by phenylephrine (PE) or angiotensin II (AII)-evoked increments in blood pressure was evaluated in rats. A highly significant negative correlation existed under control conditions between the changes in MAP and HR. HEX (10-20 mg/kg) did not influence the baroreceptor HR response of anesthetized and conscious rats, suggesting anesthesia was not involved in the failure of HEX to abolish the baroreceptor HR response. A combination of HEX and AMB (full ganglionic blockade) substantially attenuated but did not abolish the HR response to baroreceptor activation, but this effect was not significantly different from that produced by AMB alone. In a marked contrast to HEX, chlorisondamine (CHL) abolished the baroreceptor HR response both in anesthetized and in conscious rats. Efficacy of ganglionic blockade was tested by examining the effects of HEX or CHL on the frequency-bradycardic response relationship evoked by electrical stimulation of the peripheral end of the right vagus; HEX only attenuated the response whereas CHL abolished it. It is concluded that, even in doses which lower blood pressure, HEX: 1) does not adequately block the baroreceptor HR response; 2) when combined with a muscarinic blocker to induce full ganglionic blockade, the decrease in baroreceptor HR response is largely, if not totally, attributable to muscarinic blockade; 3) is much weaker than CHL in blocking ganglionic transmission and, even when combined with a muscarinic blocker, it does not abolish the baroreceptor HR response whereas CHL does, and 4) CHL represents a better choice for studies that require complete ganglionic blockade in anesthetized or conscious rats.

Impairment of central mediation of the arterial baroreflex by acute ethanol administration.

We investigated the possibility that the impairment of baroreflex control of heart rate was due to an action of ethanol on the central component of the baroreflex arc. Baroreceptors and baroreceptor afferents were removed from the arc by sino-aortic denervation and the central end of the left aortic depressor nerve was stimulated. Stimulation frequency response curves relating the decreases in blood pressure, heart rate and sympathetic efferent nerve discharge to the frequency of stimulation were constructed before and after the administration of 0.33, 0.66 and 1 g/kg of ethanol administered systemically. Except for a small decrease in blood pressure following the 1 g/kg dose, ethanol administration did not produce any change in baseline heart rate or blood pressure but the frequency response curve of heart rate was reset by the two lower doses of ethanol whereas the dose of 1 g/kg produced frank impairment of baroreflex control. Similarly the dose of 1 g/kg also impaired the depressor response to aortic nerve stimulation whereas it did not impair the baroreflex control of sympathetic efferent discharge. These data suggest a differential effect of ethanol on central pathways that control baroreflex responses. To ensure that the effect of ethanol was not due to an action of ethanol on an end organ, the heart, a separate group of rats were prepared with sino-aortic denervation and the peripheral end of the cut right vagus nerve was stimulated with increasing frequency. Ethanol did not affect the response to stimulation of the vagus nerve showing that the impairment of baroreflex control of cardiovascular variables was primarily of central origin.

A differential action for ethanol on baroreceptor reflex control of heart rate and sympathetic efferent discharge in rats.

The acute effects of ethanol (0.33, 0.66, or 1 g/kg) on baroreflex control of heart rate (HR) and sympathetic efferent discharge (SED) were investigated in chloralose-anesthetized rats. The two higher doses of ethanol caused a progressive and significant increase in baseline SED and a slight increase in HR. That these effects were ethanol mediated is suggested by the absence of any change in blood pressure following ethanol injection in any amount used and the finding that equivolume saline had no effect on any of the tested parameters. On the other hand, the baroreflex slope of the MAP-SED relationship after ethanol was similar to the control (preethanol) value in contrast to a significant decrease in the baroreflex slope of MAP-HR under the same conditions. These findings suggest that the sensitivity of the reflex control of SED was preserved whereas that of HR was impaired after acute ethanol administration. Since these findings were obtained in the same animals, our data suggest that acute ethanol has a differential action on reflex control of SED and HR. Further, the significant increase in SED after moderate and high doses of ethanol suggests an increased central sympathetic tone as recordings were made from preganglionic nerve fibers (splanchnic nerve). The absence of an increase in baseline MAP, in spite of a significant increase in baseline SED following acute ethanol injection, could be explained, at least in part, by an ethanol-evoked reduction in pressor responsiveness to phenylephrine, an alpha-adrenergic agonist.

Acute effects of ethanol on baroreceptor reflex control of heart rate and on pressor and depressor responsiveness in rats.

In rats anesthetized with alpha-chloralose, doses of 0.1, 0.5, and 1 g/kg of ethanol produced an upward shift of baroreflex curves constructed by plotting the heart rate response against mean arterial pressure following evoked rises in mean arterial pressures by phenylephrine or angiotensin II. Whereas the upward shift of baroreceptor curves may be related, at least in part, to a higher base-line heart rate after ethanol, the data showed that the 1 g/kg dose of ethanol significantly depressed baroreflex sensitivity, suggesting that higher doses of ethanol impair baroreflex-mediated bradycardia. The phenylephrine, but not the angiotensin II or the nitroprusside, dose-response curves were shifted to the right after ethanol, indicating a decreased pressor responsiveness and suggesting that ethanol may have alpha-adrenergic blocking activity. This effect was also obtained in conscious rats. That this effect was not influenced by changes in baroreflex sensitivity was supported by the finding that a similar shift of the phenylephrine pressor-response curve was obtained in bilaterally vagotomized and hexamethonium-treated rats. Whether this effect of ethanol on baroreflex control of heart rate was influenced by anesthesia was investigated in conscious rats; the 1 g/kg dose of ethanol that produced the most significant decrease in baroreflex sensitivity was used in these experiments. Ethanol was still able to significantly inhibit baroreflex sensitivity in conscious rats, but the upward shift of the baroreflex curve and the elevated base-line heart rate no longer occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acute ethanol administration on the baroreceptor reflex control of heart rate in normotensive human volunteers.

The effects of acute ethanol administration on blood pressure, heart rate and the baroreceptor reflex control of heart rate were studied in normotensive subjects who served as their own control. Baroreceptor reflex control of heart rate was measured by two methods: the ramp method and the steady state method. None of the doses of ethanol had any effect on blood pressure during the observation period, except for the highest dose where a slight elevation was evident for a short period of time. On the other hand, the heart rate showed a slight but consistent dose-related increase. In general, ethanol attenuated the baroreceptor mediated bradycardia but this effect was dependent on the way in which blood pressure was elevated. A dose-related impairment of baroreceptors was evident when the ramp method was used, i.e. ethanol significantly depressed baroreflex sensitivity, expressed as delta heart period (HP)/delta mean arterial pressure (MAP). In contrast, delta HP/delta MAP was not influenced by ethanol when the steady state method was used. However, the steady state baroreflex curves were reset about a higher median blood pressure (MAP50), suggesting that the baroreceptors will be operative at higher blood pressure levels after ethanol. The pressor responsiveness was also influenced differently by ethanol depending on the method of injecting phenylephrine. An increase in pressor responsiveness was evident, though not dose-related, after ethanol only when blood pressure was elevated by the ramp method, suggesting that the inverse relationship between baroreflex sensitivity and pressor responsiveness is more prominent with the ramp method and/or when impairment rather than resetting of baroreceptors occurs. That the decrease in baroreflex sensitivity and the increase in MAP50 were related to peak ethanol levels in blood and that the blood pressure was not influenced by ethanol strongly suggest these effects were ethanol mediated. The weakened buffering action of the baroreflexes would be expected to favour the development of higher blood pressure.

Similarities and differences in the effects of verapamil, diltiazem and nifedipine on arterial baroreflexes of anesthetized cats.

The effects of verapamil, diltiazem and nifedipine on baroreflex sensitivity (BS) were investigated in anesthetized cats at equihypotensive doses of 100, 100 and 10 micrograms/kg, respectively. The gain in BS (ms/mmHg) was calculated from the ratio delta heart period/delta systolic pressure following evoked rises and falls in arterial pressure. Verapamil and diltiazem significantly augmented BS while nifedipine depressed BS during evoked rises in arterial pressure. By contrast, BS was significantly depressed by diltiazem and nifedipine in response to depressor challenges with nitroprusside, while it was unaffected by verapamil. The augmentatory action of verapamil on BS after pressor challenges, was abolished by bilateral vagotomy while the inhibitory action of nifedipine was still evident after vagotomy, suggesting a vagal augmentatory action for verapamil and an involvement of the cardiac sympathetic nerves in the inhibitory action of nifedipine on BS. The differences between the actions of the 3 drugs on BS are not readily explainable by our data but they cannot be attributed to alterations of cardiac autonomic function since at the doses employed none of the drugs affected the cardiac responses to carotid occlusion, i.v. isoproterenol or electrical stimulation of the right vagus. It is concluded that BS is affected differently by the 3 chemically unrelated calcium channel blockers in a way which could either be contributory or deleterious to the antihypertensive effectiveness of these drugs.

Effect of chronic ethanol administration on arterial baroreceptor function and pressor and depressor responsiveness in rats.

The effect of chronic ethanol administration on arterial baroreflexes was investigated in rats. Comparison of the results with those obtained from rats kept on an isocaloric control diet revealed that chronic ethanol had a differential action on baroreflex sensitivity (BS). The BS after evoked graded rises in arterial pressure was inhibited significantly whereas that tested after an evoked fall in arterial pressure was augmented significantly in chronic ethanol rats. These changes in BS were not secondary to changes in blood pressure as resting arterial pressure was similar in both groups. However, the heart rate was slightly, but significantly lower in the ethanol group. Challenging isocaloric control and chronic ethanol rats with an acute dose of 0.5 g/kg of ethanol produced nonsignificant changes in BS when evoked changes in blood pressure were both pressor and depressor. A dose of 3 g/kg of ethanol decreased the BS tested after phenylephrine-evoked rises in pressure in both groups; however, the percentage of inhibition of BS was greater in the isocaloric control group. The pressor responsiveness to phenylephrine was reduced slightly in chronic ethanol-treated rats, in contrast to that evoked by angiotensin II which was augmented slightly as compared to the control group. There was no significant difference in the depressor responsiveness to nitroprusside. After injection of acute doses of 0.5 and 3 g/kg of ethanol, the dose-response curves to phenylephrine were shifted to the right in a dose-related fashion in both groups, whereas the angiotensin II and nitroprusside dose-response curve remained unchanged after 0.5 g/kg of ethanol in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)